[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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