The Next Front in Cancer Care

As More Patients Survive, Cancer Centers Handle Disease’s Knock-On Effects




Dec. 9, 2013 7:34 p.m. ET
For cancer patients, getting through the rigors of treatment is the first hurdle. Then, life as a cancer survivor poses its own daunting physical and emotional challenges.

A growing number of hospitals and community cancer centers, which treat the majority of the nation’s cancer patients, are launching survivorship-care programs. These include treatment follow-up plans, physical rehabilitation and emotional assistance, such as counseling and support groups. They resemble programs currently offered by big urban cancer centers like MD Anderson in Houston and Memorial Sloan-Kettering in New York.


As more cancer patients are treated successfully, treatment centers are focusing on the next phase and discovering it can pose daunting challenges that require new approaches to care. Laura Landro explains on Lunch Break. Photo: Greenville Health System.

Chemotherapy and radiation can damage vital organs such as the heart and liver, possibly causing secondary diseases years later. The body can be debilitated, cognitive functions impaired and emotions distressed, making return to normal life and work difficult. Some 70% of cancer survivors experience depression at some point. Patients have higher levels of anxiety years after the disease is cured. And there is always the chance that cancer will return.

More patients are expected to face such health issues as the number of cancer survivors grows, partly due to improved early detection and treatment.

The Commission on Cancer, a consortium of professional organizations that accredits U.S. cancer centers treating 70% of newly diagnosed patients, will begin in 2015 requiring that they provide survivorship-care plans for their patients.

“I tell patients now we are going to follow you for your entire lifetime,” says W. Larry Gluck, an oncologist and medical director of the Greenville Health System’s Cancer Institute, in Greenville, S.C., which set up a Center for Integrative Oncology and Survivorship in 2011. “The mental and physical needs of cancer patients go on long after therapy has been completed.” In the past, patients typically were sent back to their family doctor, who might have little knowledge of delayed side effects or complications of treatment and recurrence risks, Dr. Gluck says.

There are close to 14 million cancer survivors living in the U.S., a number that is expected to grow to 18 million by 2022, according to the National Cancer Institute. About 40% have been alive 10 years or more after diagnosis (including this reporter, a leukemia survivor).

Private health insurers and Medicare typically cover cancer patients’ medical visits, during which some survivorship-care planning can take place. Cancer centers say some private insurers consider survivorship planning a necessary service. A bill currently in congressional committee, the Planning Actively for Cancer Treatment Act would require Medicare to cover care-planning services at diagnosis and once cancer patients finish treatment.

Nonprofit groups like Cancer Support Community, which was formed in 2009 through the merger of two of the largest support organizations, Gilda’s Club and the Wellness Community, offer free services including personalized assessment and care plans, distress screening, support groups and complementary therapies such as yoga and meditation. Last year, it announced a partnership with Greenville to incorporate its services into the hospital system as part of the recent survivorship center.

“Cancer hospitals are realizing that they have to be a one-stop shop, taking care not just of the body, but of the mind and soul of the survivor,” says Kim Thiboldeaux, chief executive officer of Cancer Support Community.


After being treated at the Greenville, S.C., Cancer Institute last year, Renee Gossman says yoga classes at the institute’s survivorship center helped her regain strength. Greg Beckner

Renee Gossman, 71, a personal trainer who teaches water aerobics, was diagnosed at the Greenville Cancer Institute with uterine cancer in January 2012. She had a hysterectomy, chemotherapy and radiation. Ms. Gossman, who doesn’t have a lot of family living nearby, says she was fatigued and felt isolated during nearly a year of treatment. “You get through all of that, and then it’s like, what’s going to happen now?” she says.

Ms. Gossman says her oncologist, Larry Puls, referred her late last year to Greenville’s survivorship center where she met with a social worker, a nurse navigator and a dietitian. She received a summary of her treatment, copies of her pathology reports, a follow-up plan and a summary of other programs and activities she might find helpful.

“They give you a team of people who are going to look after you, get you back involved in the world and see to your physical, social and emotional needs,” Ms. Gossman says. She started a 12-week exercise program at the center that focuses on restoring aerobic conditioning, muscular strength and flexibility. She also began taking yoga classes and a writing workshop through the Cancer Support Community program at Greenville. Ms. Gossman currently volunteers once a week as a greeter in the lobby of the cancer institute.

Other services offered at Greenville include free nutrition counseling and help with the after-effects of specific cancers, such as swelling, called lymphedema, that often occurs after breast-cancer surgery.

Patients, and their caregivers, are encouraged to use the survivorship center as a resource, says Regina Franco, a nurse practitioner and manager of the survivorship center. “If you hear on the news that you should be taking vitamin E, call us and ask, ‘Is this really something I should be doing?’ “

Greenville recently joined with researchers at the University of South Carolina to open a human-performance lab that will assess patients before and after treatment, billed as an office visit.

One area of research: how cancer and chemotherapy affect energy production at the cellular level and how exercise might restore some of the damage. Also being studied is the impact of complementary therapies such as yoga, massage and acupuncture, Dr. Gluck says.

Many smaller cancer centers and oncology practices are using a software program called Journey Forward, created by a group of advocacy organizations and health companies, to create customized follow-up plans. The program, which includes resources for both doctors and patients, has been downloaded about 30,000 times since it was launched in 2009, says Shelley Fuld Nasso, chief executive of the nonprofit National Coalition for Cancer Survivorship, which helped develop the software. For cancer survivors, “things can come up many years down the road that you aren’t expecting or prepared for,” she says.

Write to Laura Landro at



Differences in How Men and Women Think Are Hard-Wired

Recent Studies Raise the Possibility That Male Brains Are Wired for Focus, Female Brains for Multitasking 


Dec. 9, 2013 7:04 p.m. ET

Researchers are finding brains of women and men display distinctive differences that are shaped by the interplay of heredity, experience, and biochemistry. Science writer Robert Lee Hotz explains on Lunch Break. Photo: Getty Images.

So many things come down to connections—especially the ones in your brain.

Women and men display distinctive differences in how nerve fibers connect various regions of their brains, according to a half-dozen recent studies that highlight gender variation in the brain’s wiring diagram. There are trillions of these critical connections, and they are shaped by the interplay of heredity, experience and biochemistry.

No one knows how gender variations in brain wiring might translate into thought and behavior—whether they might influence the way men and women generally perceive reality, process information, form judgments and behave socially—but they are sparking controversy.

“It certainly is incendiary,” said Paul Thompson, a professor of neurology and director of the University of Southern California’s Imaging Genetics Center. He is directing an effort to assemble a database of 26,000 brain scans from 20 countries to cross-check neuroimaging findings. “People who look at findings about sex differences are excited or enraged,” he said.

Combined brain scans of 949 subjects, ages 8 to 22, show how neural connections differ by gender. Male brains, top, have more connections within hemispheres (blue lines). Female brains, bottom, have more between hemispheres (orange lines). Proceedings of The National Academy of Sciences/University of Pennsylvania

Researchers are looking at the variations to explain the different ways men and women respond to health issues ranging from autism, which is more common among men, and multiple sclerosis, which is more common among women, to strokes, aging and depression. “We have to find the differences first before we can try to understand them,” said Neda Jahanshad, a neurologist at USC who led the research while at the University of California, Los Angeles.

Dr. Jahanshad and her UCLA collaborators conducted a 2011 brain-imaging study of healthy twins, including 147 women and 87 men, to trace connections in the brain. She discovered “significant” sex differences in areas of the brain’s frontal lobe, which is associated with self-control, speech and decision-making.

In the most comprehensive study so far, scientists led by biomedical analyst Ragini Verma at the University of Pennsylvania found the myriad connections between important parts of the brain developed differently in girls and boys as they grow, resulting in different patterns of brain connections among young women and young men.

The team imaged the brains of 949 healthy young people, 521 females and 428 males, ranging in age from 8 to 22. Like Dr. Jahanshad’s team, Dr. Verma employed a technique called Diffusion Tensor Imaging to trace how water molecules align along the brain’s white-matter nerve fibers, which form the physical scaffolding of thought. The study was reported earlier this month in the journal the Proceedings of the National Academy of Sciences.

Pairs of scan images show gender differences in brain wiring in childhood (1), adolescence (2) and young adulthood (3). Male brains are on left, female on right.University of Pennsylvania, Proceedings of The National Academy of Sciences.

The neural patterns emerged only when combining results from hundreds of people, experts said. In any one person, gender patterns may be subsumed by the individual variations in brain shape and structure that help make every person unique.

Dr. Verma’s maps of neural circuitry document the brain at moments when it is in a fury of creation. Starting in infancy, the brain normally produces neurons at a rate of half a million a minute, and reaches out to make connections two million times a second. By age 5, brain size on average has grown to about 90% of adult size. By age 20, the average brain is packed with about 109,000 miles of white matter tissue fibers, according to a 2003 Danish study reported in the Journal of Comparative Neurology.

Spurred by the effects of diet, experience and biochemistry, neurons and synapses are ruthlessly pruned, starting in childhood. The winnowing continues in fits and starts throughout adolescence, then picks up again in middle age. “In childhood, we did not see much difference” between male and female, Dr. Verma said. “Most of the changes we see start happening in adolescence. That is when most of the male-female differences come about.”

Broadly speaking, women in their 20s had more connections between the two brain hemispheres while men of the same age had more connective fibers within each hemisphere. “Women are mostly better connected left-to-right and right-to-left across the two brain hemispheres,” Dr. Verma said. “Men are better connected within each hemisphere and from back-to-front.”

That suggests women might be better wired for multitasking and analytical thought, which require coordination of activity in both hemispheres. Men, in turn, may be better wired for more-focused tasks that require attention to one thing a time. But the researchers cautioned such conclusions are speculative.

Experts also cautioned that subtle gender differences in connections can be thrown off by normal disparities in brain size between men and women and in the density of brain tissue. Other factors, such as whether one is left- or right-handed, also affect brain structure.

Also affecting results are differences in how computer calculations are carried out from one lab to the next. “With neuroimaging, there are so many ways to process the data that when you do process things differently and get the same result, it is fantastic,” Dr. Jahanshad said.

Write to Robert Lee Hotz at


How Your Knees Can Predict the Weather

Granny was right: Scientists find link between achy joints and the forecast


Oct. 14, 2013 7:12 p.m. ET
The Wolff family of Paramus, N.J., was eyeing the gathering clouds and debating whether to cancel a planned park trip when 6-year-old Leora piped up with an idea: “Let’s call Grandma. Her knees always know when it’s going to rain!”

Leora’s grandmother, Esther Polatsek, says she started being sensitive to the weather in her 20s, when a fracture in her foot would ache whenever a snowstorm approached. Now 66 and plagued by rheumatoid arthritis, Mrs. Polatsek says she suffers flare-ups whenever the weather is about to change.

“It’s just uncanny. Sometimes it’ll be gorgeous out, but I’ll have this awful pain. And sure enough, the next morning it rains,” she says. “It may be just a few drops, but it makes my body crazy.”

Do weather conditions really aggravate physical pain?

It is one of the longest running controversies in medicine.

Weathering the Pain

You can’t change the forecast, but you can lessen its impact.

  • Take a pain reliever or anti-inflammatory in advance if a storm or cold weather is forecast.
  • Dress warmly in the cold, including thermal socks, gloves and a vest.
  • Keep out drafts at home by sealing doors and windows and carpeting floors.
  • Apply heat to aching joints.
  • Use a dehumidifier to avoid spikes in dampness.
  • Consider visiting a warm, dry climate, although the benefits may wear off after a prolonged stay.
  • Maintain a healthy body weight.
  • Stay active, keeping muscles strong around damaged joints.

Hippocrates in 400 B.C. noticed that some illnesses were seasonal. The traditional Chinese medicine term for rheumatism (fengshi bing) translates to “wind-damp disease.”

But modern scholars have gotten inconsistent results in studies that tried to match weather patterns to reported pain symptoms—leading some to dismiss the connection as highly subjective or all in sufferers’ minds.

“People’s beliefs about arthritis pain and the weather may tell more about the workings of the mind than of the body,” concluded the late Stanford psychologist Amos Tversky in the mid-1990s, after comparing the pain reports of 18 rheumatoid-arthritis patients with local weather conditions for a year and finding no connection.

Still, other studies have linked changes in temperature, humidity or barometric pressure to worsening pain from rheumatoid arthritis and osteoarthritis, as well as headaches, tooth aches, jaw pain, scar pain, low-back pain, pelvic pain, fibromyalgia, trigeminal neuralgia (a searing pain in the face), gout and phantom-limb pain.

Bill Balderaz had a rheumatoid-arthritis flare-up last year—just before a surprise storm hit Ohio.Jason Joseph

Scientists don’t understand all the mechanisms involved in weather-related pain, but one leading theory holds that the falling barometric pressure that frequently precedes a storm alters the pressure inside joints. Those connections between bones, held together with tendons and ligaments, are surrounded and cushioned by sacs of fluid and trapped gasses.

“Think of a balloon that has as much air pressure on the outside pushing in as on the inside pushing out,” says Robert Jamison, a professor of anesthesia and psychiatry at Harvard Medical School. As the outside pressure drops, the balloon—or joint—expands, pressing against surrounding nerves and other tissues. “That’s probably the effect that people are feeling, particularly if those nerves are irritated in the first place,” Dr. Jamison says.

Not everyone with arthritis has weather-related pain, says Patience White, a rheumatologist at George Washington University School of Medicine and a vice president of the Arthritis Foundation. “It’s much more common in people with some sort of effusion,” an abnormal buildup of fluid in or around a joint that frequently occurs with inflammation.

Many patients swear that certain weather conditions exacerbate their pain. Consequently, orthopedists, rheumatologists, neurologists, family physicians, chiropractors, physical therapists—even personal trainers—report an increase in grousing among their clients when the temperature drops or a storm approaches.

“I can tell you emphatically there are certain days where practically every patient complains of increased pain,” says Aviva Wolff, an occupational therapist at the Hospital for Special Surgery in New York City, and Mrs. Polatsek’s daughter. “The more dramatic the weather change, the more obvious it is.”

Both the Weather Channel and AccuWeather have indexes on their websites that calculate the likelihood of aches and pains across the country, based on barometric pressure, temperature, humidity and wind. Changes in those conditions tend to affect joints even more than current conditions do, says AccuWeather meteorologist Michael Steinberg, which is why the Arthritis Index shows more risk the day before a storm or a sharp drop in temperature is forecast.

Some sufferers say their joints can be more accurate than meteorologists. Rheumatoid-arthritis sufferer Bill Balderaz, 38, president of a digital-marketing firm in Columbus, Ohio, recalls feeling “the worst arthritis pain I’ve ever had—I could barely move” one day last year, even though it was sunny and clear. By midafternoon, a land-based hurricane known as a derecho with 80 mile-per-hour winds unexpectedly buffeted Ohio and three other states, traveling 600 miles in 10 hours and knocking out power for 10 days. “The storm caught everyone off guard. It was clear one minute and then the skies opened up,” Mr. Balderaz says.

Tests on animals seem to bear out the impact of weather. In one study, guinea pigs with induced back pain exhibited signs of increased pain by pulling in their hindpaws in low barometric pressure.

Cold weather seems to raise the risk of stroke, heart attacks and sudden cardiac death, some research shows. Heart-attack risk rose 7% for every 10 degrees Celsius (18 degrees Fahrenheit) drop in temperature, according to a study of nearly 16,000 patients in Belgium, presented at the European Society of Cardiology last month. British researchers studying years of data on implanted defibrillators found that the risk of ventricular arrhythmia—an abnormal heart rhythm that can lead to sudden death—rose 1.2% for every 1.8 degrees Fahrenheit drop, according to a study in the International Journal of Biometerology last month.

Once blamed on physically demanding tasks like shoveling snow, the increased heart risk due to cold may be due to thickening blood and constricting blood vessels, researchers think.

And rising humidity may cause joints to swell and stiffen. In fact, tendons, ligaments, muscles, bones and other tissues all have varying densities, so they may expand or contract in different ways in changing conditions, Dr. Jamison says.

In people with chronic inflammation from arthritis or past injuries, even slight irritations due to the weather can aggravate sensory nerve cells, known as nociceptors, that relay pain signals to the brain. That may explain why some people with neuropathic pain and phantom-limb pain also report weather-related flare-ups.

“Fibromyalgia patients seem to be the most sensitive,” says Susan Goodman, a rheumatologist at the Hospital for Special Surgery. She also notes that while some people seem to be extremely sensitive to weather, others with similar conditions aren’t, for reasons that aren’t clear. That may explain why many studies find no clear association, she says.

Some weather conditions seem to relieve pain. In one study, the warm, high-pressure Chinook winds common to western Canada lessened patients’ neuropathic pain, the kind brought on by disease or injury. For other patients, the same climate increased migraines and sinus headaches.

Some pain sufferers say they feel better in warm, dry climates where weather conditions seldom change. When she went to Israel in the 1990s, “I felt like I was 20 years younger when I stepped off the plane,” says Mrs. Polatsek, the rheumatoid-arthritis patient.

But studies haven’t consistently borne out the benefits of one climate over another. “There really is no place in the U.S. where people report more or less weather-related pain,” says Dr. Jamison. He surveyed 557 arthritis sufferers in four cities in 1995 and found that more than 60% believed the weather affected their pain—regardless of whether they lived in San Diego, Boston, Nashville, Tenn., or Worcester, Mass.

Visiting a warm, dry climate may bring temporary relief, Dr. Jamison adds. “But if you live there full time, your body seems to acclimatize and you become sensitive to even subtle weather changes.”

Write to Melinda Beck at



Genetic Manipulation Extends Life of Mice 20%

But Translating Findings to Humans Faces Many Hurdles

By reducing the activity of one type of gene, scientists said they increased the average life span of mice by about 20%, a feat that in human terms is akin to extending life by about 15 years.

Moreover, the researchers at the National Institutes of Health found that memory, cognition and some other important traits were better preserved in the mice as they aged, compared with a control group of mice that had normal levels of a protein put out by the gene.

By manipulating a single gene, scientists at the National Institutes of Health said they increased the average life span of mice by about 20%, a feat that in human terms is akin to extending life to about 90 years from 75. Ron Winslow reports. Photo: Getty Images.

The findings, published Thursday in the journal Cell Reports, strengthen the case that the gene, called mTOR, is a major regulator of the aging process.

The mice were bred to put out just 25% of the normal levels of mTOR protein, indicating that suppressing the activity of the gene “clearly makes mice live longer,” said Toren Finkel, head of the laboratory of molecular biology in NIH’s National Heart, Lung and Blood Institute and senior author of the new study.

Though mouse studies don’t always translate to humans, Dr. Finkel and other researchers said the results raise the possibility that targeting the gene with drugs that inhibit its activity might one day be at least part of a strategy for prolonging longevity in people.

Such a drug, an immunosuppressant called rapamycin, and some similar agents already are on the market and used to treat certain diseases, but researchers cautioned against taking such medicines, which have side effects, for anything but approved uses.

NIH/NHLBINIH researchers found that lowering the expression of a single gene helped extend the life of mice by about 20%. A mouse with a manipulated gene on the left and an unchanged mouse on the right.

The results also build on a growing body of research challenging the belief that aging is an intractable biological process, prompting scientists to think of slowing aging as a possible way to prevent disease.

“What we need right now is for scientists and the public to wake up to the concept that you can slow aging,” said Brian Kennedy, president of the Buck Institute for Aging Research in Novato, Calif., who wasn’t involved in the new study. “If you do, you prevent many of the diseases that we’re so scared of and that are associated with aging.” They include cardiovascular disease, cancer and Alzheimer’s disease.

Major hurdles stand in the path of translating the findings to humans, including whether inhibiting the action of mTOR would have similar life-extending effects, and if it did whether the benefit would come without unwanted problems.

The mice in the study had softer bones, developed more infections—probably from a depressed immune system—and may have had a higher risk of cataracts than normal mice, the researchers found. But they were also significantly less likely to develop cancer, Dr. Finkel said.

The mTOR gene has a well-established role in the metabolism and energy balance of cells, and researchers believe it is associated with the concept of caloric restriction. It has been known for about a century that animals that eat less live longer.

When there are a lot of calories present in cells, mTOR activity is turned up, “signaling the cell to grow and divide,” Dr. Kennedy said. “If there are fewer calories, the pathway is turned down and that signals the cell to stop proliferating and become stress resistant.” That helps animals live longer, he said.

The name mTOR stands for mechanistic target of rapamycin, a drug used in certain treatments for cancer and heart disease and also to suppress the immune system to prevent rejection of organ transplants.

“It’s early days to suggest that rapamycin is something that people would want to take” to increase longevity,” said David Sabatini, professor of biology at the Massachusetts Institute of Technology and the Whitehead Institute for Biomedical Research in Cambridge, Mass., who wasn’t involved in Thursday’s study. “But [research] is clearly hinting at a pathway that matters.”

In the study, Dr. Finkel found that the median life span for the mTOR-deficient mice was 28 months for males and 31.5 months for females, compared with the span for normal mice of 22.9 months for males and 26.5 months for females.





Gene Breakthroughs Spark a Revolution in Cancer Treatment

A growing number of cancer practices are sequencing the DNA of tumors to uncover their genetic abnormalities. The aim: to pair a drug with the specific mutation fueling a patient’s disease. UC San Francisco’s Dr. Trever Bivona discusses.

Kellie Carey’s doctor finally stopped dodging questions about how long she had to live six weeks after he diagnosed her lung cancer.

“Maybe three months,” he told her in his office one sunny May morning in 2010, she recalls.

Yet she is still alive, a testament to the most extraordinary decade of progress ever in the long scientific struggle against lung cancer.

Tests found Ms. Carey’s lung cancer to be of a rare type that researchers had found just three years earlier by deciphering its genetic code. The 45-year-old businesswoman in 2010 went on a drug Pfizer Inc. PFE +0.27% was testing for that type. By pinpointing her cancer, the drug probably helped give her years more to live than chemotherapy would have, her doctors say.

Jesse Neider for The Wall Street JournalKellie Carey, who was given three months to live in 2010, discusses her lung-cancer treatment with her doctor, Roy Herbst, last month.

That is remarkable because lung cancer for decades defied efforts to find drugs that could extend an average patient’s life by even a few weeks.

But an explosion in knowledge about the genetic mutations that cause tumors is just now offering the first real promise of drugs that can control what is the most-common and most-deadly cancer.

Ms. Carey has one of at least 15 lung-cancer variations, almost all of which scientists didn’t know existed 10 years ago. Researchers have identified those variations, most of them in just the past four years, by decoding DNA in tumors—akin to how crime labs analyze DNA to genetically fingerprint suspects.

The newfound variants have led major cancer centers to revamp their approach to treating cancer and have spurred a rush among drug companies to find medicines that narrowly target each one.

The drugs don’t cure cancer and face significant hurdles. But doctors now talk of a “precision medicine” approach in which those pinpoint drugs can treat tumors far more effectively than catchall chemotherapy.

“What we’re seeing is the beginning of a revolution in therapeutics,” says Janet Woodcock, director of the Food and Drug Administration’s Center for Drug Evaluation and Research. “We can only hope that this gets us to where cancer is managed or curable.”

Among signs that revolution really is afoot: A June 2013 study found that lung-cancer patients who were treated with drugs targeted at their genetically identified varieties lived 1.4 years longer than patients on chemotherapy whose cancers weren’t genetically identified.

In effect, lung cancer is no longer a few common diagnoses. Instead, it is a growing list of rare cancers, each a target for its own drug regimen.

“It’s likely that more than half of tumors have some alteration we can target with a drug,” says John V. Heymach, a lung-cancer specialist at MD Anderson Cancer Center, Houston. “They may not all have the same success, but we know that in many cases, a targeted agent will work very well.”

The same goes for other malignancies: Scientists have decoded tumor DNA from breast, colon, kidney, skin and other cancers in recent years to discover scores of variations they didn’t know existed before.

Research hospitals like MD Anderson, Vanderbilt University and Massachusetts General Hospital are among a growing number of cancer practices that routinely decode the tumor DNA of most patients with advanced cancer.

The lists of newfound variations have invigorated the drug industry, with companies like Pfizer, Roche Holding AG ROG.VX +0.38% andMerck MRK -0.08% & Co. racing to develop drugs that target each one.

Last year, nearly 1,000 cancer drugs were in clinical development, up 52% from 2006, says the Pharmaceutical Research and Manufacturers of America, a trade group. The “vast majority” of that growth is from drugs targeted at genetic mutations, says Bill Chin, the group’s head of science and regulatory affairs.

Three drugs are on the market for newly discovered lung-cancer mutations. Dozens more are in clinical trials. Some approved for other cancers appear effective for specific lung cancers. And drug companies are targeting other mutations of all cancer types.

At least half the 27 medicines on Novartis AG’s NOVN.VX +0.74%current list of oncology drugs in clinical development target cancer mutations. Precision medicine is “fundamentally changing the way we think about cancer drug development,” says Hervé Hoppenot, president of the company’s Novartis Oncology unit.

Just last year, the FDA established a “breakthrough therapy designation” to hasten approval of experimental drugs that show striking benefits in early trials, including those targeted at cancer mutations.

Ms. Carey’s diagnosis in 2010 came just as that thinking was starting to change. Her roller-coaster ride of cancer remission and recurrence over the next three years shows the promise and shortcomings of precision medicine.

Ms. Carey, who worked for a business selling private jets, suffered an apparent seizure at her gym. Doctors discovered a nodule in her lung of cancer that had spread to her brain. Surgery and radiation treated the brain tumor.

But when the New York City resident’s doctor said she probably had three months left, “I definitely felt like there were no options,” she says.

It wasn’t an unusual prognosis for lung cancer in 2010. Three decades of research starting in the 1970s into hundreds of potential lung-cancer drugs had produced dismal results, says MD Anderson’s Dr. Heymach: Over that time, a lung-cancer patient’s median survival improved by just one month, to eight months.

Ms. Carey found hope in news accounts of a drug Pfizer was testing against a cancer type researchers had identified in 2007. The type was caused by a mutation in the so-called ALK gene—it normally plays a role in brain development—and Ms. Carey wanted to know if that was her cancer.

In 2010, precision medicine was still so nascent that Ms. Carey had to show unusual persistence. Few doctors even considered testing tumors for mutations.

She says she had to demand the test. “Are you helping to save my life,” she recalls asking her doctor at the time, “or just waiting for me to die?”

That ALK-gene mutation was only the second mutation researchers had identified using advanced DNA-sequencing technology on lung-cancer tumors. The first was in 2004, a mutation in the so-called EGFR gene that responded well to an existing drug, Tarceva, now sold by Roche. (Another mutation, KRAS was discovered previously, with earlier technology.)

The discovery of the role of the EGFR mutation in 2004 sparked the search for more cancer-causing mutations.

Before that, a pathologist would identify a patient’s lung-cancer tumors through a microscope to see if they were of the “small-cell” or “non-small-cell” variety. The difference helped determine which regimen of chemotherapy to prescribe.

After finding the ALK-gene mutation, researchers in 2007 found another mutation. By 2010, for a few lucky patients whose tumors proved to be of the newly discovered varieties, there were a few drugs on the market or in trials.

Ms. Carey was among the fortunate: Her mutation proved to be of the ALK gene, which represents about 5% of lung-cancer cases.

The discovery of the ALK-gene mutation had prompted Pfizer to test a drug already in its portfolio, brand-named Xalkori and generically called crizotinib, to see if it worked on the mutation. Pfizer’s study of the first patients showed dramatic results, which Ms. Carey read about.

Again, Ms. Carey needed persistence, this time to get the drug. She visited different sites participating in Pfizer’s trials before finding a slot at the University of Chicago.

Within six weeks, two of three cancerous nodules in her lungs had disappeared, and the third had shrunk significantly.

The FDA approved the Pfizer drug in 2011 based on 250 patients, four years after the ALK-mutation link was discovered. That is lightning speed in an industry accustomed to spending a decade with thousands of test subjects to get drug approval.

Ms. Carey in 2011 began buying the Pfizer drug by prescription. It was expensive—today Pfizer charges $10,800 a month for it—but her insurance covered it.

Prices like that raise questions about the affordability of precision medicine. But those prices, and the speed at which genetically targeted drugs can come to market, had begun changing the economics of drug development.

The “precision medicine approach requires people to change the way they look at opportunities,” says Mace Rothenberg, a senior vice president who heads cancer clinical development for Pfizer. Instead of trying to apply a drug to the largest number of patients possible, it is possible to “demonstrate very significant value of the drug to the patient, the physician, the payers and the company.”

Discovery of new mutations accelerated. A 2011 report linked a mutation of a gene called RET to lung cancer, prompting researchers at Memorial Sloan-Kettering Cancer in New York to approach ExelixisInc. EXEL -0.61% The South San Francisco biotechnology company was developing a drug called cabozantinib to treat a rare form of thyroid cancer linked to the RET mutation.

That mutation is found in only about 1% of lung-cancer patients, but Sloan-Kettering launched a drug trial. The first few patients tested had striking benefits. “These were patients who had nothing six months earlier,” says Mark Kris, a lung-cancer specialist at Sloan-Kettering.

Discovery of still-more lung cancer mutations continued in rapid fire. The count is 15 today, accounting for about 60% of all lung cancers, according to some estimates, and researchers expect to find more.

Precision medicine is no cure. A tumor with a pinpointed mutation doesn’t always respond to a drug targeted at it. The drug often shrinks tumors within weeks. But the tumors can develop resistance and come roaring back.

Ms. Carey’s cancer found a way around the treatment, in early 2012. An analysis of her tumor found the ALK-gene mutation still active. She took to calling her mutation the “Darth Vader of cells.”

Doctors think most patients will need a series of precision drugs, sometimes with chemotherapy. “The tumor will keep evading our best therapies,” says Trever Bivona, a lung-cancer researcher at University of California San Francisco. “Ultimately we’re going to have to get to combination approaches.” exdiscovery of new

Ms. Carey in the spring of 2012 went off crizotinib for another regimen of brain radiation, then went back on the drug.

By that year, interest was surging among drug companies in targeted drugs. At least three “next-generation crizotinibs” against the ALK-gene mutation were now in trials. Ms. Carey entered a trial for one of them, being developed by Ariad Pharmaceuticals Inc. ARIA +0.27%

Not all patients can find a trial. Precision drugs are approved for only two lung-cancer mutations, the ALK and the EGFR-gene mutations. A patient with a different mutation must look for a drug in development and try to join its trial.

Dr. Bivona of University of California San Francisco says he treated a patient this year who died a month before the launch of a clinical trial for a drug that matched the patient’s mutation. “We were in a black hole,” he says. “Getting drugs to the patients who need them will take an entire remodeling of the drug-development system.”

While there are drugs approved for other cancers that appear effective for some newfound lung cancers, insurers generally feel data don’t yet justify coverage of such “off-label” drugs. And for several of the 15 known lung-cancer variants, an especially promising drug has yet to emerge.

Tests for mutations are less likely to be available in smaller doctors’ offices. Even many large centers are just putting in place systems to act on the information. “A lot of places can tell you they do this now, but few really have the people in place who know what to do,” says Roy Herbst, chief of medical oncology at Yale Cancer Center, New Haven, Conn., who is Ms. Carey’s current oncologist.

But rapid diagnostic advances are making it easier for any doctor to test for the newfound cancers. Tests now can hunt for more than 200 mutations—of lung and other cancers—in one biopsy.

Evidence that precision medicine works will likely broaden its use quickly. A June 2013 report on 1,007 patients with advanced lung cancer whose tumors were sequenced by a group of researchers called the Lung Cancer Mutation Consortium found that 62% had alterations suspected of being driver mutations.

The researchers reported that the 265 patients on the study treated with a targeted drug had a median survival of 3.5 years from diagnosis, compared with 2.1 years for the 361 patients for whom a mutation wasn’t identified.

“It opens up so many more doors for patients if you can find their target,” says Alice Shaw, an oncologist at Mass General in Boston.

At Ms. Carey’s checkup late this July, her doctor said her new drug regimen is keeping her lung tumor from progressing.

She is also considering a new class of drugs called PD-1 inhibitors that enlist the immune system. Such agents from Merck, Roche andBristol-Myers Squibb Co. BMY +0.51% are creating a buzz among oncologists for use in parallel with the genomic strategy.

“Now when I look back, I’m astonished at the timing of everything,” she says.

“My quality of life is extraordinary,” she says. “The science in this and the positive response I’ve had—I wouldn’t be alive without that.”


New Study Shows Why You Should Get the Kids to Bed on Time

Going to bed at a regular time every night could give your child’s brain a boost, recent research shows.

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A large study published in June found that young children with an irregular bed time fared worse on cognitive tests several years later. Sumathi Reddy explains on Lunch Break. Photo: Getty Images.

Going to bed at the same time every night could give your child’s brain a boost, a recent study found.

Researchers at University College London found that when 3-year-olds have a regular bedtime they perform better on cognitive tests administered at age 7 than children whose bedtimes weren’t consistent. The findings represent a new twist on an expanding body of research showing that inadequate sleep in children and adolescents hurts academic performance and overall health.


Izhar Cohen

The latest study considered other factors that can influence bedtime and cognitive development, such as kids skipping breakfast or having a television in their bedroom. After accounting for these, the study found that going to bed very early or very late didn’t affect cognitive performance, so long as the bedtime was consistent.

“The surprising thing was the later bedtimes weren’t significantly affecting children’s test scores once we took other factors into account,” said Amanda Sacker, director of the International Center for Lifecourse Studies in Society and Health at University College London and a co-author of the study. “I think the message for parents is…maybe a regular bedtime even slightly later is advisable.”

The researchers suggested that having inconsistent bedtimes may hurt a child’s cognitive development by disrupting circadian rhythms. It also might result in sleep deprivation and therefore affect brain plasticity—changes in the synapses and neural pathways—at critical ages of brain development.

Sleep experts often focus largely on how much sleep children get. While that is important, “we tend to not pay as much attention to this issue of circadian disruption,” said Judith Owens, director of sleep medicine at Children’s National Medical Center in Washington, D.C., who wasn’t involved with the study.

Insufficient sleep and irregular bedtimes may each affect cognitive development through different mechanisms, Dr. Owens said. “The kid who has both [problems] may beat even higher risk for these cognitive impairments,” she said.

The study, published online in July in the Journal of Epidemiology & Community Health, examined data on bedtimes and cognitive scores for 11,178 children.

The children were participants in the U.K.’s Millennium Cohort Study, a nationally representative longterm study of infants born between 2000 and 2002.

Mothers were asked about their children’s bedtimes at 3, 5 and 7 years of age. Nearly 20% of the 3-year-olds didn’t have a regular bedtime. That figure dropped to 9.1% at age 5 and 8.2% at age 7. Mothers were also asked about socioeconomic and demographic characteristics and family routines.

When the children were 7 years old, they received cognitive assessments in reading, math and spatial abilities. The poorest test scores were recorded by children who went to bed very early or very late, and by those who had inconsistent bedtimes, said Dr. Sacker. But once other factors in the home were taken into account only the inconsistent bedtime was associated with lower scores, she said.

A consistent pattern of sleep behavior mattered. “Those who had irregular bedtimes at all three ages had significantly poorer scores than those who had regular bedtimes,” Dr. Sacker said. This was especially true for girls who didn’t establish consistent bedtimes between 3 and 7 years old.

Yvonne Kelly, a co-author of the study and a professor in the department of epidemiology and public health at University College London, said the researchers aren’t sure why girls seemed to be more affected. She noted that the difference in scores between these groups of girls and boys wasn’t statistically significant for the reading and spatial tests, but it was for the math test.

“I don’t think for one moment that boys are immune to these things and girls are more affected,” Dr. Kelly said.

The researchers didn’t have data on the total number of hours children slept overnight because mothers weren’t asked about what time the children woke up.

In general school-age kids—kindergarten through eighth-grade—should be getting about 10 hours of sleep, while 3- and 4-year-olds might need 11 to 13 hours, including day-time naps, said Shalini Paruthi, director of the pediatric sleep and research center at SSM Cardinal Glennon Children’s Medical Center at Saint Louis University.

Dr. Paruthi said the good news from the study is that the majority of the children went to bed at a consistent time, reinforcing advice from sleep specialists. “The younger the child is, the better it is to get into the habit of a regular bedtime,” said Dr. Paruthi, who wasn’t affiliated with the study. She recommends a 15-minute, pre-bedtime routine to help the brain transition from a more alert to a quiet state.

And in order to keep the body’s internal clock in sync with the brain, bedtimes on weekends and in the summer should only stray from the normal time by an hour or less, Dr. Paruthi said. “The internal clock in the brain and the body like to have consistency every day,” she said.



Links Tighten Between IQ, Breast-Feeding





Breast-feeding longer can make children smarter. That’s the conclusion of a study published Monday in JAMA Pediatrics, a journal of the American Medical Association.

In many ways, the study won’t surprise proponents of breast-feeding, who have long posited a connection between nursing and cognition and now have an additional piece of research to back up their argument. Skeptics could likely stick to the view that what matters most is how smart a baby’s mom is, or that social pressure to breast-feed can have its own problems for children’s development by creating stressed-out parents. However, the findings are likely to add muscle to public-health advocates’ push to increase breast-feeding rates, which start out around 75% but slump to an average of 25% at a baby’s first birthday, according to the Centers for Disease Control and Prevention.

The JAMA study isn’t the first to study a link between nursing and intelligence, but researchers say it is more conclusive because of its size and how it has isolated variables such as the mother’s IQ and the child’s upbringing. Previous studies have had difficulty adjusting for other factors that might influence a child’s IQ, were limited by their small size or didn’t account for length of nursing, said Mandy Belfort, the JAMA study’s lead author and assistant professor of pediatrics at Harvard Medical School.

The latest study examined and rated each child’s environment based on factors such as how many books are available, and gave each mother an IQ test. They also asked detailed questions about factors that might influence IQ, such as child care, income and parental education. They then subtracted those factors using a statistical model. Dr. Belfort said she hopes that “what we have left is the true connection” with nursing and IQ.

Breast-feeding is hard to study in a randomized trial because it is unethical to put some children in the non- group, Dr. Belfort said, which leaves researchers with observational studies such as the one she conducted. Researchers at Boston Children’s hospital followed 1,312 babies and mothers from 1999 to 2010. They found out how many of those children were still consuming their mothers’ milk at their first birthday, and then tested the children’s intelligence at ages 3 and 7.

Intelligence is a strange brew of nature and nurture and isolating one factor is challenging. Breast-feeding in the first place has a lot to do with class and wealth, with richer, better educated women typically opting to make the effort to nurse their babies.

Children who were still nursing after a year had higher receptive language scores at age 3, which means they understood what was being said to them better than their formula-fed peers. At age 7, the breast-fed children scored higher on verbal and nonverbal intelligence tests.

In 3 year olds, every month of breast-feeding raised cognition scores by an average of .21 point. Each month of breast-feeding was associated with a .35 more verbal IQ point and a .29 more nonverbal point in the 7 year olds. A full year of nursing would boost a child’s IQ by about 4 points over a child who didn’t nurse, said Dr. Belfort, a significant bump considering that IQs average around 100. That is for children getting some breast milk in their diets; those consuming only breast milk before starting to eat solid foods around six months of age saw even greater advantages.

“For an individual person, it would be hard to tell a two or three point difference in IQ, but it would matter a lot for society,” said Dr. Belfort. “If we can shift the IQ up, we would have to invest less resources at the low end.” Meaning that with improved IQ scores across the board, less funding would have to be spent on remedial education programs.

Dr. Amy Tuteur, an obstetrician who writes a blog called, is unconvinced by a four-point increase in IQ, saying the bump needs to be bigger to prove that it isn’t just random variation. “Intelligence is multifactoral and the idea that any one thing can make a big difference right away makes me skeptical,” she said. “American IQ has been increasing steadily, it rose when breast-feeding rates were going down and it rose when breast-feeding rates were going up.”

The possible link between breast milk and brain development is only starting to be teased out. Some theories suggest that it isn’t the content of the milk but the bond between mother and child developed while nursing that accounts for some of the boost. Other ideas hinge on nutrients found in breast milk such as DHA and ARA, which are fatty acids linked to brain development. Some formula companies put DHA and ARA in their offerings.

“There are nutrients in breast milk that don’t really exist anywhere else, and we don’t fully know why,” says Dimitri Christakis, a pediatrician at Seattle Children’s Hospital Research Institute and wasn’t involved in the research.

He wrote an editorial in JAMA pediatrics on the study and leads an advocacy group called the Global Breast-feeding Initiative. In the editorial he contends the JAMA study should put skepticism to rest about whether breast-feeding is best for brain development and that society should make it easier and more acceptable for moms to nurse.

For Amra Chudleigh-Neal of Thousand Oaks, Calif., intelligence is just one more reason for her to breast-feed her 6-week old daughter. She said her older child, now 7, has above average IQ, which Ms. Chudleigh-Neal said could be in part because she exclusively breast-fed until her daughter was 6- months old.

“It tends to be a little more of a sacrifice to nurse the second child, you think ‘oh my gosh is it really worth it’ but looking back with my older child I believe it did make a difference,” she said. Ms. Chudleigh-Neal receives extensive support from The Pump Station, a Los Angeles-area nursing resource center that helps with things like connecting moms to lactation professionals.

Not everyone can breast-feed successfully, and that needn’t make parents worry. “Talk to your baby, hold your baby and read to your baby,” Dr. Belfort said. “There are so many different factors in a child’s development.”

One difficulty in studying breast milk is that every feeding can vary based on the mother and what she has eaten. So the Boston researchers also examined a component in mothers’ diets that might be responsible for children’s brain development: fish, which contains DHA.

The authors found that more than two or more servings of fish per week seemed to confer IQ benefits, but that boost in children’s cognition wasn’t statistically significant.

Write to Avery Johnson at


A Battle Against Wayward Genes

The story of how ingenious medical researchers and big pharma teamed up to defeat a rare form of leukemia.



    More than 50 years ago, scientists working in the City of Brotherly Love discovered a genetic mutation that they called “the Philadelphia chromosome” in patients with chronic myelogenous leukemia, a fatal, spontaneously arising cancer of the blood.In her book of the same title, Jessica Wapner chronicles the ensuing decades of laborious scientific inquiry and industrial ingenuity that led to the discovery of Gleevec, the first drug designed to attack cancer at the genetic level. Its success in beating CML into remission and making the errant chromosome disappear has helped to revolutionize cancer research, unleashing a hunt for the genetic basis of other cancers and opening the door to comparable targeted treatments.

    While the money came from drug maker Novartis,NOVN.VX -0.07% the hero of the story is Brian Druker, an oncologist and researcher at Oregon Health & Science University. His unwavering determination kept the development of Gleevec on track against formidable odds, not least of which was the fact that CML, a rare disease with fewer than 6,000 new cases annually in the U.S., seemed to hold little potential for the blockbuster sales that typically attract pharmaceutical-company investment.

    Ms. Wapner tracks decades of work by scientists who often had little knowledge of one another but eventually proved that the Philadelphia chromosome was the sole cause of CML. The mutation causes separate genes to fuse and become one, producing an abnormal protein, tyrosine kinase, which causes white blood cells to proliferate uncontrollably. The resulting cascade becomes a “killing machine,” in Ms. Wapner’s phrase. Blood turns into “viscous sludge” as red cells plummet. Meanwhile, platelets become too few to make the blood clot, and severe bleeding precedes death.

    Having myself received the diagnosis for CML in 1992, I can testify that it is a fairly terrifying experience. At the time there was no Gleevec in sight. Patients were prescribed the drug hydroxyurea to slow things down, but it didn’t work for long, and another common treatment, interferon, was tough to tolerate and wasn’t a long-term solution in any case. The only possible cure was a bone-marrow transplant, which carried risks—including rejection—and required a suitable donor, preferably a matched sibling. (I was fortunate to have two.)




    The Philadelphia Chromosome

    By Jessica Wapner 
    (The Experiment, 303 pages, $25.95)

    Surprisingly, Ms. Wapner gives short shrift to bone-marrow transplantation, portraying it as the worst possible option when in fact it has saved the lives of many CML patients, including my own. She also dismisses the side effects of Gleevec as minimal. Having taken the drug as part of treatment for recurrences more than a decade after my transplant, I can attest to its unpleasantness, a reason that some patients have stopped using the drug. Resistance also develops, leading some patients to seek transplants after all.

    In “The Philadelphia Chromosome,” Ms. Wapner routinely translates the complexities of science for the lay reader, notably the role of tyrosine kinase and the quest to inhibit its deadly activity. Whenever the details get to be tough slogging, she offers up straight talk to explain what it all means: “In the hunt for cancer’s underlying mechanism, finding tyrosine was like a tracker finding an animal print or a broken branch. They knew they had caught the right trail.”

    The narrative picks up steam when Dr. Druker moves from the Dana-Farber Cancer Institute in Boston to a new research job at Oregon Health & Sciences University. He secures several compounds from Ciba-Geigy, the pharmaceutical company, which is also pursuing a drug. He ultimately uses the compounds to find the Holy Grail: an antibody that is able to bind to the errant protein and block its effects.

    Dr. Druker found supporters among Ciba-Geigy’s scientists, but it was hardly clear coasting from there, and Ms. Wapner’s tale shifts to the often-frustrating struggle to clear the regulatory, political and financial hurdles that kept popping up. Though the lead compound of the drug that would become Gleevec was synthesized by 1990, seven years later the first phase of human trials had yet to begin.

    The turning point came in 1996, after the merger of Ciba-Geigy and Sandoz created Novartis, whose new chief executive, Dr. Dan Vasella, allowed the evidence to prevail over business hesitations within the company. Once human trials were under way, the results were breathtaking: Abnormal white blood cells disappeared, and normal blood cells were not affected.

    Soon the Web was abuzz with news of the drug. For patient Bud Romine, it was a miracle. “The sword that had been hanging over his neck, waiting to fall, was now gone,” Ms. Wapner writes. “He’d been waiting to die, and now he knew he was going to live.” After being fast-tracked at the Food and Drug Administration, Gleevec set a record for swift approval in 2001. Gleevec must be taken daily for life and costs about $6,500 a month, though there are programs for those who can’t afford it. From 2001 to 2011, Ms. Wapner reports, world-wide sales were close to $28 billion, and Novartis and others now offer second-generation drugs that may be more tolerable and effective.

    Novartis took much of the credit for Gleevec’s success, and Dr. Vasella wrote his own 2003 book about its development, “Magic Cancer Bullet.” Dr. Druker, who did not profit from the drug, did not seem to get the credit he deserved. Thanks to Ms. Wapner, he gets it now. Dr. Druker and Dr. Vasella, since retired from Novartis, strike a conciliatory note at the end of Ms. Wapner’s account, stressing the importance of collaboration between academia and industry, especially when research funding is limited. “The drug companies aren’t evil,” Dr. Druker says from his vantage as a university scientist. “They make drugs, and we should help them.”

    Ms. Landro, a Journal editor and columnist, is the author of “Survivor: Taking Control of Your Fight Against Cancer.”

    SON DERS: Prof. Dr.Ufuk Cığızoğlu Beyazova’dan

     Sevgili sınıf arkadaşım Prof. Dr. Ufuk Cığızoğlu Beyazova’dan ogrencilerine emeklilik öncesi “SON DERS” konuşması       

    “SON DERS  


    Değerli arkadaşlarım

    Bu son dersi anlatma görevinin bana verilmiş olmasından son derece mutluyum, onur duydum.gurur duydum. Teşekkür ederim.

    Bir öğretmen, hekim olmak üzere olan arkadaşlarından ayrılırken onlara son olarak ne söylemek ister. Belki biraz öğüt vermek. “İyi bir hekim olmak” üzerine öğütler. Ancak ben tüm meslek yaşamımda öğüt vermekten çok örnek olmaya çalıştım. Kendimce iyi hekim olmak neyse öyle bir hekim olmaya çalıştım. En sık gördüğü hastalıkların tanı ve tedavisini, bu hastalıklardan korunmayı iyi bilmek, her gün yeni bir şey öğrenmeye çalışmak, öğrendiği her şeyi başkaları ile paylaşmaya çaba göstermek yardım isteyen bir şeyler danışan herkese yardımcı olmaya çalışmak, insanları sevmek, insanlar arasında ayrım gözetmemek, yurdunu sevmek, dilini sevmek, infant yerine bebek, prenatal, natal, postnatal yerine doğum öncesi, doğum, doğum sonrası demek, marker yerine belirteç sözcüğünü kullanmak, mesleğimiz çok yoğun çalışma gerektirse de yaşamda sanata, spora, yurdu ve dünyayı tanımaya zaman ayırmak, çocuklara, insanlara, mesleğe yararlı olabilmek için sivil toplum örgütlerinde çalışmalar yapmak, bu günü anlayabilmek için geçmişi bilmeye çalışmak iyi hekim olmaktı benim için, bunlarla örnek olmaya çalıştım.

    Sizlere dersleri anlatırken konu ile ilgili küçük öyküler de anlattım. Aşıları anlatırken Türkiye’nin Pasteur’u Muammer Tunçman’ın Kurtuluş savaşı sırasında aşılanmış tavşanları İstanbul’daki telkihhaneden kaçırabilmek için İngiliz işgalini nasıl yararak İneboluya geldiğini. Orada bir laboratuar kurarak nasıl kuvayı milliye için aşı ürettiğini anlattım.

    Cumhuriyetin kurulmasından sonra Dr. Refik Saydam’ın savaşın yoksul ve yorgun Ankara’sında herkesin hayal diye nitelediği Hıfzıssıhha enstitüsünü nasıl kurduğunu, o yıllarda dünyada aşı üretebilen 5 merkezden biri haline getirdiğini bir  çok Orta doğu ülkesi ve Çin’in aşılarını Türkiyenin ürettiğinin öyküsünü anlattım.

    Bu gün son dersimizde de bir kısa öykü daha anlatmak istiyorum. Fatma Müfide hanım’ın öyküsü.

    Sonradan Küley soyadını alan Fatma Müfide hanım 1900 lerin başında doğmuştu. Şimdiki lise eğitimine karşılık gelen idadiyi bitirdikten sonra 1919 da Tıp Fakültesine girip hekim olmak istemişti. Ancak 1900 lerin başında İstanbul’da bu o kadar kolay değildi. Osmanlı Sıhhiye Meclisi kadınların hekim olamayacaklarına dair bir mazbata çıkarmıştı. Bu mazbatada Kadınların evlenip aile kurduktan sonra mesleklerine devam etmeyecekleri, fakülteye girmenin “iffet ve ahlak” değerlerini zedeleyeceği, erkek hastaları muayene etmemeleri ve anatomi diseksiyonlarına da katılmamaları gerektiği belirtilmişti. İstanbul Darülfünunu Tıp fakültesine kız öğrenci almıyordu. Bu nedenle başvurusu reddedildi.

    Fatma Müfide hanım 1921 de yeniden tıp fakültesine başvurdu, kaydını yaptırdıysa da kız öğrenci kabulüne karşı olan hocalardan birisinin tıp eğitiminin zor ve uzun olması, laboratuar çalışmalarının fazlalığı üstelik tek bir kız öğrencinin o kadar erkek arasında eğitim almasının uygun olmayacağı nedeniyle Saray’a ve o zamanki hükümet yetkililerine şikâyeti ile yine derslere kabul edilmedi. Ertesi yıl 1922 ders yılında, Anadolu’daki başarıların artışı, Sarayın ve İstanbul Hükümeti’nin güçsüz kalmasından cesaretlenip 2 kız arkadaşını daha ikna etti. Yeniden başvurdu. Üniversite onları kabul etmek zorunda kaldı.

    Kurtuluş savaşının ardından Fatma Müfide hanımı 7 kız öğrenci daha örnek aldı ve Tıp Fakültesine alındılar. Fatma Müfide Küley fakülteyi bitirdikten sonra 1933 de öğretim üyesi oldu. 1973 yılına dek üniversitede çalıştı. Öğretim üyeliği dışında Çeşitli derneklerde etkin olarak görev alan Dr.Küley, üniversiteli kadınlar derneğinin kurucu üyelerindendi,  Türk Tıp Cemiyeti genel sekreterliği, ve başkanlığını yaptı. 

    Dr. Müfide Küley bana örnek oldu. Ben ondan çok daha kolay olarak Tıp Fakültesine girmiştim. Kimse bana kadınlar evlenip aile kurduktan sonra mesleklerine devam edemezler demedi, fakülteye girmenin “iffet ve ahlak” değerlerini zedeleyeceği ne benim ne ailemin aklına geldi. Kaydımı yaptırmak için başvurduğumda kimse git birkaç kız öğrenci daha bul erkek öğrencilerin arasında yalnız kalırsın demedi. Zaten bizim sınıfın yarısı kızdı. Hiçbir hocam erkek hastaları muayene etmemem ve anatomi derslerine katılmamam gerektiğini söylemediler. Bunların hiç birini kimse düşünmedi bile. Çünkü cumhuriyet döneminin söylemi bu değildi.

    1923 de Atatürk “Daha esenlikle, daha dürüst olarak yürüteceğimiz yol vardır. Bu yol,Türk kadınını çalışmamıza ortak yapmak, ilmî, ahlâkî, sosyal, ekonomik yaşamda erkeğin ortağı, arkadaşı, yardımcısı ve destekleyicisi yapmak yoludur.” demişti.

    Cumhuriyet, kadınların düşünebileceklerine inandı, kadınların okuyup yazabileceklerine inandı, kadınların da öğretmen, bilim insanı, hakim, hekim olabileceklerine inandı. Cumhuriyet bana inandı. Sizlere inandı. Gençliğe inandı.

    Çünkü Cumhuriyeti gençler kurmuşlardı. Atatürk samsuna çıktığında 38 yaşındaydı. Fikir arkadaşları Rauf Orbay ve Refet Bele, Kazım Karabekir, Ali Fuat Cebesoy hep 37-38 yaşında gençlerdi. Lozan antlaşmasını imzaladığında ismet İnönü onlardan da gençti. Kurtuluş savaşının komutanları 30 lu yaşlardaydılar. Milli Mücadeleyi destekleyen sanatçıların çoğu, Ruşen Eşref, Falih Rıfkı, Yakup Kadri 25-30 yaşlarındaydılar. Cumhuriyeti o yılların gençleri kurdu.  “Biz kurduk onu yücelterek yaşatacak olan sizsiniz”. diyerek sonraki kuşaklara emanet ettiler. 

    Gençlerin hem yurtta hem cihanda barışı koruyacağına, ülkenin bağımsızlığını ve cumhuriyeti muhafaza ve müdafaa edeceğine  ve bilimi en büyük yol gösterici olarak kabul edeceğine inandılar. 

    Onların bu inancını boşa çıkarmayacağınıza bizler de inanıyoruz. Cumhuriyetin hiçbir kazanımından geri adım atmayın. Sizlere yeni yaşamınızda başarı ve mutluluklar diliyorum. Yolunuz açık olsun.

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