Watch for Ocular Effects of Breast Cancer Drugs
When a patient with an eye condition walks into an ophthalmologist’s office, the fact that she has been treated for breast cancer may not raise warning flags for the clinician. But there’s accumulating evidence that ocular conditions such as dry eye, retinopathy, and cataracts may be at least partly due to some breast cancer medications.Only a small percentage of breast cancer patients experience clinically evident ocular side effects from their medications. Nevertheless, because these drugs are so widely used, the related eye conditions may affect many women. The breast cancer medication most commonly identified with ocular side effects is tamoxifen. However, chemotherapy agents, such as 5-fluorouracil (5-FU), can also have ocular side effects. And more researchers are becoming concerned that the drugs known as aromatase inhibitors, which now are often prescribed as adjuvant endocrine therapy, may also have adverse effects on the eye, including small retinal hemorrhages, increased incidence of floaters, and dry eye.Tamoxifen RetinopathyWhite or yellow refractile crystals around the macula are a characteristic finding in tamoxifen retinopathy (Image courtesty of Retina Image Bank. Young Hee Youn, MD; Sung Hyun Kim. 2012; #559. © American Society of Retina Specialists.)Tamoxifen Troubles
“Tamoxifen has long been known to cause eye problems, including dryness, irritation, cataracts, and deposits in the retina, in the area of the macula, that result in macular edema,” said K. V. Chalam, MD, PhD, MBA, professor and chair of ophthalmology at the University of Florida College of Medicine in Jacksonville. Most of the ocular side effects are dose related, he said. “Certainly, the side effects we see with tamoxifen are much less profound than they used to be because of the lower doses now used.” Years ago, many breast cancer patients were prescribed doses of 150 mg or more, he noted. “In such cases, the ocular side effects from tamoxifen could be profound. That’s not the case anymore with the usual dose of 20 mg or less.”Widespread effects. Tamoxifen is a selective estrogen receptor modulator (SERM) and acts against breast cancer by occupying estrogen receptors. It’s the only SERM approved for every stage of breast cancer. Because estrogen affects a wide variety of physiological functions and estrogen receptors are present in the eye, the changes in estrogenic activity brought about by tamoxifen have the potential to affect visual processing, as well as the lacrimal and meibomian glands that protect the surface of the eye, according to Alvin Eisner, PhD. Research shows that tamoxifen increases the risk of posterior subcapsular cataracts by as much as fourfold, which is significant because these types of cataracts can substantially impair visual function, said Dr. Eisner, a researcher most recently at the Northwest Sarcoma Foundation who specializes in ophthalmology, vision science, and cancer treatment.Cataract. Researchers at the University of Southern California analyzed the self-reported incidence of eye disease among 1,297 female breast cancer patients taking tamoxifen who were enrolled in a population-based case-control study. They found that women who used tamoxifen for four to five years had a relative risk (RR) of 1.4 for all types of cataracts; those who were on the drug for more than six years had an RR of 1.7. They concluded that five or more years of tamoxifen increases cataract risk and that “healthy women considering tamoxifen use to reduce the risk of breast cancer should be advised of the possibility of cataract development.”1Yet some ophthalmologists say that the question of whether tamoxifen increases risk of cataracts is still unresolved. “It’s fairly rare to find that a cataract is due to a medication, and I think that the jury is still out on whether tamoxifen may cause cataracts in some patients,” said Rick Fraunfelder, MD, MBA, professor of ophthalmology at Oregon Health & Science University and the Casey Eye Institute. Dr. Fraunfelder is also director of the National Registry of Drug-Induced Ocular Side Effects.Retinopathy. However, use of tamoxifen, particularly at higher doses and for longer periods of time, may lead to retinopathy, Dr. Fraunfelder said. “Patients on tamoxifen can get striking white to yellow refractile bodies around the macula. These effects tend to occur at least one year after therapy begins and are cumulative.”But, according to Dr. Eisner, tamoxifen retinopathy is overemphasized. A review article he coauthored states that “the initial findings of tamoxifen retinopathy at an auspicious time in the evolution of BC [breast cancer] treatment have led to an overemphasis on this condition in the sense that vision symptoms (e.g., photopsia) due to other intraocular conditions may be too readily misattributed to tamoxifen retinopathy and/or downplayed.”2 Estimates of the prevalence of retinopathy among breast cancer survivors on standard doses of tamoxifen have varied widely among published studies, with rates ranging from 0 to 6 percent, Dr. Eisner said.Pointers for following patients on tamoxifen. Dr. Fraunfelder recommends that breast cancer patients have a baseline eye exam within the first year of treatment with tamoxifen, including an examination of the macula and testing of central and color vision. Dr. Chalam recommends that most breast cancer patients on tamoxifen be followed every four to six months, and those with symptoms should be seen by an ophthalmologist as often as every three months. Any sign of symptomatic ocular conditions should prompt a discussion with the patient as well as her oncologist.According to Dr. Chalam, the ocular risks increase with long-term use of tamoxifen because the effects of the drug on the eye are cumulative over time. “The side effects usually occur at least one year after therapy begins,” Dr. Fraunfelder said. However, one condition that may occur relatively earlier is subclinical swelling within the optic nerve head, Dr. Eisner said. In addition, he noted that early, subtle cases of cystoid tamoxifen retinopathy may sometimes be detectable with optical coherence tomography (OCT).The presence of asymptomatic refractile bodies is not a sufficient reason to discontinue tamoxifen, but if a patient starts to lose color vision or central vision while on the drug, the ophthalmologist should confer with the patient’s oncologist about stopping or switching treatments. Retinal hemorrhages and cystoid macular edema—which can result from tamoxifen use—may also indicate that a patient should stop taking tamoxifen or be switched to an alternative drug, Dr. Fraunfelder said.The good news about the ocular side effects of tamoxifen is that if the drug is discontinued or the dosage reduced, ocular toxicities such as macular edema or retinal deposits are often reversible, Dr. Chalam said.However, if the patient is on a high dose of tamoxifen and exhibits chronic maculopathy, there is a very real risk of losing vision permanently, Dr. Fraunfelder said. “It’s very rare for a patient to go completely blind, but many lines of visual acuity can be lost,” he said. “If you start getting vision loss after taking tamoxifen, it can be progressive and may continue even if you stop the drug.”Alternatives to tamoxifen. Oncologists have the option of prescribing raloxifene (Evista) as an alternative to tamoxifen for breast cancer prophylaxis, and it may have a more favorable side effect profile. Although the National Surgical Adjuvant Breast and Bowel Project Study (STAR) found that there were fewer cases of breast cancer among tamoxifen users, women on raloxifene had fewer cases of uterine cancer, as well as of cataracts (RR = 0.79) and cataract surgeries (RR = 0.82).3“Oncologists now have more choices, and patients experiencing ocular effects from tamoxifen can often be switched to raloxifene, although the use of raloxifene would be off label,” said Dr. Chalam.Chemotherapy Complications
Chemotherapy drugs can also cause ocular side effects. According to Dr. Eisner, 5-FU can sometimes result in epiphora, while methotrexate can lead to conjunctivitis and other inflammation of the ocular surface.2Because chemotherapies are toxic to rapidly dividing cells (such as those in a tumor), they can also be harmful to other cells that divide and renew on a regular basis, including those in the corneal epithelium. As a result, these agents can cause dry eye, which can usually be treated with lubricating drops, according to Dr. Chalam. Docetaxel, a taxane drug, can also lead to epiphora, as a result of stenosis of the tear drainage apparatus, said Dr. Eisner.Conjunctivitis may occur when chemotherapy drugs leak into the tear film. “The chemicals irritate the eye, but the condition is temporary and goes away once the patient is done with chemotherapy,” Dr. Fraunfelder said, adding that there is no long-term damage. Topical nonsteroidal anti-inflammatory eyedrops can be used along with artificial tears if a patient has eye pain, he said.Aromatase Inhibitors
In recent years, aromatase inhibitors (AIs) such as anastrozole (Arimidex), letrozole (Femara), and exemestane (Aromasin) have been increasingly prescribed to postmenopausal breast cancer patients as adjuvant endocrine therapy, sometimes after two to three years of tamoxifen treatment. The short-term ocular side effects of AIs often seem to be mild, at least according to the limited cross-sectional studies that have looked at this question, Dr. Eisner said, although “There is theoretical potential for AI-induced estrogen depletion to increase the long-term risk of serious eye disease.”Although AIs work by inhibiting estrogen synthesis rather than by occupying estrogen receptors as tamoxifen does, some of the AI side effects are similar to those of tamoxifen, according to Dr. Eisner. The estrogen suppression that occurs with AIs might be regarded as causing an accelerated female aging that resembles an exaggerated menopause.A study by Dr. Eisner and colleagues suggests that anastrozole can cause small retinal hemorrhages in some patients.4 He said that his research indicates that breast cancer patients who take anastrozole are more likely to have retinal hemorrhages than tamoxifen users. These hemorrhages may be the result of excessive traction on the retina, caused by estrogen depletion.5Related effects, such as posterior vitreous detachments, may occur during the natural menopausal transition, he said. Dr. Eisner noted that it’s possible to assess the tractional effects of AIs through the use of OCT. Other possible effects of AIs include photopsia and increased incidence of floaters, as well as dry eye.Dr. Eisner pointed to the need for more studies of the effects of AIs, particularly longitudinal studies to better document and help clarify their ocular effects.“As many as 40 percent of women completely abandon their use of AIs before the prescribed time because they can’t tolerate the side effects. Although the ocular side effects may be less important or less compelling than well-known side effects such as arthralgia or hot flashes, they nevertheless may provide the straw that breaks the camel’s back for breast cancer patients on these drugs,” said Dr. Eisner.___________________________1 Paganini-Hill A, Clark LJ. Breast Cancer Res Treat. 2000;60(2):167-172.2 Eisner A, Luoh SW. Curr Eye Res. 2011;36(10):867-885.3 Vogel VG et al. JAMA. 2006;295(23):2727-2741.4 Eisner A et al. Optom Vis Sci. 2008;85(5):301-308.5 Eisner A et al. Breast Cancer Res Treat. 2009;117(1):9-16.___________________________Drs. Chalam and Eisner report no related financial interests. Dr. Fraunfelder is a consultant to Teva.
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Showing posts with label CANCER DRUGS. Show all posts
Showing posts with label CANCER DRUGS. Show all posts
Wednesday, May 2, 2018
Tuesday, October 7, 2014
The "eye popping" cost of cancer drugs
Lesley Stahl tells 60 Minutes Overtime about another "devastating" side effect of cancer: the bill
This week on 60 Minutes, Lesley Stahl reports on what she calls, the "eye popping" cost of cancer drugs.
The story was brought to Stahl's attention when she received an email from a close friend suffering from cancer. In the email, he told her about the astronomical bill he'd just received for his treatment and suggested Stahl do a story "on the backbreaking cost of cancer drugs."
She asked her producer, Rich Bonin, to look into the story.
What Bonin found surprised him: "The first thing I never really thought about was how expensive cancer drugs are. Secondly, I never knew that for many oncologists, when they prescribe cancer drugs, they actually get a commission."
But Bonin says the story is far more complicated than "good doctors" versus "evil drug companies."
He paraphrases one doctor's analogy, comparing it to the complex relationship with a mother-in-law: "We love them, we need them, they do good, but you know, there's this other side to the relationship that also makes it complicated."
As the 60 Minutes team reports, cancer drug prices have the potential to bankrupt a family.
"People don't just take one drug. It accumulates. They take two, or sometimes three. And each drug can cost $100,000," Stahl tells 60 Minutes Overtime. "It's really heartbreaking."
The above video was produced for 60 Minutes Overtime by Magalie Laguerre-Wilkinson and Craig Crawford.
© 2014 CBS Interactive Inc. All Rights Reserved.
Friday, November 1, 2013
The Pills of Last Resort
By DARSHAK M. SANGHAVI, M.D.
It was shortly after the breadbasket arrived last year at the Temple Bar near Harvard Square that Sarah Broom first told me about the last-ditch plan to save her own life.
Broom’s mere presence that evening was something of a miracle. Several years earlier, in 2008, while pregnant with her third child, she received a harrowing diagnosis. A 35-year-old English lecturer and poet living in New Zealand, Broom developed a persistent cough. She saw doctors in Auckland repeatedly over the course of a few months, but they didn’t want to do an X-ray on a pregnant woman. Finally, her shortness of breath became so severe that they relented, and 29 weeks into her pregnancy, she was found to have a large mass on her lung. She underwent a cesarean section — her daughter was born almost three months early — and a biopsy.
Broom had advanced-stage lung cancer. “I was told nothing could be done to cure the cancer, but that various treatments could give me time,” she recalled. Less than 1 percent of patients live more than five years.
She endured chemotherapy for weeks but then developed severe pelvic pain. To her horror, tests showed there was a new plum-size tumor on her ovary that wasn’t present at her C-section. The cancer was spreading relentlessly. Broom’s doctors predicted she had only a few months to live. She worried about her two sons, Daniel and Christopher, ages 5 and 2; her husband, Michael, whom she’d been with since they were teenagers; and her premature baby, Amelia, who was still hospitalized in the newborn unit. “My determination was to live, to live a long time — what else could I do, with three little kids depending on me — but at this time, it was clear that the situation looked pretty dire indeed,” Broom told me.
In desperation, she called friends around the world, including Meghan O’Sullivan, a former deputy national security adviser in the Bush administration, who contacted Bruce Chabner, the director of clinical research at Massachusetts General Hospital Cancer Center in Boston. Chabner asked Broom to send him her biopsy, so he could analyze its DNA. Her tumor had a mutation in a gene called anaplastic lymphoma kinase, or ALK, which occurs in about 5 percent of lung cancers. A Japanese group discovered it only a year earlier. Chabner knew that the drug company Pfizer was developing a new compound called crizotinib that might treat this mutation. The trouble was, it had been given to only two ALK-positive people before, and one died anyway. Still, it was Broom’s only hope, and Pfizer agreed to enroll her in a trial in Australia.
Incredibly, the tumors shrank by half, and Broom led an almost normal life for two years. Then the cancer returned. Various drugs were tried; none worked. Through Chabner, Broom ultimately got in touch with Alice Shaw, an oncologist who knew of two promising new compounds, AUY922 and LDK378, from Novartis, that might treat ALK-mutated lung cancers. They were two of the 23 Novartis anticancer drugs that were so early in development that they weren’t yet named or on the market. Because the company had no sites for the trial near New Zealand, Broom left her family and flew to Boston in late 2011 so that Shaw could treat her with AUY922.
But Broom did not respond to the drug and instead developed large new metastases in her brain. Her final hope was LDK378, but Broom was worried that she’d soon be too sick to travel. She decided to return home even though she would have no access to the drug.
Shortly before she left, O’Sullivan invited her out with a few other friends to the Temple Bar, where I met her. As we spoke, we discovered an unexpected connection: Alice Shaw was a college classmate of mine. Broom explained her and Shaw’s master plan to get Novartis to release the drug. It was simple, really. Broom would send a letter begging the Swiss pharmaceutical giant for compassion.
“Dear Novartis,” she wrote. “I am writing to plead with you for compassionate access to LDK378. . . . I have three small children, and I cannot yet give up.” Couldn’t the company, she asked, just sidestep the clinical trial and send her the medicine that could save her life?
Before drugs in the United States can be prescribed by doctors and bought by patients, they must undergo three stages of rigorous clinical trials and approval by the Food and Drug Administration. This safety requirement dates back to 1962, when the sedative thalidomide was revealed to have caused thousands of birth defects. This policy has helped cause drug-development costs to skyrocket to hundreds of millions of dollars and drug approval to take up to 10 years, but it has also protected the public from untold risks and side effects.
Circumventing the deliberate pace of clinical trials can be dangerous, as my own father’s story attests. Short of breath for years and told he had asthma, he actually had idiopathic pulmonary fibrosis, a disease in which the lungs quickly and fatally scar. The New England Journal of Medicine reported that interferon gamma-1B could help, but the 1999 report included only nine treated patients. The F.D.A. approved the drug a few years earlier, but for only a rare genetic bone disease or an immune-system disorder, and it could cost tens of thousands of dollars for a course of treatment. My sister and I, both doctors, wrote a letter to my father’s insurer pleading for them to cover this off-label use. Amazingly, the insurer agreed.
Three times a week, my father gave himself an injection of interferon gamma. Not only did the drug not improve his condition, but it also caused raging fevers that left him confined to bed in terrible pain. He died in 2001. Three years later, N.E.J.M. published a far more thorough study with 330 patients that concluded interferon gamma was not only ineffective against the scarring disease but also caused respiratory infections. It would have been better if my father never took it. And because we had found a backdoor way of getting it — he never joined any study — no drug company or regulator learned anything constructive from his death.
Consider what might have happened if more people with idiopathic pulmonary fibrosis followed my father’s path: 330 people may never have enrolled in the study that clearly showed that the drug was useless for his condition. Which is why last year, after the journal Science reported that the drug Targretin, already approved to treat skin cancer, reversed Alzheimer’s disease in mice within three days, federal experts writing in N.E.J.M. warned that “even if patients and families are willing to take the risks [of Targretin] for the potential benefit, the physician’s answer should be no.” Doctors, in other words, should instead tell patients to enroll in placebo-controlled trials, not least so we can learn whether Targretin really helps fight the disease.
Nevertheless, for desperate patients like Broom, the pace of clinical trials can be lethally slow, and patients have successfully argued for “compassionate access” to unapproved drugs. The first compassionate access was granted for a drug called AZT, originally created to treat leukemia, then shelved. In 1985, the Burroughs Wellcome lab sent it to the National Cancer Institute, where, incidentally, Chabner was director of the treatment division. AZT was the 11th drug tested in a shotgun approach against a new virus soon known as H.I.V., and it worked. By 1986, a key study showed the drug saved lives, but final F.D.A. approval would normally take a year. Dying AIDS patients couldn’t wait. So Robert Yarchoan, along with other N.C.I. investigators who helped develop AZT, worked with Wellcome, the F.D.A. and other federal agencies to create an “open-access clinical trial,” which served as a way to release the drug free to almost one-third of all AIDS sufferers in the country. It was a shrewd way to bypass the usual F.D.A. timeline for drug approval.
Pushed by the advocacy group Act Up, the F.D.A. agreed to allow pharmaceutical companies to offer compassionate access to other promising AIDS drugs. The activists for patients with Alzheimer’s and cancer soon demanded access to promising drugs as well. “AIDS created a terrible, wonderful model for us all,” one activist told The New York Times in 1991. In 1999, a 19-year-old college student named Abigail Burroughs unsuccessfully fought for compassionate access to experimental drugs owned by ImClone and AstraZeneca to treat her head-and-neck cancer. After her death in 2001, her father founded the Abigail Alliance, which sued the F.D.A., arguing for a constitutional right to early-phase drugs. Though the courts ultimately ruled against the family, the F.D.A. did recently create a program that would make it easier for companies to release experimental medicines — if the companies agreed to do it.
But not all companies willingly allow compassionate access to drugs in their pipelines, and ImClone’s and AstraZeneca’s reluctance makes sense on some level. Only 6 percent of early-stage cancer drugs ever come to market, because many are found to have severe side effects or simply don’t work. Given those odds, companies hesitate to do anything to jeopardize a product too soon. If they give drugs away, a disastrous side effect or other poor outcome could spur bad publicity and extra scrutiny from regulators. Even more important, if doctors simply let people take untested medicines without going through all the clinical trials, drug companies would most likely never get anyone to enroll in them, never get the data on safety and efficacy for F.D.A. approval and never pass the gateway to big sales. “Even if patients with cancer are willing buyers,” writes George Annas, a Boston University expert on medical law, “drug manufacturers are not willing sellers.”
As a public-health advocate, I know that if we simply let people have access to untested medicines without those trials, we will never learn which ones are effective and how best to use them. But to a physician coming face to face with frightened and desperate patients in the clinic, the case for the greater good seems less compelling. After all, the promising drug may be the patient’s last and only chance. Every now and then, desperation leads to success. That’s the hope that led Broom to write to Novartis.
Not long after our dinner, Novartis responded to Broom’s letter begging for LDK378, denying her request but giving no reason. Shaw decided to make a more personal appeal. She asked Broom to have her three children and husband hand-write letters. Daniel’s letter read: “Dear Drug Company . . . Mummy needs to finish reading ‘The Lord of the Rings’ to Christopher and I, we are at ‘Return of the King,’ siege of Gondor, page 853. There are 1,069 pages. . . . I love my mum, please help her to get better.” Shaw topped it off with a montage of photos: Broom holding her daughter, Amelia, in an angel costume; Broom wading with her kids in a lake. In her own letter, Shaw made the detailed scientific case for LDK378 and referred to her authority as a Harvard Medical School professor and the lead recruiter for major cancer trials.
She gathered the packet and sent it to Barbara Weber, Novartis’s head of early-development oncology and senior vice president, who had the authority to release LDK378. “I apologize for e-mailing you directly,” Shaw wrote, “but I have exhausted all other options.” She also sought Weber out in person at an oncology conference in California. Weber was so moved by the packet that she decided to give Broom the LDK378.
Right now, there are no specific guidelines that determine who is eligible for compassionate access. Weber told me that she gets only a handful of requests and that she usually approves them. (Shaw told me she made numerous requests for Broom to get compassionate access to Novartis’s LDK378 but was repeatedly denied. Weber said she was not aware of those requests.) The fact that Broom’s appeal was so personal and got directly into Weber’s hands made the difference, but few patients actually have the resources and connections to make that happen.
Novartis mailed Broom a package of LDK378, and she began taking the pills. Within weeks, her headaches were gone, and scans showed that her tumor almost entirely disappeared. In August 2012, she was on vacation with her family at a national park near her home when I reached her by Skype. We talked about a children’s-book character she created named Freya Fantail, a small bird who helped ill animals. Broom was particularly grateful that a close friend had illustrated the manuscript with vivid crayon drawings. She’d resumed reading “The Return of the King” to her sons.
To be sure, the events leading to Broom’s miraculous improvement arose from a series of advantages. She was a well-connected, highly literate Oxford graduate who could afford to travel to Boston from New Zealand. She happened to know O’Sullivan, who in turn knew Chabner, a globally respected cancer researcher. And of course, Shaw, her oncologist, wouldn’t accept Novartis’s initial denial of LDK378 and knew how best to navigate the system. Few people are so lucky, as Broom was the first to admit.
Still, access to unproven medicines cannot be an absolute right; it must depend on review by an experienced doctor, like Shaw, who can weigh complex medical data to make educated guesses for treatment. Otherwise, patients are too vulnerable to charlatans. Recently, Shinya Yamanaka, who won the 2012 Nobel Prize in Medicine for his work on human stem cells, described to me the pleas he and his colleagues receive. His work has created the possibility of one day growing new organs, and patients come to him asking for all sorts of unproven treatments. When they’re inevitably denied, they may seek out people like the Beijing neurosurgeon who treats paralysis by injecting aborted fetal tissue into the spine, even though there is no conclusive testing to suggest it works.
This is where patient-advocacy groups could make an impact: by creating easily accessible tools to help such patients better understand their options, connect them with the latest science and point them to promising drugs under development. The fact that Barbara Weber gets only a half-dozen or so requests for compassionate use each year suggests that very few patients know the possibility even exists. Advocacy groups could also ensure that companies price new therapies fairly. (Last fall, after doctors from Memorial Sloan-Kettering hammered Sanofi and Regeneron for the high price of one of their cancer drugs in a New York Times Op-Ed, the companies dropped their price by half.) Government resources like clinicaltrials.gov could better organize and curate studies for patients and disclose which drugs are in the development pipeline. In these ways, compassionate access could become less about luck and more about what’s best for patients and for science.
Broom’s cancer responded to treatment with LDK378. But her reprieve again proved temporary. After almost a year, LDK378 stopped working, and Broom truly was left with no options. Earlier this year she stopped responding to my e-mails. She died on April 18 in Auckland, surrounded by her family.
Around that time, her husband, Michael, had taken to wearing three bracelets carved from bone. An American woman named Linnea Duff had given Broom the bracelets to symbolize that she was the third person to get crizotinib, the cancer drug Chabner first prescribed. Duff was the fourth to get it, for her advanced-stage lung cancer, and she bought four bracelets for herself. Like Broom, Duff had a remarkable response, and the drug kept her cancer at bay for years. She recently began a trial of LDK378 after having a relapse, but she has already survived almost seven years since her diagnosis, longer than even the best prognosis.
Broom, too, survived for years beyond what doctors first told her she could expect. She wasn’t supposed to see Amelia’s first birthday, and instead she was able to celebrate her fourth. For long stretches of that time, Broom was able to live a normal, relatively healthy life. All this was undoubtedly due to the various drugs she was able to get through compassionate access.
Duff and Broom used to playfully refer to each other as “No. 3” and “No. 4,” Duff told me, but now only No. 4 is left. “I resolve to never give up,” she said, “and I start each day saying, ‘I’m alive, I’m alive, I’m alive.’ ”
Saturday, June 1, 2013
Five Promising Cancer Drug Results
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A quick run-down of studies presented this morning at a press conference at the annual meeting of the American Society for Clinical Oncology, the biggest gathering of U.S. cancer doctors.
http://www.forbes.com/sites/matthewherper/2013/06/01/five-promising-cancer-drug-results/
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