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Thursday, April 21, 2011

Re: [ALOCHONA] Muslim women should be thankful to France.--Your disparagement show you lack civility; you lack decency in your language.



If religious dogmatism is better than,

 

Prosperity

Employment

Knowledge

Education

Honour

Dignity

Equality

Social Security

Rule of Law

Security

 

 Please go for it.

 

Akbar Hussain

 



On Tue, Apr 19, 2011 at 8:11 AM, S A Hannan <sahannan@sonarbangladesh.com> wrote:
 

Per capita income does not determine happiness or peace. Most French and for that matter ultra-materialized western people live  like animals, just eat and drink and die, no higher objective in life.

People in my own village are much happier though they are just lower middle class people.

Akbar Hossain, it does not behove you to say that French are not investing in Jannat, none has requested them to do so. Your disparagement show you lack civility; you lack decency in your language.

 

Shah Abdul Hannan

 


From: alochona@yahoogroups.com [mailto:alochona@yahoogroups.com] On Behalf Of Akbar Hussain
Sent: Monday, April 18, 2011 1:05 AM
To: alochona@yahoogroups.com
Subject: Re: [ALOCHONA] Muslim women should be thankful to France.

 

 

France has a population of 65 million and a few thousand of them occasionally goes naked in the secluded areas. This you know very well because this is very sensational for people like you. But you do not know that they have a per capita income of 33000.00 USD and only 6.2 pc lives below poverty line. I hope you know their standard of poverty line. If today France announce that they will take 5 million Muslim immigrants from Indonesia to Morocco how may of your imander brothers and sisters are going to apply to migrate?  The reason for your anger may be that the French people are not investing in the jannats where you want to go after death. When this burden of ignorance will go away?

 

Akbar Hussain

 

 

On Sun, Apr 17, 2011 at 2:49 AM, Mohammed Ramjan <mramjan@hotmail.com> wrote:

 

Mr. Akbar Hussain
 
Long writing no time to read.
 
Mulla is follower of Islam. Islam is the only way of life piece for the human being in all respects.
 
French Ban Veil, they will , because they decayed, one island in Frence for nudity, man and women run in the jungle in nude state so how they will allow veil ?
 
Know thyself
 
Mohamed Ramjan
 
Kuwait
 

 


To: alochona@yahoogroups.com
From: akbarh1950@gmail.com
Date: Tue, 12 Apr 2011 21:15:26 -0400
Subject: [ALOCHONA] Muslim women should be thankful to France.



 

The French ban on Islamic veil is in effect from 11 Apr. By law it has been prohibited and any violation will face penalties. The mullahs are cursing France by asking Allah's wrath in the country. As per the statistics the handful of Muslim women who wear niqab or veil are numbering around 2000 only. But the western world, especially France has taken such a stern measure against this primitive practice? The rise of extremist Islam since 9/11 has taken a vow to establish a brand of Islam rooted in the 7th century Arabian culture and according to them veil is an essential part of it. The social and cultural history of the Arabs does not essentially mention this practice.

Veiling did not exist in early Arabia, but Mohammed admonished women to cover them modestly, and his own wives were veiled in public. Mohammed's wives set the example, and gradually the veil became a sign of prestige.

 

Adherence to traditional dress varies across Arab societies. Saudi Arabia is more traditional, while Egypt is less so. Women are required to wear abayas in only Saudi Arabia; this is enforced by the religious police. This restricts their economic participation and other activities and also demeans them as equal citizens. In most countries, like Kuwait, Lebanon, Libya, Jordan, Syria and Egypt, the veil is not mandatory. In Tunisia, the secular government has banned the use of the veil in its opposition to religious extremism. Former Tunisian President called the veil sectarian and foreign and has stressed the importance of traditional Tunisian dress as a symbol of national identity. Islamic feminism counters both sorts of externally imposed dress codes.

 

Outside the Arab world veil was never a dress for the women. When Islam was shipped to those lands the preachers made the Arab culture an essential part of it.In the contemporary world where the importance of an individual has become an important issue this veil negates the very foundation of the principles of individualism. In the western world the practice wearing veil in public simply voids the existence of a person.

 

The enlightened and open minded Muslims denounce veil as oppressive and shameful. The important reason to denounce it because any dogmatic Islamic practice gives encouragement to the Islamic extremists. Despite full throated claims Islam does not really believe in the equality of men and women. A pre medieval practice to subjugate women is not a matter of faith; it's a tribal culture which does not exist any more.

 

Akbar Hussain

 

 

 

 

 

 

    

 

 

 




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[ALOCHONA] WikiLeaks - Prof. Yunus considers entering Bangladesh politics



WikiLeaks - Prof. Yunus considers entering Bangladesh politics expecting bruising response

On February 12, ConGen spoke with Nobel Prize winner Dr. Muhammad Yunus about his plans to enter Bangladesh politics. Yunus, on a two-day visit to Kolkata, expressed a strong interest to enter the political fray and said that he was reviewing his options. He expressed support of the present Caretaker Government and its decision to declare a "State of Emergency," saying it had averted a possible civil war. Yunus felt that Muslim fundamentalists represented a fringe and that while the dominant parties had developed ties with fundamentalists for political gain, most Bangladeshis did not favor the extremism. Yunus was also receptive to closer commercial and trade relations with India. Yunus recognized the risk of entering politics and its potential to tarnish his exemplary image. However, even as he professed that he was still considering his options, he indicated a strong intent to plunge into the maelstrom of Bangladesh politics.

                                                                                                                                

Full Cable -

 

http://deshcalling.blogspot.com/2011/04/wikileaks-prof-yunus-considers-entering.html

 



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Re: [WideMinds] Re: [ALOCHONA] Minority in West Bengal - (from unheard voice)



HAKKA HUA ALAMGIR - DONT NEGLECT YOUR PILLS.  YOU ARE BRAYING AGAIN!

-----Original Message-----
From: Faruque Alamgir
Sent: Apr 14, 2011 8:18 AM
To: abid bahar , WideMinds@yahoogroups.com, alochona@yahoogroups.com, notun_bangladesh@yahoogroups.com, dahuk , ovimot yahoogroups , Sonar Bangladesh , Amra Bangladesi , Bangla Zindabad , qar
Subject: Re: [WideMinds] Re: [ALOCHONA] Minority in West Bengal - (from unheard voice)

 

The patriots Bangladeshis except the HIDU  Staaani boot licker K.Jibis  are aware of the vicious game plan of the dadas and prepared to  defend the entity of of Bangladeshis like 1971 and to uphold the dignity of the  blood spilled by the "Shahid Mukti Jodhdhas" .The Bangladeshis also know who are the enemy to the Bangladeshis cause and dreaming to be Sikkim.

The majority populace of Bangladesh hates Hidu Staaan  from the very core of their heart for their uneven and unbecoming big brotherly and heinous acts against the sanctity,entity,dignity and sovereignty of our hard earned  BANGLADESH.

On Thu, Apr 14, 2011 at 7:04 PM, abid bahar <abid.bahar@gmail.com> wrote:

 

Watch Out the Harmful Hindu Communalism among the "Progressive West Bengali dadas!"

-----------------------------------------------------------------------------------------------------------------------------
There is a tradition of communalism among the so-called West Bengali dadas.
 
*Don't forget, during the Sepoy Mutiny Calcutta babus overwhelmingly supported the British..

*In the infamous Gujrat riot we see many of the Hindu fanatics that killed Muslims were from West Bengal.

*The left front of Buddhoda always found the West Bengali terrorists infiltrated from Bangladesh!

*That is the face of progressive babu tradition first began by Ram Mohon Roy who once said
"Muslims are the invaders of India," triggering communal distrast among Bengalis."Unknown

to most Bangladeshis Ram Mohan was a Hindu reformer but was a Muslim hater' the founder of Brahmo Samaj.

 Contrary to Ram Mohan's notions, in reality most Indian Muslims were Indians and were

 converts from Buddhism and Hinduism.

*When Felenis die in Bengali soil or dams were built on Bengali soil by India to punish Bangladesh, no dada says a word.

*Bangladesh's Awami League's cultural and political godfathers like Pronobda and others pretends

like they are great well-wisher of Bangladesh who even helped secure 1 billion dollar Indian loan to help Indian crocodiles

to invade Bangladesh portes.

*If these communal communist ("progressive"d)adas could be Bangladesh's great friends, why not Bangladeshis prepared to swim with crocodiles and shirks!

Ofcourse we are not talking about all the dadas.

 
On Thu, Apr 14, 2011 at 5:20 AM, Faruque Alamgir <faruquealamgir@gmail.com> wrote:
 

Friends


Should there no comment from the die hard Secular HINDU  STAAANI lover Sitangsho Guho/rue bean n several hidu staaani paid agents about the status of the secular Muslims in the fanatic blood monger HIDU staaan ???????????

joy bharat mata zindabad/murdabad !!!!!!!!!!!!!!!!!!!!!!!

On Thu, Apr 14, 2011 at 12:10 AM, qar <qrahman@netscape.net> wrote:
 

With a "Secular" government like this who needs religious zealots?





 

Spotlight on West Bengal — the minority report




How much do we know about our closest neighbor?
I definitely was surprised to learn that Muslims might have better economic opportunity in Narendra Modiâ's Gujarat than the red secular West Bengal. All are Anti-Muslims
Full Times of India article over the fold. Hat tip: Comrades from Kafila. 

The Times of India

Bengal worse than Gujarat for Muslims?

Abantika Ghosh, TNN, Mar 23, 2011, 03.39am IST
NEW DELHI: These are figures the Left Front should be wary of as it prepares to defend its citadel of 34 years in West Bengal.
 
An analysis of data on the Muslim community released by the chief economist of the National Council of Applied Economic Research, Abu Saleh Sheriff, reveals that the state's minority has benefited little from development measures. In terms of human development indices, the Muslims have fared very poorly.
Of the 25.2% Muslim population, only 2.1% have government jobs and 50% children are out of school at the primary level. Only 12% go on to complete matriculation. These numbers are all the more astonishing given the fact that Left swears by its secular credentials and positions itself as a protector of minority rights.
 
Alarm bells have already started ringing, especially after a postmortem of the Left's poor showing in the civic elections last year. An important factor which could have resulted in the dismal performance was Muslim disenchantment. In what may be viewed as the party's efforts to make amends, there is a steep 33% hike in the number of Muslim candidates fielded by Left Front. It has gone up from 42 in 2006 to 56 this time in the 292-member Assembly.
Throughout his lecture, Sheriff â€" who has also been the member secretary of the Sachar panel â€" spoke of Gujarat and West Bengal in the same breath. In fact, he used the data to project the Left-ruled state in a far worse light than the state ruled by Narendra Modi, not regarded by many as a benefactor of the minorities. And this comparison appeared all the more relevant because the West Bengal government had gone out of its way to provide shelter to Qutubuddin Ansari, the man who became the face of the post-Godhra riots with his folded hands and tearful eyes.
 
"If a substantial fraction of the state's 25% Muslim population have traditionally voted for the alliance it could be because of the projected gains of the land reforms even though if you look at the figures, it shows that these reforms do not seem to have made any significant difference to the living standards of the community. With the elections coming, it is time this reality is brought to the knowledge of the public," Sheriff said. He was addressing a seminar on "Relative development of West Bengal and Socio-Religious Differentials" organized by the Institute of Objective Studies at the India Islamic Cultural Cultural Centre.
 
Shariff's figures on education, sourced, according to him from the census database and the Planning Commission, show 50% Muslim children attend school at the primary level, 26% remain in middle school and only 12% complete matriculation against 54%, 30% and 13% respectively for SC/STs and 80%, 58% and 38% for others.
 
Of the 90 minority-concentrated districts in the country, West Bengal has 12. "The worst are the state government employment figures where even Gujarat with its 9.1% Muslim population and with a 5.4% share in jobs is way ahead of West Bengal which is by far the worst in the country. We had to try very hard to get these figures out from the state government because, for obvious reasons, they are very secretive about this," Shariff said.
 
A look at OBC statistics in Bengal shows only 2.4% of its Muslims belong to that category. This, Sheriff says, is not the real picture and simply exposes the state government's reluctance to undertake the enumeration exercise.
 
 Muslim demograhy, India
 
West Bengal Facts and Figures


Date of formation

State Capital

Area

Latitude (capital)

Longitude (capital)

Population (2001)

Population Density

Male population

Female population

Sex Ratio

Literacy rate

Per Capita Income

No. of Districts

No. of towns

Largest City

No. of Villages

No. of Lok Sabha seats

No. of Rajya Sabha seats

No. of assembly seats

Religion

Official Language

Time zone

Temperature

Average Rainfal
01-05-1960

Kolkata

88,752 km²

22.82° N

88.2° E

80,176,197

903 per sq. km

41,465,985

38,710,212

934 females per 1000 males

69.22 %


19

375

Kolkata

51,043

42

16

294

Hindu, Muslims, Christians and others

Bengali

IST (UTC+5:30)

Min. 12-150C; Max. 38-420C

4170 mm
 
 
Gujarat Facts and Figures


Date of Formation 1st May 1960
Area 196,024 sq km
Capital Gandhinagar
Latitude 20-6' N to 24-42' North
Longitude 68-10'E to 74-28' East
Population (2001) 50,596,992
Male population 26,344,053
Female population 24,252,939
Population Density 258 persons per sq. km
Sex Ratio 921
Literacy rate 69.97%
Per Capita Income (04-05) Rs.28, 355
No. of villages 18,539
No. of towns 242
No. of Districts 25
No. of assembly seats 182
No. of Lok Sabha seats 26
No. of Rajya Sabha seats 11
Biggest city Ahmedabad
Major Religions Hinduism, Islam
Chief Language Gujarati
Other languages spoken Hindi, English and Marathi
Time zone IST (UTC+5:30)
Variation of Temperature 23°C-43°C (summer),
15°C-36°C (winter)
Annual average rainfall 1685 mm
Railway Length 5310 Km
Highways Total Length 74031 Km

  
 
 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


Left's worries in Bengal include disenchanted Muslims

Kolkata: As the Left in West Bengal heads into what’s being described as its toughest election in the state, it must contend with its growing gap from the Muslims, who once were on its side.
 
The minority community makes up 25% of the state’s population. In 2006, the report of the Sachar Committee said West Bengal was among the worst states for Muslims to live in. Headed by retired judge Rajinder Sachar, the committee was appointed by Dr Manmohan Singh to assess the social, economic and educational status of Muslims in India.
 
Days ago, a member of that committee, Abu Selah Shariff, who is an eminent economist, dealt a heavy blow by declaring that Muslims are better off in Gujarat than in Bengal. Chief Minister Buddhadeb Bhattacharjee dismissed that allegation. “In our state, minorities live in peace and harmony but in Gujarat they live with fear and mistrust. You should not compare Gujarat with West Bengal,†he said.
 
As part of his argument, Mr Shariff pointed out that in Bengal, Muslims hold 2.1% of government jobs. In Gujarat, that figure is 5.4 per cent. Mr Shariff also said that half of Bengal’s Muslim children don’t go to primary school. Nobel Laureate Amartya Sen has said that there is 99% enrollment in Bengal’s primary schools. Mr Shariff says that while Muslim parents may sign their children up for school, they’re not attending class.
 
The Left has long argued that the Sachar report â€" is based on incomplete statistics. Even if that is the case, the general elections of 2009 showed that there was a 9 per cent swing in Muslim votes away from the Left.
 
“This is correct. This is a factor. The Sachar and Ranganath Mishra reports showed a terrible picture. That’s why Muslims are depending on us. The people of Bengal want us in politics,†said Siddiquallah Chowdhury, a leader of the People’s Democratic Alliance of India that is contesting 40 seats this election.
 
It could be the results of the general election that have nudged both the Left and its political rival â€" Mamata Banerjee’s Trinamool Congress â€" to field a record number of Muslim candidates this time around â€" 56 for the Left, 42 for Ms Banerjee’s party.
 
 
 
 
 
 
 
 
 
 
 






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[ALOCHONA] Please read: Mody Cohen of Dacca Television circa 1960s




All

those of you old enough to remember pre-1971 television in the former East Pakistan will recall the TV announcer Mordy Cohen who spoke fluent Bangla and was permanent presence on the small screen daily. He mysteriously disappeared a few years before Bangladesh became free. I just came across this story!

 

Ignore the orientalist nature of the article published in the Jerusalem Post and focus on the fact that a jewish Bengali (ok not a real bengali as per traditional ethno-nationalistic point of view but a Bengali nevertheless) could become a newscaster in a predominantly muslim country and not feel insecure.

 

But I am happy about how in some ways then we were so much more tolerant then.  Saddened that ever since nationalism (religious or linguistic) has taken root there is no scope for such people in our lands.

 

Robin

 

 

Bangladesh – with Jewish connections

By DAVID ZETLER 

04/21/2011 20:58

Jerusalem POST

http://www.jpost.com/Travel/TravelNews/Article.aspx?id=217443

 

Being a tourist here is a singular experience because the people aren't used to seeing visitors.   Iwas interested in including Bangladesh in our tour to Asia, but there would be problems involved, the main one being that as Israelis, my wife and I were not allowed into the Muslim country. An Israeli diplomat in Asia told me about Mordecai Cohen, who grew up in what is today Bangladesh. I contacted him in Kolkata, where he now lives, and planned how to get our Bangladeshi visas using our foreign passports. A Bangladeshi mission person kindly granted us visas and even warned us about the traffic in Dhaka.

 

We arrived in Kolkata, where we were made very welcome by Mordy and Jo Cohen. Mordy's great-grandparents, Jews from Iran and We arrived in Kolkata, where we were made very welcome by Mordy and Jo Cohen. Mordy's great-grandparents, Jews from Iran and Iraq, settled in East Bengal in the 1800s in what was then India. Very few Jews settled in East Bengal, as opposed to West Bengal, which had a thriving Jewish community of more than 5,000 at its peak in and around Kolkata (then Calcutta).

 

When the Indian subcontinent became independent from Britain in 1947, it was partitioned between India and the divided country of East and West Pakistan.

 

Mordy went to school in Rajshahi in East Pakistan and was one of the pioneers of television in Dhaka (then Dacca), which was its capital. He was an announcer and news reader in English and two local languages.

 

Each news broadcast was accompanied by "the news, presented by Mordecai Cohen." Mordy had attended school with boys who later held important positions in the government and in the defense services. He gave us the name and phone number of a former cabinet minister in Dhaka if we encountered any problems there. After the Six Day War in 1967, questions were raised about the Jew presenting the news. His parents, who were still living in Rajshahi, were threatened and were given police protection. He and his parents left for Calcutta in 1968.

 

Mordy told us about his uncle, Gen. J.F.R. (Jack) Jacob, who was born in Calcutta in 1923. In 1941, after hearing reports of the Holocaust, he enlisted in the Indian army, which was under British command. After completing an officer's course, he served in North Africa, Burma and Sumatra. By 1971 he had been promoted to chief of staff of the Eastern Command of the Indian army.

 

It was the year that East Pakistan started a guerrilla war against the Pakistani army, as the East Pakistanis (Bengalis) were very unhappy with being ruled by West Pakistan and Bengali not being accorded the status of an official language. The army retaliated by ruthlessly raping and killing local students, academics and Hindus who still remained in East Pakistan. Ten million East Pakistanis fled their homes to seek refuge in neighboring India. The leaders of the liberation struggle appealed to Indian prime minister Indira Gandhi for help, and it was left to Jacob to plan an invasion and defeat the Pakistan army.

 

It was a difficult project as, besides having to cross wide rivers, it was the height of the Cold War and although the USSR was an ally of India, the US, an ally of Pakistan, positioned its Seventh Fleet in the Bay of Bengal. He planned a short war and within two weeks he met General Niazi, the head of the Pakistan army in Dacca and instead of getting a hoped for cease-fire, Niazi surrendered to him. The Pakistan army of 93,000 had surrendered to a Jew and, in doing so, had created the new Muslim country of Bangladesh. It was one of the biggest surrenders in the history of warfare.

 

Jacob wrote a book on the war, Surrender at Dacca: Birth of a Nation, which has been translated into many languages, including Hebrew. He has been invited to Israel and has been a guest of its prime ministers. After he retired from the army, he served as the governor of the Indian states of Goa and Punjab. Today he lives in New Delhi and recently told me that Bangladesh was going to present him and Indira Gandhi (posthumously) with a gold medal this year, the 40th anniversary of independence.

 

WE VISITED the Liberation Museum in Dhaka, where only one panel is devoted to the Indian army, and Jacob's name is not mentioned. It reminded me of my visit to Darjeeling in northern India, the birthplace of Sherpa Tensing Norgay, who accompanied Edmund Hillary on the conquest of Mount Everest. There is a museum devoted to Norgay and his climb up Everest, and right at the end of the exhibits it says that he was accompanied by Hillary.

 

We decided to plan and pay for our Bangladesh trip in Kolkata, as we could not draw any money there with our Israeli credit cards. We took dollars with us for meals and any other expenses. We also took the precaution of leaving our Israeli passports and Hebrew documents in Kolkata.

 

Our visit to Dhaka, a city of 13 million, was spoiled by the impossible (read "impassable") traffic congestion.

 

Thirty years ago Dhaka had a population of only a million. The traffic consists of new cars, old buses and tens of thousands of artistically decorated threewheeled bicycle rickshaws. Rickshaw art can be described as colorful moving graffiti and adds to the character of Bangladesh.

 

To get anywhere took hours, but we did manage to get to the National Assembly building, a very impressive piece of architecture and the largest parliament building in the world. Our guide told us it was designed by an American, Louis Kahn. As Khan is a very common last name in Pakistan, we assumed he was a Muslim.

 

I later learned that he was a well-known Jewish architect from Philadelphia, and that this building is considered by some to be his finest.

 

We visited the harbor area on the river where ferries of all sizes take passengers to various parts of Bangladesh. There were also little boats loaded with colorful fruit, such as pineapples and green coconuts.

 

From Dhaka we took a bus trip to Cox's Bazaar, in the extreme southeast of the country. It was supposed to be a nine-hour trip but took 14 hours due to an accident and the great volume of traffic using the narrow, twolane road, which is in very poor condition. On the positive side, the bus was very comfortable, and there were frequent toilet stops.

 

At one of the rest stops, we got talking to a young photojournalist. He sometimes did work for an American newspaper and his English was very good. When we told him we were tourists, he said, "Tourists in Bangladesh! That's funny." We did not meet any white tourists, only a few aid workers.

 

Cox's Bazaar reminded me of Eilat, as it is a holiday resort by the sea, the Bay of Bengal, and far from the center of the country. It boasts 120 km. of sandy beach, the longest natural beach in the world. From there we rented a car with a driver and did a day trip to the southernmost corner of the country, wedged between the Bay of Bengal and Myanmar. We visited the Taknef Park, which has a herd of wild elephants. We only saw their large footprints but did manage to become attached to a few leeches.

 

Returning to Cox's Bazaar, we drove the last 30 km.next to the beach, which was dotted with picturesque fishing boats, each with its high, pointed front and back. Early the following morning we walked on the beach, where souvenir peddlers were selling their wares to local and Indian tourists. There were also fishermen repeatedly walking into the sea with their nets and pulling them in, but the fish were very small. I decided not to swim, as there are many rivers emptying into the Bay of Bengal and they pass through the most populated and poorest region of the world.

 

Our last stop was Chittagong, the larger of Bangladesh's two ports. Our guide's name was Joji. He was born in Libya, where his Bangladeshi parents worked for many years, and was 16 when his parents returned to Bangladesh. Chittagong has a huge garment industry, and Joji took us to an industrial park with 5,000 apparel factories. We visited the yards near Chittagong, where giant ships are beached and dismantled by hand. The industry has come under international criticism for employing children and the many deaths and injuries that befall the workers. Many of the factories have large signs at the entrances saying they do not employ children. Bangladesh is the most densely populated country in the world – more than 1,000 people per square kilometer – and its 160 million people work wherever they can find it. For many, the choice is simple: work in the ship-breaking yards or starve.

 

One quiet corner in the heart of Chittagong is the World War II British and Commonwealth cemetery. In this immaculately kept cemetery with edge-to-edge green lawns, we found one Jewish grave with a Magen David on it, of a 19-year-old RAF sergeant from England.

 

We photographed it, and Joji and the caretaker came to see what we were photographing but did not ask any questions.

 

Our guide took us to the immaculately kept Bhatiari golf club, hoping to eat lunch in the restaurant, but it had been booked for a party. Right next to the clubhouse was a small mosque where worshipers were performing their midday prayers.

 

We drove to a riverbank, hoping to see the sunset, but as soon as we approached it, we were surrounded by locals and had to leave after a few minutes. Wherever we stopped, we were surrounded by locals. Most of them only had one question, "What country?" Some of them would talk to us, and many of them posed next to us for their friends to photograph. A white person is a source of intense interest.

 

In spite of the present and a former prime minister being women, a Bangladeshi woman can only book into a hotel if she is accompanied by her father or husband.

 

Unfortunately, we could not visit the Chittagong hill tracts, the most picturesque and interesting part of the country. It has a high incidence of a virulent type of malaria and, because it is a problematic tribal area, we would have had to engage a police escort.

 

The hotels we stayed at were good, and so were the restaurants. The problem with being a tourist in Bangladesh is that the people aren't used to tourists.

 

Our guide in Dhaka spoke very poor English and didn't even know which banks change foreign currency or which places to take us, while none of our drivers spoke English.

 

We were in Bangladesh a few days before the Id al- Adha festival, celebrated by slaughtering a male animal, and in every town and village we went through, there were rows of bulls of all sizes waiting to be sold.

 

I asked a few of the people we met why so many terrorists have Pakistan connections and yet one never hears of a Bangladeshi terrorist. No one could give me an answer, but maybe the answer lies in the name. Pakistan is the Islamic Republic of Pakistan, while Bangladesh is the People's Republic of Bangladesh.  

 




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[ALOCHONA] Do NOT criticize Hasina in FACEBOOK - or else . . . (freedom of speech)

**Freedom of Speech, democracy of ROYAL FAMILY **

----
" Unb, Gazipur - A student of Dhaka University of Engineering and Technology was suspended for one year for making objectionable remark against the family of Prime Minister Sheikh Hasina in the social networking website FACEBOOK. "


http://www.thedailystar.net/newDesign/news-details.php?nid=182689

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[ALOCHONA] What did they do in 1971?



Please read this statement of a Pakistani retired Colonel ...!

----- Forwarded Message ----
From: Riaz Jafri <jafri@rifiela.com>

Dear Shazia:
 
Since you addressed your post to me, I am obliged to respond.
 
Firstly, about your saying "do good at this age".  What do you mean at this age?  Lady, though I am 82 yet am quite 'young' looking and by the Grace of Allah (SWT) much fitter than many half my age. Those who know me will bear me out on this count, or, you can Google my image (Col. Riaz Jafri (Retd)) to see it for yourself. Next, I don't have to do good at this age ONLY.  Allah be praised HE helped me ALL my life to do good whatever little I could.
 
Next, you asked me to tell you what did we people do in 1971.  It is a long story to tell. A story entirely different to what the Indian influenced  hostile media fed to the world and many gullible and prone to suspicion in Pakistan too accepted it blindly. Probably, I wrote it earlier on some forum that I was GSO-1 (Principal Staff Officer) to late Gen Rao Farman Ali, who was incharge Martial Law Civil Affairs (running the entire civil administration of East Pakistan). Chief Secretary Muzzafar Hussain had to go through me to see Gen. Farman or Governor Tikka Khan.  Believe you me, I am as such witness to many an historic event and privy to some inside stories including that of ZAB.  Someone has questioned on this forum as to why don't we discuss the atrocities, killings and burying alive of the West Pakistanis and Biharis also on the forum? (900 Biharis were stoked alive to the Railway Engines' fire at Santhar Railway Station)  Do you have any idea as to what happened to some of the West Pakistani officers and their families in East Pakistan?  These officers were posted to East Pakistan Rifles (sort of Rangers there), various East Pakistan Regiments stationed in 1971 then,  East Pakistan Regimental Centre at Chittagong, Cadet College Faujdar Ghat, Peelkhana Dacca etc.  They were almost all massacred in the most unimaginable and inhumane manner.  Some of the walls of the rooms were seen splattered with the blood of the children's head smashed against them.  People were buried in the ground with only the heads protruding out on which the Muktis spat, urinated and finally stoned them to death. Women were paraded stark naked forced to keep standing in large cages where they tried (unsuccessfully) to hide their bodies with their hair. The tales are too horrific to continue.
 
And most of us on the forum only remember the 2 million Bengali women to have been raped by the West Pakistani soldiers!!  As if Pak Army had nothing else to do.  A figure impossible to achieve under the given circumstances and period.  What an irony?!!
 
And, what is more astonishing is that some of us are writing on the forum that the same is being repeated in Balochistan now !!  Can any body in his real senses imagine it happening in Baluchistan?  Are we people aware of the strong tribal traditions (honour killing etc.) of Baluchis and Pushtoon in this regard?  Can they allow such a thing to happen to their womenfolk in their midst?  Please ask a Baluchi before you hurt their feelings by uttering such nonsense that could such a thing ever happen in their area?
 
Again, if some of us are bent upon maligning the army, I have a simple question for them.  Agreed, it  happened in erstwhile East Pakistan as it was a military regime then and it looked the other way when it all happened.  But now that we have a duly elected democratic government,  why doesn't it stop the genocide and the rape and what not happening in Baluchistan?  If the army and agencies are involved in such inhuman activities the government should order them to stop it. So simple.  If not, is the government also party to it, in which case it MUST also be maligned and blamed for it.  Why only the army and the agencies?
 
Finally, let me tell you all what I heard Maj Nawaz of 4 Baluch on 19 September 1965 while yelling at his men.  I happened to be with him - don't ask me how and why - in his bunker at the BRB when the field telephone rang up. There was a soldier on the other end who informed him that he had spotted some Indians moving towards Lahore on his right. Maj Nawaz yelled at the top of his voice," Oye Roko unko. Woh Lahore nahin jaa rahey.  Woh hamari maan ki tarf jaa rahey hein.  Woh tumahri banan ki taraf jaa rahey hein. Roko unko".  Maj Nawaz is dead now, but he must be turning in his grave that some of us think that his men are raping their own sisters and mothers in Baluchistan !!!!!
 
Col. Riaz Jafri (Retd)
   
----- Original Message -----


Col sahib:

do good at this age and tell us what did you guys do in 1971?

and do you regret it?


Sent from Shazia's 4G magical iPhone.


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[ALOCHONA] Biographer of Cancer & pulitzer prize winner Siddhartha Mukherjee

Sounds like an excellent read! Check out the new book! I plan to

Emperor of All Maladies

-----Forwarded Message-----
>From: Sekhar Ramakrishnan
>Sent: Apr 20, 2011 6:50 PM
>To:
>Subject: [foil] pulitzer winner siddhartha mukherjee
>
>When I first read about Siddhartha Mukherjee's "Biography of Cancer," it
>seemed a gimmick to distinguish a standard book on cancer from hundreds
>like it. But he has won a Pulitzer now, and he does write for the reading
>public from a scientific point of view on issues in the public mind, which
>is wonderful. The topic in the last article, a possible link between
>cellphones and brain cancer, is covered very well indeed, and should be a
>model for people, on the left or on the right, who are too quick to blame
>some pet "evil" technology for assorted health problems - microwave ovens,
>nuclear energy, dental fillings, vaccines, etc.
>
>Below are
>http://www.nytimes.com/2010/11/09/books/09mukherjee.html with a profile,
>http://www.nytimes.com/2010/11/11/books/11book.html
>http://www.nytimes.com/2010/11/14/books/review/Weiner-t.html with two
>reviews, one negative and one positive, and two by Mukherjee:
>http://www.nytimes.com/2010/10/31/magazine/31Cancer-t.html
>http://www.nytimes.com/2011/04/17/magazine/mag-17cellphones-t.html
>
>Parts of the 592-page book can be viewed at
>http://books.simonandschuster.biz/Emperor-of-All-Maladies/Siddhartha-
>Mukherjee/9781439107959/browse_inside
>
>Sekhar
>
> NY Times November 9, 2010
>
> How Cancer Acquired Its Own Biographer
>
> By CHARLES McGRATH
>
>In Dr. Siddhartha Mukherjee´s lab, a Stanley Kubrick-like space at the
>Herbert Irving Comprehensive Cancer Center at Columbia University,
>enormous white freezers with digital temperature readouts keep tissue at
>80 below zero. Sterile work stations with transparent hoods and bacteria-
>scattering blowers emit an unearthly blue light. And there is a bountiful
>supply of mice that, thanks to the addition of a jellyfish gene, literally
>glow either red or green in the dark.
>
>Under the microscope, their blood-forming stem cells, a particular
>interest of Dr. Mukherjee´s right now, shine like tiny Christmas lights.
>Just recently, he said, he and his team had discovered what may be a new
>mutation associated with the precancerous condition myelodysplasia.
>
>"Cell culture is a little like gardening," he added. "You sit and you look
>at cells, and then you see something and say, `You know, that doesn´t look
>right.´ "
>
>Dr. Mukherjee, an oncologist and assistant professor of medicine at
>Columbia, known as Sid by his friends, is married to the MacArthur award-
>winning artist Sarah Sze and looks less like a scientist than like the
>leading man in a Bollywood musical. He belongs to that breed of
>physicians, rapidly multiplying these days, who also have literary DNA in
>their genome, and his first book, "The Emperor of All Maladies: A
>Biography of Cancer," comes out from Scribner on Nov. 16.
>
>The book tells the stories of several cancer patients, and also of heroic
>researchers like Sidney Farber, who pioneered the treatment of childhood
>leukemia. But its main character, as the subtitle suggests, is the disease
>itself as it has been diagnosed, treated and thought about over the last
>4,000 years.
>
>In the early 1950s, Dr. Mukherjee points out in the book, cancer was still
>considered so unmentionable that a woman seeking to place an advertisement
>in The New York Times for a support group was told that the paper could
>not print either the word "breast" or the word "cancer." How about
>"diseases of the chest wall," an editor helpfully suggested. Then, a few
>decades later, cancer was in the public limelight, thought to be virtually
>curable if we just waged sufficient "war" against it.
>
>What we understand now, thanks to advances in cell biology, Dr. Mukherjee
>writes, is that cancer is normalcy of a sort. Cancer cells are
>"hyperactive, survival-endowed, scrappy, fecund, inventive copies of
>ourselves," he says, and adds: "We can rid ourselves of cancer, then, only
>as much as we can rid ourselves of the processes in our physiology that
>depend on growth - aging, regeneration, healing, reproduction."
>
>Dr. Mukherjee grew up in New Delhi; his father was a manager for
>Mitsubishi, and his mother had been a schoolteacher. He went to a Roman
>Catholic school there, where he was required to learn by heart a
>staggering amount of poetry, but attended college at Stanford, which he
>chose mostly because some cousins lived in California. After studying
>immunology at Oxford on a Rhodes scholarship, he went to Harvard Medical
>School.
>
>By the time he got there, Dr. Mukherjee had pretty much decided to
>specialize in oncology, but the experience of actually encountering
>patients was transforming. "All of a sudden it´s as if the world had
>turned," he said. "Everything suddenly becomes real, and your emotional
>responses become hyper-acute."
>
>And it was because of a patient, he added, that he began to write "The
>Emperor of All Maladies." "I was having a conversation with a patient who
>had stomach cancer," he recalled, "and she said, `I´m willing to go on
>fighting, but I need to know what it is that I´m battling.´ It was an
>embarrassing moment. I couldn´t answer her, and I couldn´t point her to a
>book that would. Answering her question - that was the urgency that drove
>me, really. The book was written because it wasn´t there."
>
>He wrote most of it in bed, propped up on pillows, and by mastering what
>he called the "art of full indiscipline."
>
>"Instead of saying, `I´ll get up every day at 5:30´ or, `I´ll write from 9
>to 12,´ I did the complete opposite," he said. "I said: `I will write
>during the day for 5 minutes, 10 minutes, whatever. I´ll write in
>stretches until the book is done."
>
>"The Emperor of All Maladies" (which Dr. Mukherjee adapted into an article
>for The New York Times Magazine last month) employs a complicated
>structure, looping around in time, juggling several themes at once and
>toggling between scientific discussions and stories of people, and yet Dr.
>Mukherjee says he wrote it in pretty much linear fashion from start to
>finish, without moving things around. He was influenced by both Richard
>Rhodes´s study "The Making of the Atomic Bomb" and Randy Shilts´s "And the
>Band Played On," each a big book about a historical moment, but his real
>breakthrough came, he said, when he conceived of his book as a biography.
>
>"I began wondering, can one really write a biography of an illness?" he
>said. "But I found myself thinking of cancer as this character that has
>lived for 4,000 years, and I wanted to know what was its birth, what is
>its mind, its personality, its psyche?" At times in the book he even
>personifies the illness, talking about its "saturnine" quality, its
>"moody, volcanic unpredictability."
>
>Last week Dr. Mukherjee gave an upbeat lunchtime talk to a group of cancer
>fellows at Columbia, young physicians who are preparing to become
>oncologists. He spoke quickly, clicking through a series of PowerPoint
>slides, but occasionally slowed down to remind the fellows about the kinds
>of questions that were bound to come up in their board exam. Talking about
>drug treatments, he reminded them: "If something is good, more is not
>necessarily better. Not always."
>
>"Are cancer patients living longer?" he asked, and then answered his own
>question: it depends on which cancer and on when you start measuring. And
>yet in the treatment of myeloma, his main theme that day, changes had come
>so fast, he said, that everything he had learned at their age was already
>out of date, and a new generation of drugs - über-thalidomides, he called
>them - were changing the picture even as he spoke. Myeloma, a cancer of
>blood plasma cells, is still not curable but often now is very treatable.
>
>Dr. David Scadden, a Harvard hematologist and oncologist who supervised
>Dr. Mukherjee when he was a cancer fellow, recalled that his enthusiasm
>was such that he sometimes seemed to levitate off the laboratory floor.
>"People who take care of cancer patients and also have the research
>dimension are people who are unsatisfied with how things are but
>optimistic about how they might be," he said. "Sid has an internal hope
>machine."
>
>At one point in "The Emperor of All Maladies" Dr. Mukherjee calls oncology
>a "dismal discipline," but, sitting in his office, he said his work did
>not make him feel dispirited. "What does it mean to be an oncologist?" he
>explained. "It means that you get to sit in at a moment of another
>person´s life that is so hyper-acute, and not just because they´re
>medically ill. It´s also a moment of hope and expectation and concern.
>It´s a moment when you get to erase everything that´s irrelevant and ask
>the most elemental questions - about survival, family, children, legacy."
>
>"Most days," he added, "I go home and I feel rejuvenated. I feel
>ebullient."
>
> NY Times November 11, 2010
>
> Cancer as Old Foe and Goad to Science
>
> By JANET MASLIN
>
>On its first page "The Emperor of All Maladies" sets forth its intention:
>to be a definitive history of how cancer has been understood, treated,
>feared and politicized throughout all of recorded human history. That´s a
>staggeringly tall order. Yet the author, Dr. Siddhartha Mukherjee, seeks
>to make it even taller. His book also aspires to be "a biography of
>cancer," even though Dr. Mukherjee (a cancer specialist and researcher
>with stellar credentials) cannot exactly explain what that phrase means.
>
>"This book is a `biography´ in the truest sense of the word," he claims at
>the outset. It is "an attempt to enter the mind of this immortal illness,
>to understand its personality, to demystify its behavior." He ventures
>even farther into the realm of the impossible when he promises to address
>these two questions: "Is cancer´s end conceivable in the future? Is it
>possible to eradicate this disease from our bodies and societies forever?"
>
>With objectives so vast, and with such a beautiful title, "The Emperor of
>All Maladies" is poised to attract a serious and substantial readership.
>And it is an informative, well-researched study. But it is in no way a
>biography of anyone or anything, and Dr. Mukherjee winds up acknowledging
>as much before his book is over.
>
>He points out that there is both folly and scientific partisanship in
>treating "cancer, a shape-shifting disease of colossal diversity," as "a
>single, monolithic entity."
>
>Likewise, questions about whether cancer can be eradicated eventually run
>up against hard reality. "Cancer is a flaw in our growth, but this flaw is
>deeply entrenched in ourselves," the book says. "We can rid ourselves of
>cancer, then, only as much as we can rid ourselves of the processes in our
>physiology that depend on growth - aging, regeneration, healing,
>reproduction."
>
>How did Dr. Mukherjee allow his otherwise sophisticated book to be
>presented so reductively? It´s an all too fitting flaw, since the same
>kind of oversimplification has long been the bane of cancer theory. "The
>Emperor of All Maladies" provides a survey of the different ways in which
>cancer has been understood in different eras, from the Greeks´ idea that
>it was caused by black bile, one of the four liquid humors, to the 19th-
>century conviction that the most drastic and disfiguring surgery would
>lead to the best cure. He also writes about the fund-raising, Nixon-era
>idea of waging war on cancer as if illness were an enemy to be faced in
>battle.
>
>The biographical aspects of "The Emperor of All Maladies" have more to do
>with the personalities of anti-cancer combatants than with concocting one
>for cancer itself. This book pays considerable attention to pioneering
>figures like William Stewart Halsted, an advocate in the 1870s and 1880s
>of extreme breast cancer surgery; Sidney Farber, who in the 1940s made
>great breakthroughs in treating childhood leukemia with dangerously toxic
>chemicals; and Min Chiu Li, who in the 1950s lost his job at the National
>Cancer Institute for providing chemotherapy to patients whose symptoms had
>receded, even though this extended therapy meant the first
>chemotherapeutic cure of cancer in adults.
>
>In a maneuver as transparently glib as that of calling his book a
>biography, Dr. Mukherjee also inserts occasional glimpses of his own
>patients, whose experiences are markedly overdramatized. ("It was now 9:30
>in the morning. The city below us had stirred fully awake. The door shut
>behind me as I left, and a whoosh of air blew me outward and sealed Carla
>in.") But none of this personal material is as compelling as the story of
>how cancer research has progressed through so many different phases.
>
>Here Dr. Mukherjee´s writing is at its most candid and grim. The
>overarching point made by his narrative is that the whole subject of
>cancer is dauntingly complex. Even the statistics about mortality rates
>are tricky, since so much of researchers´ thinking about the prevalence of
>cancer depends on how they measure progress. And the unmistakable effect
>of our progress in curing other previously fatal diseases is to make
>cancer, which is most often found in older patients, look more prevalent
>than ever.
>
>"The Emperor of All Maladies" is at its most honest in describing the push-
>pull dynamics of scientific progress. Dr. Mukherjee links a decline in
>extremely punishing chemotherapy regimens to the fact that patients became
>less passive. (He credits much of this forcefulness to AIDS activists.) He
>describes the conflicting interests of surgeons and chemotherapists. He
>writes most promisingly about the effects of genome mapping on scientists´
>ability to understand how cancers progress, and he cites the similar ways
>in which different cancers create genetic pathways within mutating cells.
>He is confounding yet fair in writing that "this is either very good news
>or very bad news."
>
>Late in "The Emperor of All Maladies" Dr. Mukherjee provides especially
>apt metaphors for a subject so difficult to grasp. He quotes the Red Queen
>from Lewis Carroll´s "Through the Looking Glass" to describe the alacrity
>with which research must move: "It takes all the running you can do, to
>keep in the same place." He describes one patient´s maneuvers to keep up
>with her illness as "like watching someone locked in a chess game." And he
>says that the patterns in cancer research repeat themselves just as
>history does. Among the constants in this struggle are "the hypnotic drive
>for universal solutions" and "the queasy pivoting between defeatism and
>hope."
>
> NY Times November 14, 2010
>
> The Mind of a Disease
>
> By JONATHAN WEINER
>
>All patients begin as storytellers, the oncologist Siddhartha Mukherjee
>observes near the start of this powerful and ambitious first book. Long
>before they see a doctor, they become narrators of suffering, as Mukherjee
>puts it - travelers who have visited the "kingdom of the ill."
>
>Many doctors become storytellers too, and Mukherjee has undertaken one of
>the most extraordinary stories in medicine: a history of cancer, which
>will kill about 600,000 Americans by the end of this year, and more than
>seven million people around the planet. He frames it as a biography, "an
>attempt to enter the mind of this immortal illness, to understand its
>personality, to demystify its behavior." It is an epic story that he seems
>compelled to tell, the way a passionate young priest might attempt a
>biography of Satan.
>
>Mukherjee started on the road to this book when he began advanced training
>in cancer medicine at the Dana-Farber Cancer Institute in Boston in the
>summer of 2003. During his first week, a colleague who´d just completed
>the program took him aside. "It´s called an immersive training program.
>But by immersive, they really mean drowning," he said, lowering his voice
>the way many of us do when we speak of cancer itself. "Have a life outside
>the hospital," the doctor warned him. "You´ll need it, or you´ll get
>swallowed."
>
>"But it was impossible not to be swallowed," Mukherjee writes. At the end
>of every evening he found himself stunned and speechless in the neon
>floodlights of the hospital parking lot, compulsively trying to
>reconstruct the day´s decisions and prescriptions, almost as consumed as
>his patients by the dreadful rounds of chemotherapy and the tongue-
>twisting names of the drugs, "Cyclophosphamide, cytarabine, prednisone,
>asparaginase. . . ."
>
>Eventually he started this book so as not to drown.
>
>The oldest surviving description of cancer is written on a papyrus from
>about 1600 B.C. The hieroglyphics record a probable case of breast cancer:
>"a bulging tumor . . . like touching a ball of wrappings." Under
>"treatment," the scribe concludes: "none."
>
>For more than 2,000 years afterward, there is virtually nothing about
>cancer in the medical literature ("or in any other literature," Mukherjee
>adds.) The modern understanding of the disease originated with the
>recognition, in the first half of the 19th century, that all plants and
>animals are made of cells, and that all cells arise from other cells. The
>German researcher Rudolph Virchow put that in Latin: omnis cellula e
>cellula.
>
>Cancer is a disease that begins when a single cell, among all the
>trillions in a human body, begins to grow out of control. Lymphomas,
>leukemias, malignant melanomas, sarcomas all begin with that microscopic
>accident, a mutation in one cell: omnis cellula e cellula e cellula. Cell
>growth is the secret of living, the source of our ability to build, adapt,
>repair ourselves; and cancer cells are rebels among our own cells that
>outrace the rest. "If we seek immortality," Mukherjee writes, "then so,
>too, in a rather perverse sense, does the cancer cell."
>
>Mukherjee opens his book with the story of one of the founders of the
>hospital where he trained - Sidney Farber, a specialist in children´s
>diseases who began as a pathologist. In 1947, Farber worked in a tiny,
>dank laboratory in Boston, dissecting specimens and performing autopsies.
>He was fascinated by a sharklike species of cancer called acute
>lymphoblastic leukemia, which can move so fast that it kills an apparently
>healthy child within only a few days. A patient would be "brought to the
>hospital in a flurry of excitement, discussed on medical rounds with
>professorial grandiosity" and then sent home to die.
>
>In the summer of 1947, a 2-year-old boy, the child of a Boston shipyard
>worker, fell sick. Examining a drop of the baby´s blood through the
>microscope, Farber saw the telltale signs of acute lymphoblastic leukemia,
>billions of malignant white cells "dividing in frenzy, their chromosomes
>condensing and uncondensing, like tiny clenched and unclenched fists." By
>December, the boy was near death. In the last days of the year, Farber
>injected his patient with an experimental drug, aminopterin, and within
>two weeks he was walking, talking and eating again. It wasn´t a cure, only
>a remission; but for Farber it was the beginning of a dream of cures, of
>what one researcher called "a penicillin for cancer."
>
>The next year, Farber helped start a research fund drive around a boy who
>suffered from a lymphoma in his intestines, a disease that killed 90
>percent of its victims. The boy was cherubic and blond, an enormous fan of
>the Boston Braves, and his name was Einar Gustafson. For the sake of
>publicity, Farber rechristened him Jimmy. That May, the host of the radio
>show "Truth or Consequences" interrupted his usual broadcast to bring his
>listeners into Jimmy´s hospital room to listen in as players on the Braves
>marched into Jimmy´s room and sang "Take Me Out to the Ball Game."
>
>By the summer of 1952, Farber had built an imposing new hospital, Jimmy´s
>Clinic. Soon, he was working on an even grander scale, with the help of an
>extraordinary socialite and medical philanthropist, Mary Lasker. ("I am
>opposed to heart attacks and cancer," she once told a reporter, "the way
>one is opposed to sin.") Mary and her husband, Albert, an advertising
>executive, joined forces with Farber. They wanted, as Mukherjee writes, "a
>Manhattan Project for cancer." Together, through masterly advertising,
>fund-raising and passion for their common cause ("The iron is hot and this
>is the time to pound without cessation," Farber wrote to Mary Lasker),
>they maneuvered the United States into what would become known as the war
>on cancer. Richard Nixon signed it into law with the National Cancer Act
>in 1971, authorizing the spending of $1.5 billion of research funds over
>the next three years.
>
>In political terms, the war was well timed, coming at a time when
>America´s collective nightmares were no longer "It Came From Outer Space"
>or "The Man From Planet X," but "The Exorcist" and "They Came from
>Within." Mary Lasker called the war on cancer the country´s next moon
>shot, the conquest of inner space.
>
>In scientific terms, however, the war was disastrously premature. The moon
>race had been based on rocket science. But in the early 1970s, there
>really wasn´t a science of cancer. Researchers still did not understand
>what makes cells turn malignant. Now that they were so much in the
>spotlight, and in the money, they fell into bickering, demoralized,
>warring factions. The "iconic battleground" of the time was the
>chemotherapy ward, Mukherjee writes, "a sanitized vision of hell."
>Typically it was a kind of limbo, almost a jail, in which absolutely no
>one spoke the word "cancer," the inmates´ faces had an orange tinge from
>the drugs they were given, and windows were covered with heavy wire mesh
>to keep them from committing suicide. "The artifice of manufactured cheer
>(a requirement for soldiers in battle) made the wards even more poignantly
>desolate," Mukherjee writes.
>
>"The Emperor of All Maladies" is a history of eureka moments and decades
>of despair. Mukherjee describes vividly the horrors of the radical
>mastectomy, which got more and more radical, until it arrived at "an
>extraordinarily morbid, disfiguring procedure in which surgeons removed
>the breast, the pectoral muscles, the axillary nodes, the chest wall and
>occasionally the ribs, parts of the sternum, the clavicle and the lymph
>nodes inside the chest." Cancer surgeons thought, mistakenly, that each
>radicalization of the procedure was progress. "Pumped up with self-
>confidence, bristling with conceit and hypnotized by the potency of
>medicine, oncologists pushed their patients - and their discipline - to
>the brink of disaster," Mukherjee writes. In this army, "lumpectomy" was
>originally a term of abuse.
>
>Meanwhile, more Americans were dying of cancer than ever, mainly because
>of smoking. Back in 1953, the average adult American smoked 3,500
>cigarettes a year, or about 10 a day. Almost half of all Americans smoked.
>By the early 1940s, as one epidemiologist wrote, "asking about a
>connection between tobacco and cancer was like asking about an association
>between sitting and cancer." In the decade and a half after Nixon declared
>his war on cancer, lung cancer deaths among older women increased by 400
>percent. That epidemic is still playing itself out.
>
>Mukherjee is good on the propaganda campaign waged by the tobacco
>companies, "the proverbial combination of smoke and mirrors." As one
>internal industry report noted in 1969, "Doubt is our product, since it is
>the best means of competing with the `body of fact.´ " This episode makes
>particularly interesting reading to anyone following the current
>propaganda campaigns against the science of climate change.
>
>Meanwhile, those who studied the causes of cancer in the laboratories and
>those who treated it in the clinics were not always talking to each other.
>As Mukherjee puts it, "The two conversations seemed to be occurring in
>sealed and separate universes." The disease was hard to understand either
>intellectually, in the lab, or emotionally, in the clinic. In the lab,
>because it is so heterogeneous in its genetics and its migrations in the
>body. In the hospital, because its course is horrible and so often slow,
>drawn out. When it comes to cancer, Mukherjee writes, "dying, even more
>than death, defines the illness."
>
>Mukherjee stitches stories of his own patients into this history, not
>always smoothly. But they are very strong, well-written and unsparing of
>himself: "Walking across the hospital in the morning to draw yet another
>bone-marrow biopsy, with the wintry light crosshatching the rooms, I felt
>a certain dread descend on me, a heaviness that bordered on sympathy but
>never quite achieved it."
>
>The heroes of the last few decades of this epic history are Robert
>Weinberg, Harold Varmus, Bert Vogelstein and the other extraordinary
>laboratory scientists who have finally worked out the genetics of cancer,
>and traced the molecular sequence of jammed accelerators and missing
>brakes that release those first rebel cells. As James Watson wrote not
>long ago, "Beating cancer now is a realistic ambition because, at long
>last, we largely know its true genetic and chemical characteristics." We
>may finally be ready for war.
>
>As a clinician, Mukherjee is only guardedly optimistic. One of the
>constants in oncology, as he says, is "the queasy pivoting between
>defeatism and hope." Cancer is and may always be part of the burden we
>carry with us - the Greek word onkos means "mass" or "burden." As
>Mukherjee writes, "Cancer is indeed the load built into our genome, the
>leaden counterweight to our aspirations for immortality." But onkos comes
>from the ancient Indo-European nek, meaning to carry the burden: the
>spirit "so inextricably human, to outwit, to outlive and survive."
>Mukherjee has now seen many patients voyage into the night. "But surely,"
>he writes, "it was the most sublime moment of my clinical life to have
>watched that voyage in reverse, to encounter men and women returning from
>that strange country- to see them so very close, ­clambering back."
>
>Jonathan Weiner is the Maxwell M. Geffen professor of medical and
>scientific journalism at Columbia University. His latest book is "Long for
>This World: The Strange Science of Immortality."
>
> NY Times October 31, 2010
>
> The Cancer Sleeper Cell
>
> By SIDDHARTHA MUKHERJEE
>
>In the winter of 1999, a 49-year-old psychologist was struck by nausea -a
>queasiness so sudden and strong that it seemed as if it had been released
>from a catapult.
>
>More puzzled by her symptoms than alarmed - this nausea came without any
>aura of pain - she saw her internist. She was given a diagnosis of
>gastroenteritis and sent home to bed rest and Gatorade.
>
>But the nausea persisted, and then additional symptoms appeared out of
>nowhere. Ghostly fevers came and went. She felt perpetually full, as if
>she had just finished a large meal. Three weeks later, she returned to the
>hospital, demanding additional tests. This time, a CT scan revealed a nine-
>centimeter solid mass pushing into her stomach. Once biopsied, the mass
>was revealed to be a tumor, with oblong, spindle-shaped cells dividing
>rapidly. It was characterized as a rare kind of cancer called a
>gastrointestinal stromal tumor, or GIST.
>
>A surgical cure was impossible: her tumor had metastasized to her liver,
>lymph nodes and spleen. Her doctors halfheartedly tried some chemotherapy,
>but nothing worked. "I signed my letters, paid my bills and made my will,"
>the patient recalled. "I was told to go home to die."
>
>In June, several months after her diagnosis, she stumbled into a virtual
>community of co-sufferers - GIST patients who spoke to one another online
>through a Listserv. In 2001, word of a novel drug called Gleevec began to
>spread like wildfire through this community. Gleevec was the exemplar of a
>brand-new kind of cancer medicine. Cancer cells are often driven to divide
>because of mutations that activate genes crucial to cell division; Gleevec
>directly inactivated the mutated gene driving the growth of her sarcoma,
>and in early trials was turning out to be astonishingly effective against
>GIST.
>
>The psychologist pulled strings to enroll in one of these trials. She was,
>by nature, effortlessly persuasive, and her illness had made her bold. She
>enrolled in a Gleevec trial at a teaching hospital. A month later, her
>tumors began to recede at an astonishing rate. Her energy reappeared; her
>nausea vanished. She was resurrected from the dead.
>
>Her recovery was a medical miracle, emblematic of a new direction in
>cancer treatment. Medicine seemed to be catching up on cancer. Even if no
>cure was in sight, there would be a new generation of drugs to control
>cancer, and another when the first failed. Then, just short of the third
>anniversary of her unexpected recovery, cancer cells suddenly began
>multiplying again. The dormant lumps sprouted back. The nausea returned.
>Malignant fluid poured into the cisterns of her abdomen.
>
>Resourceful as always, she turned once more to the online community of
>GIST patients. She discovered that there were other drugs - second-
>generation analogues of Gleevec - in trial in other cities. Later that
>year, she enrolled in one such trial in Boston, where I was completing my
>clinical training in cancer medicine.
>
>The response was again striking. The masses in her liver and stomach
>shrank almost immediately. Her energy flowed back. Resurrected again, she
>made plans to return home. But the new drug did not work for long: within
>months she relapsed again. By early winter, her cancer was out of control,
>growing so fast that she could record its weight, in pounds, as she stood
>on the hospital´s scales. Eventually her pain reached a point when it was
>impossible for her to walk.
>
>Toward the end of 2003, I met her in her hospital room to try to reconcile
>her to her medical condition. As usual, she was ahead of me. When I
>started to talk about next steps, she waved her hand and cut me off. Her
>goals were now simple, she told me. No more trials. No more drugs. She
>realized that her reprieve had finally come to an end. She wanted to go
>home, to die the death that she expected in 1999.
>
>The word "relapse" comes from the Latin for "slipping backward," or
>"slipping again." It signals not just a fall but another fall, a recurrent
>sin, a catastrophe that happens again. It carries a particularly chilling
>resonance in cancer - for it signals the reappearance of a disease that
>had once disappeared. When cancer recurs, it often does so in treatment-
>resistant or widely spread form. For many patients, it is relapse that
>presages the failure of all treatment. You may fear cancer, but what
>cancer patients fear is relapse.
>
>Why does cancer relapse? From one perspective, the answer has to do as
>much with language, or psychology, as with biology. Diabetes and heart
>failure, both chronic illnesses whose acuity can also wax and wane, are
>rarely described in terms of "relapse." Yet when a cancer disappears on a
>CT scan or becomes otherwise undetectable, we genuinely begin to believe
>that the disappearance is real, or even permanent, even though statistical
>reasoning might suggest the opposite. A resurrection implies a previous
>burial. Cancer´s "relapse" thus implies a belief that the disease was once
>truly dead.
>
>But what if my patient´s cancer had never actually died, despite its
>invisibility on all scans and tests? CT scans, after all, lack the
>resolution to detect a single remnant cell. Blood tests for cancer also
>have a resolution limit: they detect cancer only when millions of tumor
>cells are present in the body. What if her cancer had persisted in a
>dormant state during her remissions - effectively frozen but ready to
>germinate? Could her case history be viewed through an inverted lens: not
>as a series of remissions punctuated by the occasional relapse, but rather
>a prolonged relapse, relieved by an occasional remission?
>
>In fact, this view of cancer - as tenaciously persistent and able to
>regenerate after apparently disappearing - has come to occupy the very
>center of cancer biology. Intriguingly, for some cancers, this
>regenerative power appears to be driven by a specific cell type lurking
>within the cancer that is capable of dormancy, growth and infinite
>regeneration - a cancer "stem cell."
>
>If such a phoenixlike cell truly exists within cancer, the implication for
>cancer therapy will be enormous: this cell might be the ultimate
>determinant of relapse. For decades, scientists have wondered if the
>efforts to treat certain cancers have stalled because we haven´t yet found
>the right kind of drug. But the notion that cancers contain stem cells
>might radically redirect our efforts to develop anticancer drugs. Is it
>possible that the quest to treat cancer has also stalled because we
>haven´t even found the right kind of cell?
>
>Even the earliest theories of cancer´s genesis had to contend with the
>regenerative power of this illness. The most enduring of these theories
>was promulgated by Galen, the Greek physician who began practicing among
>the Romans in A.D. 162. Galen, following earlier Greek physiologists,
>proposed that the human body was composed of four cardinal fluids: blood,
>phlegm, yellow bile and black bile. Each possessed a unique color (red,
>white, yellow and black) and an essential character, temperature and
>taste. In normal bodies, these fluids were kept in a perfect, if somewhat
>precarious, balance. Illness was the pathological overabundance or
>depletion of one or more fluids. Catarrh, pustules, tuberculotic glands -
>all boggy, cool and white - were illnesses of the excess of phlegm.
>Jaundice was obviously an overflow of yellow bile. Heart failure arose
>from too much blood. Cancer was linked to the most malevolent and complex
>of all fluids - black bile, imagined as an oily, bitter fluid also
>responsible for depression (melancholia takes its name from black bile).
>
>Fantastical as it was, Galen´s system nonetheless had one important
>virtue: It explained not just cancer´s occurrence but also its recurrence.
>Cancer, Galen proposed, was a result of a systemic malignant state, an
>internal overdose of black bile. Tumors were the local outcroppings of a
>deep-seated bodily dysfunction, an imbalance that pervaded the entire
>corpus. The problem with treating cancer with any form of local therapy,
>like surgery, was that black bile was everywhere in the body. Fluids seep
>back to find their own levels. You could cut a tumor out, Galen argued,
>but black bile would flow right back and regenerate cancer.
>
>Galen´s theory held a potent grip on the imagination of scientists for
>centuries - until the invention of the microscope quite literally threw
>light on the cancer cell. When 19th-century pathologists trained their
>lenses at tumors, they found not black bile in overabundance but cells in
>excess - sheet upon sheet of them that had divided with near-hyperactive
>frenzy, distorting normal anatomy, breaking boundaries and invading other
>tissues. The crucial abnormality of cancer was unbridled cellular
>proliferation, cell growth without control.
>
>We now have a vastly enriched understanding of how this runaway growth
>begins. Cancer results from alterations to cellular genes. In normal
>cells, powerful genetic signals regulate cell division with exquisite
>control. Some genes activate cellular proliferation, behaving like
>minuscule accelerators of growth. Others inactivate growth, acting like
>molecular brakes. Genes tell a limb to grow out of an embryo, for example,
>and then instruct the limb to stop growing. A cut prompts the skin to heal
>itself, but heaps of skin do not continue to grow in excess. In a cancer
>cell, in contrast, the accelerators of growth are jammed permanently on,
>the brakes permanently off. The result is a cell that does not know how to
>stop growing.
>
>Uncontrolled cell division imbues cancer cells not just with the capacity
>to grow but also with a crucial property that often accompanies growth:
>the capacity to evolve. Cancer is not merely a glum cellular copying
>machine, begetting clone after clone. Every generation of cancer cells
>produces cells that in turn bear additional mutations, changes beyond
>those already present in the accelerator and brake genes. And when a
>selective pressure like chemotherapy is applied to a cancer, resistant
>mutants escape that pressure. Just as antibiotics can give rise to
>resistant strains of bacteria, anticancer drugs can produce resistant
>cancer cells.
>
>This process - evolution´s slippery hand driving cancer´s adaptation and
>survival - provided biologists with an explanation for cancer´s recurrence
>after treatment. Relapse occurs because cancer cells that are genetically
>resistant to a drug outgrow all the nonresistant cells. Chemotherapy
>unleashes a ruthless Darwinian battle in every tumor. A relapsed cancer is
>the ultimate survivor of that battle, the direct descendant of the fittest
>cell.
>
>And yet this theory seemed incomplete. Some cancers relapse months or even
>years after a chemotherapeutic drug has been stopped - a delay that would
>make little sense if relapse were simply due to resistance. In other
>instances, treating a recurrent cancer with the same drug can lead to a
>second remission - an outcome difficult to explain if the recurring cancer
>has acquired resistance to the original drug. Could there be a deeper
>explanation for cancer´s persistence and regenerative power beyond simple
>mutations and resistance?
>
>In 1994, a researcher at the University of Toronto named John Dick
>performed a striking experiment that would upend the received wisdom about
>cancer relapses. Trained as a stem-cell biologist, Dick was particularly
>interested in blood stem cells.
>
>Stem cells, regardless of their origin, are defined by two cardinal
>characteristics. The first is hierarchy, or potency. A stem cell is the
>originator of the many different cell types in a tissue; it sits, like the
>founder of a massive clan, at the tip of a pyramid of growth. The second
>is self-renewal: even as stem cells create the cells that make up a
>tissue, they must also renew themselves. This dynast doesn´t just produce
>a clan; in each generation, it rebirths itself. The perpetual rebirth of a
>founding cell yields a virtually inexhaustible supply of cells in a
>tissue, a reservoir of growth that can be tapped repeatedly on demand.
>
>In humans, all circulating blood cells - white cells, red cells and
>platelets - arise from a population of blood stem cells exclusively
>dedicated to the genesis of blood. In their normal, unperturbed state,
>these blood-founding cells hibernate deep in the cavities of the bone
>marrow. But when circulating blood cells are killed - by chemotherapy, say
>- the stem cells awaken and begin to divide with awe-inspiring fecundity,
>generating millions of cells that gradually mature into blood cells. A
>defining feature of this proc­ess is its regenerative capacity: in
>generating blood, the blood stem cells also regenerate themselves. Each
>round of blood formation restores their supply. If the entirety of blood
>is again depleted, by another round of chemo, it can be regenerated again
>and yet again - theoretically, an infinite number of times - because the
>stem cells replenish themselves in every cycle.
>
>Blood, in short, is hierarchically organized. Its reservoir of renewal is
>concentrated in a rare population of highly potent cells. As long as these
>cells exist in the marrow, blood can be regenerated. Eliminate this
>reservoir, and the vast organ-system of blood gradually collapses.
>
>Now imagine that cancer is also hierarchically organized - with a secret
>cellular reservoir dedicated to its renewal. Typically, cancer is
>envisioned as a mass of dividing cells, with no difference between one
>cell and its neighbor. But what if some cells in a tumor are dedicated
>"founders," capable of infinite regeneration, while others are limited in
>their capacity to divide and unable to continuously generate new cells?
>Cancer cells bear mutations that enable rapid growth, but what if only
>some cells within a tumor possess indefinite growth? Such a model of
>cancer would still retain the essential pathological features of the
>disease - distorted growth, invasiveness, the capacity to mutate and
>evolve. Yet the driver of regeneration would be different: as with blood,
>only a certain subpopulation of cells in the tumor would be responsible
>for a cancer´s regeneration. Might such cells lie at the root of relapse?
>
>John Dick had an obvious place to begin looking for such cancer-
>regenerating cells - in leukemia, or cancers of white blood cells. Dick
>implanted human leukemia cells into immune-paralyzed mice and found that
>these leukemias could survive and grow in these mice. But not every
>leukemia cell could. Dick and his students implanted fewer and fewer
>leukemia cells - one million, 100,000, 1,000 and so on - to determine the
>smallest number of cells required to cause cancer in a mouse. The answer
>was surprising: one needed to implant between a quarter-million and one
>million cells to be sure of implanting at least one cell that could
>generate leukemia. The rest could not; the other 999,999 cells, in short,
>had evidently grown out of that single cell - but were themselves
>incapable of regenerating the cancer.
>
>When Dick´s team focused on defining the characteristics of this one-in-a-
>million cell, there was another surprise. All cells express subsets of
>proteins on their cell surface that correspond to their identity like tiny
>bar codes. The bar codes on the surface of the leukemia-generating cell
>bore a familiar mark: of all cell types found in blood, it most closely
>resembled the blood stem cell. And when Dick transplanted this cell from
>one mouse to the next, he found that he could generate and regenerate the
>leukemia - just as a blood stem cell would generate blood cells.
>
>Dick´s leukemia-forming cell was, in effect, the normal stem cell´s
>malignant doppelgänger. It possessed the blood stem cell´s incredible
>regenerative ability - but unlike a normal stem cell, it could not stop
>regenerating, dividing and producing more cells. It, too, was an
>inexhaustible reservoir of growth, but of unstoppable growth. Noting the
>analogy between this cell and the blood stem cell, Dick called the one-in-
>a-million cell the "leukemia stem cell."
>
>In time, biologists began to see the implication of Dick´s experiment. If
>leukemia possessed stem cells, then - much like normal blood - its
>regenerative capacity may be contained exclusively within that select
>population. And if so, it was this rare stem cell - not the other 999,999
>- that had to be attacked by a new generation of drugs. Traditional
>chemotherapy, of course, makes no distinction between a cancer´s stem
>cells and any other of its cells, between the roots and the shoots of a
>tumor. All cells are treated equal - and what is poison to one growing
>cell is largely poison to another. Indeed, most forms of chemotherapy in
>use today are derived from enormous chemical hunts begun in the 1970s,
>decades before the birth of the cancer-stem-cell theory. Many of these
>chemicals came into use because of their ability to kill dividing cancer
>cells in a petri dish. The fact that most such drugs turn out to be nearly
>indiscriminate poisons of cellular growth should hardly come as a
>surprise: they were selected to be generic cell killers.
>
>But if tumors contain dedicated stem cells, then delivering maximal doses
>of poisons to kill the bulk of the tumor might achieve one response - a
>shrinkage of the tumor - but have no effect on relapse. If the rare stem
>cell lurking within a tumor somehow escapes death, then it will reassert
>itself and grow again. Cancers will come back like a garden that has been
>cleared by hacking at its weeds while leaving the roots behind.
>
>The publication of John Dick´s paper eventually produced an avalanche of
>interest in cancer stem cells. In 2003, another laboratory, led by Michael
>Clarke at the University of Michigan, isolated a rare population of cancer-
>regenerating cells from human breast cancers, thereby extending Dick´s
>model beyond leukemia to a "solid" tumor. In 2005, a Harvard professor
>named Martin Nowak used mathematical modeling to demonstrate that another
>human leukemia known as CML also possesses a rare subpopulation of
>regenerating cells. In the winter of 2006, Dick´s lab and an Italian team
>independently discovered cancer stem cells in colon cancers. Laboratories
>around the United States rushed to extract cancer stem cells from brain,
>prostate, lung and pancreatic cancers. Pharmaceutical companies joined the
>bandwagon, spending millions, and then tens of millions, on mammoth
>chemical searches for drugs that might destroy cancer stem cells. The
>National Institutes of Health issued dozens of grant requests to study and
>isolate cancer stem cells. The paradox of this moment was not lost on
>researchers. For decades, cancer had been imagined as a degenerative
>disease - an illness caused by the corruption of genes and cells over
>time, often a side-effect of aging. Yet in the search for a new generation
>of anticancer drugs, it was to the science of regeneration - to embryos
>and stem cells - that the field turned.
>
>In 2005, by the time I finished my training, the cancer-stem-cell model
>had acquired an overheated quality. The boil and froth inevitably brought
>challenges. In Michigan, a stem-cell biologist named Sean Morrison
>returned to John Dick´s original test for stem cells - diluting and
>rediluting cells to find the cells that could regenerate a cancer.
>Morrison first tested the model in mouse leukemias and confirmed Dick´s
>results in human leukemias. He subsequently tried the experiment with
>another type of cancer - melanoma, deadly blue-black cancers that arise in
>the skin and metastasize often to the lungs and brain. Others had
>suggested that only a few cells - about one in a million - could
>regenerate the tumor in mice. But when Morrison tested the melanoma cells´
>regenerative capacity by conducting a variation of Dick´s experiment, he
>found that some 25 percent of the cells from a melanoma could grow a tumor
>in a mouse. If stem cells were this common in tumors - if one in four
>cells could grow cancer - then their very definition might be reduced to
>semantic oblivion. How could a tumor have a stem-cell-like "hierarchy" if
>every cell occupied the primary spot?
>
>New questions emerged again in May this year at the Wistar Institute in
>Philadelphia. A group there was working on melanoma, the cancer that
>Morrison studied. As previous studies had, the Wistar study also
>identified a subpopulation of self-renewing cells marked by a distinct bar
>code within human melanomas. But when these cells were studied more
>deeply, they appeared to possess no greater ability to regenerate cancers
>in mice than the nonrenewing cells - thus seemingly disconnecting the link
>between self-renewal and cancer regeneration.
>
>The Wistar and the Morrison studies are among the many that have begun to
>challenge the universality and the reliability of the cancer-stem-cell
>model. "Look," Morrison told me, "this is all going to become more
>complicated. Some cancers, including myeloid leukemias, really do follow a
>cancer-stem-cell model. But in some other cancers, there is no meaningful
>hierarchy, and it will not be possible to cure a patient by targeting a
>rare subpopulation of cells. The field has a lot of work to do to figure
>out which cancers, or even which patients, fall in each category."
>
>Even Morrison, however, acknowledges that the existence of such cells
>would have a transformative impact on cancer. "For a model to be useful,
>it need not be universal," he says. "Even if the stem-cell model applies
>only to certain forms of cancer, it would be absolutely worthwhile
>studying the biology of these stem cells. Universal cures and theories of
>cancer have so often failed that we may as well spend time talking about
>specific theories for specific forms of cancer. And it´s in specific
>cancers that the stem-cell theory might still apply - and powerfully so."
>
>My patient, the psychologist, returned to her hometown in the South. "No
>bed like your own bed," she told me in parting, smiling her pointed,
>distinctive smile. A week later, when I called her, there was no answer on
>the phone. I assume that she died - in her own bed, on her own terms -
>with the same dignity with which she lived. I finished my clinical
>fellowship in Boston in 2005 and then moved to New York four years later
>to set up a laboratory. Our lab studies leukemia stem cells. We, too, have
>joined the quest to create drugs that will wipe out malignant stem cells
>while sparing normal stem cells.
>
>How might someone go about finding such a drug? Traditionally, three
>strategies have produced anticancer drugs. The first relies on
>serendipity: someone hears of a chemical that works on some cell, it is
>tested on cancer and - lo! - it is found to kill cancer cells while
>sparing most normal ones.
>
>The second approach involves discovering a protein present or especially
>active in cancer cells - and relatively inactive in normal cells - and
>targeting that protein with a drug. Gleevec, the drug used against GIST,
>was designed to destroy the functioning of a family of proteins that are
>uniquely hyperactive in GIST and in certain leukemias. (There are only a
>few drugs with such exquisite specificity for cancer cells.)
>
>The final strategy involves identifying some behavior of a cancer cell
>that renders it uniquely sensitive to a particular chemical. Most
>traditional chemotherapies, for instance, attack the rapid division of
>cells. These drugs kill cancer cells because those divide the most
>rapidly, resulting in a narrow discrimination between cancer cells and
>normal cells.
>
>Nearly every drug in oncology´s current pharmacopeia can trace its origins
>to some variation or combination of these three approaches. But notably,
>while each method depends crucially on discriminating between normal cells
>and cancer cells, almost none make any distinction among the cells of any
>cancer.
>
>The stem-cell hypothesis of cancer poses new challenges for all three
>modes of drug discovery. To start, cancer stem cells might be fleetingly
>rare - one in a million, in Dick´s original case. A serendipitous
>discovery involving a rare cell demands an unusual confluence of luck -
>chance multiplied by chance. Defining specific targets in cancer stem
>cells might work, but here again there is a battle against numbers.
>Finding such genes unique to cancer stem cells first requires isolating
>and extracting these rare cells from real tumors, a formidable technical
>hurdle.
>
>The most difficult challenge for drug discovery, though, lies perhaps in
>modeling the self-renewing behavior of cancer stem cells. To create drugs,
>researchers typically begin with a simple cell behavior - say, its growth
>or death, or its capacity to change shape. Chemicals are then tested for
>their ability to alter this behavior. But in order to reach cancer stem
>cells, we might need to devise assays far more complex than conventionally
>used. The most traditional metric by which an anticancer chemical is
>judged - its ability to reduce the size of a tumor, or to kill cancer
>cells in a petri dish - won´t work, of course. If a chemical kills only
>the one-in-a-million cell that drives relapse, then it may not register as
>a tumor-shrinking or cancer-killing agent. A traditional drug hunt would
>most likely miss this kind of chemical - and yet this is precisely what is
>needed to attack the roots of cancer. To find drugs for cancer stem cells,
>then, we will need not just to find new chemicals, but also to find new
>strategies to test these chemicals.
>
>Still, for cancer researchers, the stem-cell hypothesis is as exciting as
>it is vexing. The capacity to tear out the roots of a tumor, and thereby
>dispel the specter of relapse, represents a sea change in our thinking
>about cancer. Indeed, the effort to isolate and target cancer stem cells
>is central to a much larger paradigm shift sweeping through cancer
>biology. Until recently, much of the field was focused on understanding
>the most salient feature of the cancer cell: its ability to divide
>uncontrollably. But our understanding of cancer has reached far beyond
>distorted cell division. Cancer cells co-opt neighboring blood vessels to
>supply themselves with oxygen. They enable their own movement through the
>body by hijacking genes that allow normal cells to move. When some cancers
>metastasize and punch holes in the bone to support their survival, they
>imitate an accelerated form of osteoporosis - in effect, recapitulating
>the aging process in bone.
>
>Cancer, it seems, is not merely mimicking the biology of rapidly dividing
>cells, but that of organs - or even organisms. At its cellular core, a
>tumor might nourish itself with its own supply of oxygen; it might
>organize its environment to fuel its growth; it might regenerate itself
>from a dedicated population of stem cells. Perhaps if we looked at cancers
>using appropriate conceptual lenses, we might find that tumors possess
>their own anatomy and physiology - a parallel universe to that of normal
>cells and organs. Such a tumor can hardly be described as a disorganized
>group of cells. It is a cellular empire, with its own sustenance, grammar,
>logic and organization. It is a growing being within a growing being.
>
>Hence the quest to discriminate between normal and malignant cells is
>progressively beginning to resemble one of those devastating surgical
>operations to separate conjoined twins. Every drug that kills cancer stem
>cells might also kill the normal stem cells. This operation, too, might
>end in tragedy for both twins.
>
>But it might not - and therein resides the hope for a next generation of
>drugs. If stem cells can be found for certain forms of cancer, and if a
>drug can be found to kill these cells in humans, then the clinical impact
>of such a discovery would obviously be enormous. And its scientific impact
>would be just as profound. Centuries after the discovery of cancer as a
>disease, we are learning not just how to treat it - but what cancer truly
>is.
>
> NY Times November 11, 2010
>
> April 13, 2011
>Do Cellphones Cause Brain Cancer?
>By SIDDHARTHA MUKHERJEE
>
>On Jan. 21, 1993, the television talk-show host Larry King featured an
>unexpected guest on his program. It was the evening after Inauguration Day
>in Washington, and the television audience tuned in expecting political
>commentary. But King turned, instead, to a young man from Florida, David
>Reynard, who had filed a tort claim against the cellphone manufacturer NEC
>and the carrier GTE Mobilnet, claiming that radiation from their phones
>caused or accelerated the growth of a brain tumor in his wife.
>
>"The tumor was exactly in the pattern of the antenna," Reynard told King.
>In 1989, Susan Elen Reynard, then 31, was told she had a malignant
>astrocytoma, a brain cancer that occurs in about 6,000 adults in America
>each year. To David Reynard, the shape and size of Susan´s tumor - a hazy
>line swerving from the left side of her midbrain to the hindbrain -
>uncannily resembled a malignant shadow of the phone (but tumors, like
>clouds, can assume the shapes of our imaginations). Suzy, as she was
>known, held her phone at precisely that angle against her left ear, her
>husband said. Reynard underwent surgery for her cancer but to little
>effect. She died in 1992, just short of her 34th birthday. David was
>convinced that high doses of radiation from the cellphone was the cause.
>
>Reynard v. NEC - the first tort suit in the United States to claim a link
>between phone radiation and brain cancer - illustrated one of the most
>complex conceptual problems in cancer epidemiology. In principle, a risk
>factor and cancer can intersect in three ways. The first is arguably the
>simplest. When a rare form of cancer is associated with a rare exposure,
>the link between the risk and the cancer stands out starkly. The
>juxtaposition of the rare on the rare is like a statistical lunar eclipse,
>and the association can often be discerned accurately by observation
>alone. The discipline of cancer epidemiology originated in one such a
>confluence: in 1775, a London surgeon, Sir Percivall Pott, discovered that
>scrotal cancer was much more common in chimney sweeps than in the general
>population. The link between an unusual malignancy and an uncommon
>profession was so striking that Pott did not even need statistics to prove
>the association. Pott thus discovered one of the first clear links between
>an environmental substance - a "carcinogen" - and a particular subtype of
>cancer.
>
>The opposite phenomenon occurs when a common exposure is associated with a
>common form of cancer: the association, rather than popping out,
>disappears into the background, like white noise. This peculiar form of a
>statistical vanishing act occurred famously with tobacco smoking and lung
>cancer. In the mid-1930s, smoking was becoming so common and lung cancer
>so prevalent that it was often impossible to definitively discern a
>statistical link between the two. Researchers wondered whether the
>intersection of the two phenomena was causal or accidental. Asked about
>the strikingly concomitant increases in lung cancer and smoking rates in
>the 1930s, Evarts Graham, a surgeon, countered dismissively that "the sale
>of nylon stockings" had also increased. Tobacco thus became the nylon
>stockings of cancer epidemiology - invisible as a carcinogen to many
>researchers, until it was later identified as a major cause of cancer
>through careful clinical studies in the 1950s and 1960s.
>
>But the most complex and most publicly contentious intersection between a
>risk factor and cancer often occurs in the third instance, when a common
>exposure is associated with a rare form of cancer. This is cancer
>epidemiology´s toughest conundrum. The rarity of the cancer provokes a
>desperate and often corrosive search for a cause ("why, of all people, did
>I get an astrocytoma?" Susan Reynard must have asked herself). And when
>patients with brain tumors happen to share a common exposure - in this
>case, cellphones - the line between cause and coincidence begins to blur.
>The association does not stand out nor does it disappear into statistical
>white noise. Instead, it remains suspended, like some sort of peculiar
>optical illusion that is blurry to some and all too clear to others. (A
>similarly corrosive intersection of a rare illness, a common exposure and
>the desperate search for a cause occurred recently in the saga of autism
>and vaccination. Vaccines are nearly universal, and autism is relatively
>rare - and many parents, searching to explain why their children became
>autistic, lunged toward a common culprit: childhood vaccination. An
>avalanche of panic ensued. It took years of carefully performed clinical
>trials to finally disprove the link.)
>
>The Florida Circuit Court that heard Reynard v. NEC was quick to discern
>these complexities. It empathized with David Reynard´s search for a
>tangible cause for his wife´s cancer. But it acknowledged that too little
>was known about such cases; "the uncertainty of the evidence . . . the
>speculative scientific hypotheses and [incomplete] epidemiological
>studies" made it impossible to untangle cause from coincidence. David
>Reynard´s claim was rejected in the spring of 1995, three years after it
>was originally filed. What was needed, the court said, was much deeper and
>more comprehensive knowledge about cellphones, brain cancer and of the
>possible intersection of the two.
>
>Allow, then, a thought experiment: what if Susan Reynard was given a
>diagnosis of astrocytoma in 2011 - but this time, we armed her with the
>most omniscient of lawyers, the most cutting-­edge epidemiological
>information, the most powerful scientific evidence? Nineteen years and
>several billion cellphone users later, if Reynard were to reappear in
>court, what would we now know about a possible link between cellphones and
>her cancer?
>
>To answer these questions, we need to begin with a more fundamental
>question: How do we know that anything causes cancer?
>
>The crudest method to capture a carcinogen´s imprint in a real human
>population is a large-scale population survey. If a cancer-causing agent
>increases the incidence of a particular cancer in a population, say
>tobacco smoking and lung cancer, then the overall incidence of that cancer
>will rise. That statement sounds simple enough - to find a carcinogen´s
>shadow, follow the trend in cancer incidence - but there are some
>fundamental factors that make the task complicated.
>
>The most important of these is life expectancy, which is growing almost
>everywhere. The average life expectancy of Americans has increased - from
>49 in 1900 to 78 in 2011. Several cancers are strongly, often
>exponentially, age-dependent. An aging population will seem more cancer-
>afflicted, even if the real cancer incidence has not changed.
>
>But what if we make an "age adjustment" for the population and shrink or
>expand the cancer incidence to match the changes in age structure? To ask
>whether cellphones increase the risk of brain cancer, then, we might begin
>by turning to this question: Has the age-adjusted incidence of brain
>cancer increased in the recent past?
>
>The quick answer is no. Brain cancer is rare: only about 7 cases are
>diagnosed per 100,000 men and women in America per year, and a striking
>increase, following the introduction of a potent carcinogen, should be
>evident. From 1990 to 2002 - the 12-year period during which cellphone
>users grew to 135 million from 4 million - the age-adjusted incidence rate
>for overall brain cancer remained nearly flat. If anything, it decreased
>slightly, from 7 cases for every 100,000 persons to 6.5 cases (the reasons
>for the decrease are unknown). In 2010, a larger study updated these
>results, examining trends between 1992 and 2006. Once again, there was no
>increase in overall incidence in brain cancer. But if you subdivided the
>population into groups, an unusual pattern emerged: in females ages 20 to
>29 (but not in males) the age-adjusted risk of cancer in the front of the
>brain grew slightly, from 2.5 cases per 100,000 to 2.6. These cancers
>appear in the frontal lobe - a knuckle-shaped area immediately behind the
>forehead and the eye. It is difficult to imagine that cellphones caused
>these frontal-lobe tumors: how, or why, would a phone´s toxicity have
>skipped over the area nearest to it and caused a tumor in a distant site?
>Most epidemiologists and biologists do not find such a tissue-skipping
>mechanism plausible and most doubt that there is any causal link between
>frontal tumors and phones.
>
>But a populationwide survey, you might argue, has its limits. The
>carcinogenic effect of a phone might be so subtle that it never registers
>in such a survey. A phone may cause cancer after a long lag time - say, 20
>years - and it may be too early to look for an effect in a general
>population. The survey data could be incomplete or of poor quality, thus
>limiting an epidemiologist´s ability to ever find a discernible link.
>
>Epidemiologists, fortunately, possess a more powerful alternative to
>uncover a link between a risk factor and cancer. Consider the classic
>studies that finally revealed the association between tobacco and lung
>cancer. In the late 1940s, Sir Richard Doll and Sir Austin Bradford Hill,
>working in London, and Ernst Wynder and Evarts Graham, working in St.
>Louis, began investigating whether tobacco smoking increased the risk of
>lung cancer.
>
>Working independently, Doll and Hill, and Wynder and Graham, devised
>remarkably similar kinds of surveys to reveal a possible link. Using
>hospital records, they identified a "case" group (a cohort of men with
>lung cancer) and a matched group of men without lung cancer (a "control"
>group).
>
>The case group and the control group were asked the same questions,
>including how much and how often they smoked. By comparing the responses
>of lung-cancer-afflicted men and nonafflicted men, the two teams of
>researchers stumbled on a striking association: men with lung cancer had a
>much longer and deeper history of smoking compared with men without lung
>cancer.
>
>What if you perform a similar case-control study with cellphones -
>comparing men and women suffering from brain cancer (cases) and men and
>women without brain cancer (controls) - looking at their past cellphone
>use? In 2010, an enormous study, called Interphone, tried to accomplish
>this task. Setting up the study took years: Interphone recruited
>participants in 13 countries, ran for a decade and included 5,117 brain-
>tumor cases and 5,634 controls. The study was coordinated by the World
>Health Organization and financed primarily by the European Union and
>cellphone companies, although by agreement industry representatives did
>not have privileged access to results before publication.
>
>Trials like Interphone are undertaken in the hope that they cleanse the
>field of doubts. In fact, Interphone achieved just the opposite effect: it
>ignited even more puzzling questions. Over all, the study found little
>evidence for an association between brain tumors and cellphones. But when
>the two cohorts - cancer and no cancer - were subdivided according to the
>frequency of cellphone use, bizarre results emerged. To start with, there
>was an apparently decreased risk of brain tumors in regular phone users,
>compared with rare users or nonusers. In other words, regular cellphone
>use seemed to reduce the risk of brain tumors. In stark contrast, very
>high cellphone use (measured as a user´s cumulative call time) seemed to
>increase the risk of a particular subtype of brain tumor. Needless to say,
>it is biologically implausible that these results are simultaneously true:
>how can regular cellphone use protect against cancer while frequent phone
>use increases risk? To most epidemiologists, including the authors of
>Interphone, the results point to a systemic flaw in the trial.
>
>Similar case-control studies have examined other kinds of brain tumors,
>including a rare nonmalignant tumor called an acoustic neuroma. Here, too,
>the trials have been contradictory. Multiple studies found no association
>with cellphone use. In contrast, one study from Sweden found an increased
>risk in people who used their phones for more than 10 years.
>
>How can trials that seem so similar at face value arrive at such disparate
>and contradictory results? The most likely common problem is bias - built
>into the very structure of these trials. In a case-control trial, patients
>are asked to remember their risk of exposure after the fact. In the
>Interphone study, for instance, participants were asked to recall the
>extent of their phone use years or even decades in their past. And memory,
>we now know, is a terribly slippery entity. A patient´s memory of his or
>her past is a particularly charged and malleable thing; burned into David
>Reynard´s memory, poignantly, is the shape of the cellphone in his wife´s
>hand and the imprint of the cancer on her brain.
>
>In fact, our memories turn out to be systematically fragile, especially
>when we are summoning our past to understand illness. In 1993, a Harvard
>researcher named Edward Giovannucci set out to measure this phenomenon.
>Giovannucci identified a cohort of women with breast cancer and an age-
>matched cohort without cancer, and asked each group about its previous
>dietary habits. The survey produced a reliable and reasonable trend: women
>with breast cancer were more likely to have consumed diets high in fat.
>
>But the women in Giovannucci´s study had also completed a dietary survey
>before their diagnosis of breast cancer. How did a woman´s memory of her
>diet compare with the actual diet that she recorded before her cancer
>diagnosis?
>
>Giovannucci´s study illustrates the insidious nature of "recall bias." In
>women with no cancer, there was no change between the actual and
>remembered diet. But women with breast cancer typically recalled a much-
>higher-fat diet than they actually consumed. The diagnosis of breast
>cancer had not just changed a woman´s present and the future; it had
>altered her sense of her past. Women with breast cancer had
>(unconsciously) decided that a higher-fat diet was a likely predisposition
>for their disease and (unconsciously) recalled a high-fat diet. It was a
>pattern poignantly familiar to anyone who knows the history of this
>stigmatized illness: these women, like thousands of women before them, had
>searched their own memories for a cause and then summoned that cause into
>memory.
>
>It is very likely that similar effects undid the Interphone trial: some
>men and women with brain cancer recalled a disproportionately high use of
>cellphones, while others recalled disproportionately low exposure. Indeed,
>10 men and women with brain tumors (but none of the "controls") recalled
>12 hours or more of use every day - a number that stretches credibility.
>In a substudy of Interphone, researchers embedded phones with special
>software to track phone usage. When this log was compared with the
>"recalled" usage, there were wide and random variations: some users
>underreported, while others overreported use.
>
>The trouble is that even the largest, longest, best-designed retrospective
>studies that rely on memory are likely to be riddled by recall bias.
>Typically, it is not the failure of memory that produces this bias, but
>its hyperactivity - its desire to explain the uncertainty of the present
>with the certainty of the past.
>
>There are certainly methods in epidemiology to counteract the biases
>created by selective memory: Interphone researchers could have initially
>identified a cohort of high-volume cellphone users and of nonusers, and
>followed them over time to determine who developed or did not develop
>cancer. Such a study - called a "prospective trial" - would certainly
>erase the biases of memory. But it would be logistically impossible to
>perform. Since the rates of brain cancer are small, about 6.5 cases per
>100,000 persons, a trial of this design would need to follow an enormous
>cohort of cellphone users - hundreds of thousands of participants - to
>record even a few cancers. And where on earth would you find the nonusers
>for the study? In most nations, cellphone usage is so common that finding
>500,000 people who will not use phones for a decade is hard to imagine.
>
>There are yet more powerful epidemiological methods that seem even more
>far-fetched. A trial that forcibly randomizes men and women to use
>cellphones or restrict phone use - a "randomized trial" - would certainly
>guarantee the most bias-free result, but would trespass inviolable ethical
>and practical concerns. Another study might try to minimize a person´s
>biased memory of exposure by collecting actual data on phone use from
>phone networks (scanning phone minutes and call logs from real bills), but
>this would violate privacy laws. Thus far, individual call logs - even
>anonymized logs - have not been made public to researchers.
>
>What if we moved the studies from humans to animals? Benzene,
>benzopyrenes, methylcholanthrene and some aniline derivatives (among many
>other chemicals) were first discovered as cancer-causing agents using
>mice, rats and rabbits. Decades before Doll and Hill´s elaborate studies
>on tobacco smokers in London, an Argentine biologist, Angel Roffo,
>"painted" rabbits with a grey-black solution containing distilled
>cigarette tar and demonstrated that the smoky residue caused cancer.
>
>Might an animal experiment identify the carcinogenicity of cellphone
>radiation that Interphone missed? Prototypical animal studies for
>carcinogens involve exposing one group of animals to the suspected agent
>and comparing it to the unexposed group. But as the 16th-century physician
>Paracelsus reminds us, "It is the dose that makes the poison." Determining
>the appropriate amount to test and delivering it to the right part of an
>animal´s body is often crucial to the experiment.
>
>At face value, testing "radiation," which is measured in standardized
>doses, would seem to make this simple. But all radiation is not created
>equal. The word "radiation" refers to energy that emanates from a source -
>but the spectrum of radiant energy is broad. On the highly energetic end
>of the spectrum is ionizing radiation - like X-rays or cosmic rays - that
>are so powerful they can tear away electrons from atoms and molecules and
>penetrate barriers like the skull and the brain. On the way into - and
>through - the body, they deposit powerful bursts of energy, generate
>corrosive chemicals, ruffle up DNA, kill cells and, most notably, mutate
>growth-controlling genes to cause cancer.
>
>Nonionizing radiation lies on the other end of the energy spectrum. These
>rays can warm cells, boil water and stimulate chemical reactions, but they
>cannot strip electrons away from atoms or damage DNA. They have no
>capacity to mutate genes directly and thereby no simple and direct means
>of initiating cancer. Radiation from microwaves, from cellular phones and
>from light bulbs are examples of nonionizing radiation.
>
>All of this makes cellphone radiation a relatively unlikely culprit as a
>mutation-causing agent. Nonetheless, biologists have exposed mice and rats
>to chronic nonionizing radiation (comparable to that emitted by phones) to
>determine whether it causes cancer. In rats prone to developing breast
>cancer, there was no acceleration of breast cancer. In another experiment,
>rats were treated with a chemical carcinogen in utero (to "prime" them to
>develop brain tumors) and then exposed to radiant energy comparable to
>cellphone radiation for two hours per day, four days a week, for 22
>months. The experiment revealed no increased incidence of brain tumors in
>rats. Nor was there any accelerated growth in previously established brain
>tumors. From 1997 to 2004, six independent experiments on mice and rats
>studied the effects of chronic radiation on brain cancer. No experiment
>revealed an increased risk of brain cancer.
>
>But radiant energy need not penetrate the brain and mutate genes to have a
>biological effect on it. A cellphone user might experience changes in
>physiology that have nothing to do with the ionizing capacity of
>radiation. Might a cellphone leave a physiological mark on the brain
>through a yet unknown mechanism?
>
>A recent study by Nora Volkow, published in The Journal of the American
>Medical Association (JAMA) and reported in this newspaper on March 30, has
>raised this unusual possibility. Volkow is an innovative brain researcher
>who is director of the National Institute on Drug Abuse in Bethesda, Md.
>She recruited 47 people and placed an "active" phone next to one ear (the
>phone was on - generating radiation, but silent, so that Volkow could
>eliminate the effects of sound and conversation). She then used a
>specialized brain scanner capable of detecting alterations in glucose.
>Glucose - a sugar - is the metabolic fuel for the brain. When parts of the
>brain are activated, brain cells begin to metabolize glucose at an
>increased rate. Volkow´s scanner was equipped to detect even marginal
>changes in glucose metabolism.
>
>When Volkow compared subjects with phones turned on with subjects who had
>their phones turned off, she found a striking pattern: there was a
>telltale sign of increased brain-glucose activity in the area of the brain
>immediately adjacent to the antenna of the phone.
>
>But as Volkow points out, there is still a long conceptual leap from
>"increased brain-­glucose activity" to "brain cancer." Our brains are
>constantly altering the metabolism of sugar - the flux of glucose changes
>when we remember Grandma´s house in Texas or listen to Bach or smell
>roses. When human beings dream during sleep, the increase in glucose
>metabolism in some parts of the brain is just as striking as the increase
>found in Volkow´s study with phones. "It´s not a dramatic increase," she
>says. "When our eye responds to a visual cue, glucose metabolism in the
>brain increases much more dramatically" - and, surely, we do not think
>that visual stimulation causes cancer. Her study proves, importantly, that
>cellphone radiation has a biological effect on the brain. But whether this
>effect is consequential - whether it causes cancer or, for that matter,
>protects against it - is entirely speculative.
>
>The most exquisite - and arguably the most sensitive - means to identify a
>carcinogen is to study the effects of the substance not on humans or
>animals but on cells. In the 1970s, a Berkeley biochemist named Bruce Ames
>devised a cellular test to do just that. Ames´s test is based on a series
>of simple principles. Normal cells in the body grow through cell division,
>or mitosis, which is carefully regulated by genes. Certain genes
>accelerate growth, while other genes dampen or stop it. Cancer originates
>when the "accelerator" genes are permanently activated or when the "brake"
>genes are permanently damaged. Since genes are encoded by DNA, chemicals
>that mutate DNA - mutagens - can alter the growth-controlling genes and
>thereby cause cancer. Ames devised a special strain of bacterial cells
>that act as a "sensor" for mutations and therefore can also detect
>mutagenic chemicals. Chemical mutagens are so commonly carcinogenic that
>versions of the Ames test represent the gold standard by which most
>carcinogens are found.
>
>Cellphone radiation is not a chemical, of course, but the rules about
>mutagenicity still apply (X-rays, for instance, are known to cause cancer
>and are detectable by Ames´s test). Laboratory experiments that link phone
>radiation to DNA mutation using a version of the Ames test have been
>largely contradictory. In 2005, a panel of experts, including a biomedical
>engineer, an epidemiologist, a genetic toxicologist and a radiation
>biologist, published a review of nearly 1,700 scientific papers on the
>cellular effects of radiation emitted by phones. In the review of more
>than 50 experiments linking phone radiation to DNA damage in animal or
>bacterial cells, evidence of damage has been negative in more than two-
>thirds of the studies. Since nonionizing radiation cannot directly affect
>the structure of DNA, experiments linking phone radiation to DNA damage
>are generally unconvincing. The most striking study linking cellular phone
>radiation to DNA damage, published in 2005 by researchers from the Medical
>University of Vienna, has recently been embroiled in even deeper
>scientific controversy: researchers studying the data intensively have
>argued that the original study is fraudulent.
>
>But it is possible for something to be a carcinogen without directly
>damaging DNA. Some chemicals might activate growth pathways or survival
>pathways in cancer cells (eventually damaging DNA and mutating genes - but
>indirectly). Exogenous estrogen, for instance, activates growth pathways
>in breast cells and can cause breast cancer but doesn´t damage DNA. Others
>may provoke inflammation, creating a physiological milieu in the body that
>allows malignant cells to grow and survive. Yet others - the class of
>substances that we know least about - might not damage DNA directly but
>chemically modify genes so that their regulation is changed. These
>substances are like the dark matter of the carcinogenic world: they are
>barely visible to our current tests for carcinogens and thus lie at the
>boundaries of the knowable universe. Cellphones and their radiation have
>been tested for many of these properties - for instance, their ability to
>chemically modify DNA without causing mutations - but evidence linking
>this form of radiation to such cellular changes remains largely negative.
>
>In the expert panel´s 2005 review, the authors summarized the evidence:
>"There is little theoretical basis for anticipating that RF energy [from
>cellular phones] would have significant biological effects at the power
>levels used by modern mobile phones and their base station antennas. The
>epidemiological evidence for a causal association between cancer and RF
>energy is weak and limited. Animal studies have provided no consistent
>evidence that exposure to RF energy at nonthermal intensities causes or
>promotes cancer. Extensive in vitro studies have found no consistent
>evidence of [DNA damage] potential, but in vitro studies assessing the
>epigenetic potential of RF energy are limited. Over all, a weight-of-
>evidence evaluation shows that the current evidence for a causal
>association between cancer and exposure to RF energy is weak and
>unconvincing."
>
>The word "carcinogen," it is believed, was first coined by the surgeon
>James Paget in an obscure passage of a lecture on surgical pathology in
>1853. Paget asked if there is "one material for cancer, one carcinogen,"
>that "may form different but closely allied compounds?"
>
>Our vision of carcinogenesis has become vastly more complex since 1853. We
>now know that there is no "one cancer." Breast, lung, prostate and blood
>cancer share a similarity - the uncontrolled growth of cells - but the
>specific genes and behaviors of these cancers are far from identical.
>
>Nor is there "one material for cancer" - one archetypal carcinogen. Agents
>that cause cancer are chemically diverse and cancer-specific. Estrogen can
>provoke cancer in the breast, but destroys prostate-cancer cells; vinyl
>chloride is exquisitely carcinogenic to the liver but not to the skin;
>chlorine and nitrogen mustard are both poison gases, but only one causes
>leukemia.
>
>Notably, there is also no "one test" for carcinogens. Scientific studies
>to capture the association between an agent and cancer cast an
>astonishingly wide net. On one end of that spectrum lie populationwide
>human trials involving hundreds of thousands of men and women. On the
>other end are precise laboratory experiments that plumb the molecular
>depths of cells and genes. The tests range from the telescopic to
>microscopic, from statistics to biochemistry - from observations of
>chimney sweeps to bacteria on a petri dish. Often one test must be
>corroborated by another. Asbestos and tobacco were identified by case-
>control studies and validated in animal models. Estrogens were implicated
>by studies on human and animal physiology and then found to be
>carcinogenic in prospective human trials.
>
>Finding a carcinogen, in short, is not like solving a mathematical
>equation, with a single formula and solution. It is more like solving an
>epic detective case, with individual pieces of evidence that, taken
>together, suggest a common culprit.
>
>But thus far, this extraordinarily wide-cast net has yet to find solid
>proof of risk for cellphone radiation: not a single trial or test that has
>attributed carcinogenic potential has been free of problems.
>Populationwide studies have failed to demonstrate an increased incidence;
>retrospective trials have been contradictory and riddled with biases;
>animal studies negative; human physiological experiments inconclusive;
>cellular studies inconsistent and weak. What is clearly needed, experts
>agree, is a single, definitive, unbiased study - "one trial," to borrow
>Paget´s terminology. Logistically speaking, the simplest such human trial
>is a case-control study that compares cancer patients with healthy
>patients, using phone-log data that companies have thus far been reluctant
>to provide. The simplest animal study involves subjecting rats and mice to
>long-term exposure to cellphone radiation. The National Toxicology Program
>has begun such a study. Cellphone radiation will be turned on and off for
>10-minute stretches for 20 hours each day. This experiment - the closest
>we will get to making mice use actual cellphones - is likely to be
>published in 2014.
>
>It is possible, of course, that even these sophisticated experiments will
>be unable to determine the risk. The lag time of cancer development with
>phone use may be 50 or 70 years - and cellphones have been around for only
>three decades or so. Yet even a slow-lagging cancer is unlikely to arise
>at a single point in time after exposure. Like most biological phenomena,
>cancer risk typically rides a statistical curve, with some patients
>developing cancer early, others peaking in the middle and yet others
>trailing off decades later. Thus far, no such statistical curve has been
>evident for brain cancer.
>
>Might the cellphone industry have already performed such experiments and
>conspired to keep real data on brain cancers from us - just as the tobacco
>industry conspired to obfuscate real data on tobacco and carcinogenesis in
>the 1950s? It´s possible, but there are important differences in comparing
>these trials with the tobacco studies. With smoking, despite active
>attempts by the industry to stifle data, the epidemiological trials were
>incontrovertibly positive, human physiological data markedly suggestive
>and animal studies (including Roffo´s painted-rabbit experiment) striking.
>
>As we await the definitive trial, then, it´s probably wise to also start
>thinking differently about the cause of Susan Reynard´s cancer. When a
>suspected cause for a devastating illness begins to slip away, there is
>often frustration and turmoil, paranoia and nihilism. In a short story by
>Lorrie Moore, the mother of a toddler with cancer rattles off a list of
>potential causes of her child´s illness - "giant landfills, agricultural
>run-off"; "lurid water"; "toxic potatoes"; "Joe McCarthy´s grave."
>
>The trouble with this kind of grasping is that it is indiscriminate. In
>truth, many substances of modern life do not - cannot - cause cancer. Some
>do, and it´s absolutely critical to identify and reduce exposure to them.
>Others don´t, and it´s absolutely worthwhile identifying these, so that we
>can focus on the real carcinogens around us. If we lump everything into
>the category of "potentially carcinogenic," from toxic potatoes to
>McCarthy´s grave, then our scientific language around cancer begins to
>degenerate. The effect is like crying "wolf" about cancer: the public
>progressively numbs itself to real environmental toxins and becomes
>disinvested in finding bona fide carcinogens.
>
>To keep ourselves on the right path on environmental carcinogens, then, we
>need not just standards to rule carcinogens "in" but also standards to
>rule them "out." The final, definitive trials on phone radiation may
>settle this issue - but, as of now, the evidence remains far from
>convincing. Understanding the rigor, labor, evidence and time required to
>identify a real carcinogen is the first step to understanding what does
>and does not cause cancer.
>
>Siddhartha Mukherjee (smukherj2011@gmail.com) is an assistant professor of
>medicine in the division of medical oncology at Columbia University. He is
>the author of "Emperor of All Maladies: A Biography of Cancer." Editor:
>Ilena Silverman (i.silverman-MagGroup@nytimes.com).
>
>

------------------------------------

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