Much of the confusion surrounding the benefits of screening comes from interpreting the statistics.  A patient’s survival period—how long a person lives after a cancer diagnosis—is often taken to imply that the test saves lives. But a screening test can only save lives if it advances the time of diagnosis and earlier treatment is more effective than later treatment.

Biases Inherent in Survival Statistics

One type of statistical bias occurs when screening does find a cancer earlier than that cancer would have been diagnosed due to symptoms, but the earlier diagnosis does nothing to change the course of the disease. For example, a man experiencing a persistent cough and weight loss is diagnosed with lung cancer at age 67 and dies of the disease at age 70. Statistically, his 5-year survival is 0 percent.

If the same man is screened and his cancer is detected at age 64, but he still dies at age 70, his life has not been extended by its earlier discovery. But his 5-year survival is 100 percent, even though the man lives not a second longer. If the effectiveness of his screening is measured by survival period, the test would seem to have a dramatic impact. But the test had no impact on the man’s mortality.

Another bias is due to the fact that screening is more likely to pick up slower-growing, less aggressive cancers that may exist in the body long before symptoms develop. In some cases, a slow-growing (nonprogressive) cancer found by screening would not have caused harm or required treatment during the patient’s lifetime. Including these patients in survival statistics artificially inflates 5-year survival rates – they would have survived regardless of the test.  And the ”overdiagnosis” of these patients can lead to other concerns.

Following discovery through screening, some slow-growing cancers are treated aggressively, often at the patient’s insistence. The cost can be significant, both economically and physically.

Physicians Also Confused

Doctors are bombarded with the same conflicting information as are patients. A study published March 6 in the Annals of Internal Medicine by Drs. Lisa Schwartz and Steven Woloshin, professors of medicine at the Dartmouth Institute for Health Policy and Clinical Practice, showed how relatively small reductions in mortality from screening can confuse even experienced doctors when pitted against large—but potentially misleading—improvements in survival. They surveyed 412 doctors specializing in family medicine, internal medicine, or general medicine regarding the effects of two hypothetical tests in terms of 5-year survival and mortality reduction.

The results of the survey showed widespread misunderstanding. More than three quarters of the doctors believed—incorrectly—that an improvement in 5-year survival shows that a test saves lives. And 68 percent said they were more likely to recommend the test if evidence showed that it detected more cancers at an early stage.

Debate Continues

Clearly, early detection of treatable cancers has saved and extended lives. But the debate about which tests to administer and when continues. Last October the US Preventative Services Task Force issued draft recommendations for prostate cancer where they advised against routine PSA-based screening in healthy asymptomatic men of any age.

In March the USPSTF recommended several new screening guidelines for cervical cancer, including testing for women ages 21 to 65 years with cytology (Pap  smear) every 3 years or, for women ages 30 to 65 years who want to lengthen the screening interval, screening with a combination of cytology and human papillomavirus (HPV) testing every 5 years. And just today, the NCI Cancer Bulletin reported on a study indicating that women at high risk for breast cancer may benefit from starting mammography at age 40.

Dr. Woloshin says patients need to know the right questions to ask their doctors. “You see these ads with numbers like ‘5-year survival changes from 10 percent to 90 percent if you’re screened.’ But what you always want to ask is: ‘What’s my chance of dying [from the disease] if I’m screened or if I’m not screened?’”

>> Original article by Sharon Reynolds

The Gala’s theme will salute Hollywood’s music and movies. Event Chairs (make that, Directors) Gabrielle Patout and Lory Tauber have been hard at work planning the event and securing the entertainment.“We’ve been working with Nancy Ames, Nancy Riviere, and Danny Ward to sign a major star.” said Gabrielle. ”So when Danny told us Kenny Loggins had confirmed, we were thrilled. His music appeals to everyone, and the Hollywood theme will be a perfect match.”

With twelve platinum selling albums, Loggins’ list of hits is impressive: Footloose – Danger Zone – I’m Alright (Caddyshack theme) – Danny’s Song – House at Pooh Corner – Celebrate Me Home – This is It - Your Mama Don’t Dance - Whenever I Call You Friend – Meet Me Halfway – A Love Song – Heart to Heart – I Would Do Anything – Angry Eyes - and on and on. And guests won’t get a break when Kenny leaves the stage. Skyrocket!, the “wickedly original party band” from Austin will take over to keep the dance floor rockin’ until the wee hours.

The Friends of the Stehlin Foundation is an independent 501(c)(3) charitable organization whose annual events have netted over $11 million. All of the proceeds have been donated to CHRISTUS Stehlin Foundation’s research, clinical, and education programs. Friends founder (and Foundation vice chairman) Mike Meagher summed up the Friends’ motivation: “There’s a lot of excitement about the new cancer drugs and research projects on the horizon, but it takes money to make those possibilities come true. That’s why we’re here – to raise money. We just always have a good time doing it.”

For information on the 2012 Gala and to receive ticket and table information, please contact Colleen Colton at the Foundation (713-659-1336).

Key Messages:

• Women who have been through natural menopause are at greater risk for developing cancer because they are older, which is a risk factor for cancer.
• Some cancer treatments may cause menopause or menopausal symptoms in women and menopausal-like symptoms in men.
• Postmenopausal hormone therapy may increase a woman’s risk of cancer.

Menopause does not cause cancer, but the risk of developing cancer increases as a woman ages. Women who have been through natural menopause are more likely to develop cancer because they are older. In addition, cancer treatment can cause menopause and menopausal symptoms.

About menopause

Menopause occurs when a woman’s ovaries stop producing eggs; her menstrual periods become irregular, then stop completely; and her body decreases production of the hormones estrogen and progesterone. It begins during a woman’s mid-40s or early- to mid-50s. It can also begin before a woman’s 40s if cancer treatment has stopped the ovaries from working (called premature menopause).

The symptoms of menopause include hot flashes, night sweats, vaginal dryness, sleeplessness, decreased sex drive, and mood swings. Learn about managing menopausal symptoms.

Menopause and cancer risk

A woman who began menopause after age 55 has an increased risk of ovarian, breast, and uterine cancer. This risk is greater if a woman also began menstruating before age 12.

A woman who menstruates longer than normal during her life is exposed to more estrogen and has more ovulations. Excess exposure to estrogen increases a woman’s risk of uterine and breast cancers, and having a greater number of ovulations increases a woman’s risk of ovarian cancer.

Does cancer treatment cause menopause or menopausal symptoms?

Some cancer treatments may cause menopause or menopausal symptoms. Menopause caused by medical treatment is called medical (or surgical) menopause. The symptoms of medical menopause may be worse because the decrease in hormones happens quickly. Even if cancer treatment does not cause menopause immediately, it may cause menopause to start sooner.

The following cancer treatments may cause menopause:

Oophorectomy (surgical removal of the ovaries). This type of surgery is used to treat or prevent ovarian, uterine, and vaginal cancers. It causes menopause immediately because the source of estrogen and progesterone is removed.

Radiation therapy or chemotherapy. Radiation therapy to the pelvis and chemotherapy that damages the ovaries can cause early menopause. Menstrual periods may return for some younger woman after treatment, but women older than age 40 are less likely to have their menstrual periods return.

Hormonal therapy. Hormonal therapy is used to treat breast cancer that is estrogen receptor- and/or progesterone receptor-positive, meaning that cancer uses estrogen and/or progesterone to grow. Hormonal or anti-estrogen therapies include the aromastase inhibitors—including anastrozole (Arimidex), letrozole (Femara), exemestane (Aromasin)—and tamoxifen.

The drugs tamoxifen (Nolvadex) and raloxifene (Evista) are used to reduce the risk of breast cancer for women who have been treated for breast cancer or who have a higher risk of breast cancer. The side effects of these drugs are similar to the symptoms of menopause.

Women taking hormonal therapy who have not been through menopause may have lighter and fewer regular menstrual periods, or their menstrual periods may stop completely. A woman’s menstrual periods may come back after hormonal therapy ends, but this is less likely for women who are closer to their natural menopausal age. Menopausal symptoms may come back for women taking hormonal therapy who have already reached menopause.

Men with prostate cancer who receive hormonal therapy or have their testicles removed may also experience symptoms similar to menopause. These include hot flashes, irritability, decreased sex drive, fatigue, osteoporosis (thinning of the bones), and erectile dysfunction (inability to have an erection).

Can the treatment of menopausal symptoms increase my risk of cancer?

The Women’s Health Initiative study found that women taking combined hormone therapy (also known as postmenopausal hormone therapy or hormone replacement therapy) to manage menopausal symptoms may have increased risk of breast cancer. Combined hormone therapy is a combination of estrogen and progestin (a form of progesterone made in a laboratory). It is used to help women cope with menopausal symptoms and prevent osteoporosis and heart disease. Hormone therapy with estrogen alone is only given to women who have had a hysterectomy (the removal of the uterus) because estrogen increases the risk of uterine cancer.

The Women’s Health Initiative also found that women taking combined hormone therapy had an increased risk of heart attack, stroke, and blood clots. However, they had a decreased risk of colorectal cancer and bone fractures. Because of the increased risks, many doctors recommend that women do not take combined hormone therapy or only take low doses for a short time. Combined hormone therapy is not usually recommended for women with a history of breast cancer or those who have an increased risk of breast cancer.

Recent research also showed that women who received combined hormone therapy have a higher risk of dying from non-small cell lung cancer (NSCLC) if they develop the disease. However, woman in the study taking combined hormone therapy were not more likely to develop NSCLC than women who were not taking combined hormone therapy. The study also showed that the risk of dying from lung cancer was higher for women with NSCLC who smoke and take combined hormone therapy.

Research on combined hormone therapy is controversial and ongoing. The risks and benefits of the treatment are different for each woman. Be sure to talk with your doctor about the benefits and risks before deciding to receive combined hormone therapy.

More Information

Emotional and Physical Matters

What to Know: ASCO’s Guideline on Hormone Therapy for Advanced Prostate Cancer

Additional Resources

National Institute on Aging: Menopause

National Cancer Institute: Menopausal Hormone Replacement Therapy Use and Cancer

National Institutes of Health: Menopausal Hormone Therapy Information

Pancreatic adenocarcinoma, the most common type of pancreatic cancer, is notoriously resistant to chemotherapy and radiation therapy, leading to an overall 5-year relative survival rate of less than 5 percent. Using mice with tumors that are genetically similar to human pancreatic adenocarcinomas, the researchers found that, as the tumors grow, a thick matrix develops and surrounds the tumors’ cells.

The matrix exerts tremendous pressure on the tumors—pressure that greatly exceeds the normal pressure found within blood vessels—causing the tumors’ blood vessels to collapse. This collapse prevents chemotherapy drugs in the blood stream from reaching the tumor cells.

Dr. Hingorani and his colleagues identified a substance called hyaluronic acid that forms a large part of this pressurized matrix. When they treated the mice with an enzyme called PEGPH20, which breaks down hyaluronic acid, the pressure within the tumors returned to normal, and the blood vessels regained their normal shape and function.

When the researchers treated mice with a combination of PEGPH20 and the chemotherapy drug gemcitabine, 83 percent of tumors within the pancreas shrank after only one cycle of treatment, and all tumors shrank after three cycles. Similar responses were seen in metastatic tumors. Mice that received the combination therapy survived almost twice as long as mice that received PEGPH20 plus a placebo.

“When able to penetrate the tumor bed, gemcitabine can indeed be an effective agent against this disease,” wrote the authors. An early phase clinical trial is testing the combination of PEGPH20 and gemcitabine in people with metastatic pancreatic cancer.

In the 1960s two young scientists in Philadelphia, Dr. Peter Nowell from the University of Pennsylvania and Dr. David Hungerford from Fox Chase Cancer Center, spent their days peering through microscopes at white blood cells. They noticed that when they stained cells from patients with chronic myeloid leukemia (aka chronic myelogenous leukemia, or CML), they would very often see an odd, minute chromosome in addition to the normal set.

We know today that this was a landmark observation. Dr. Nowell and Dr. Hungerford named their discovery the “Philadelphia Chromosome” in keeping with the tradition of the day, and it soon became an important way to diagnose CML.

In the 1970s, Dr. Janet Rowley at the University of Chicago used newly-developed techniques that highlighted different regions of chromosomes to look more carefully at the Philadelphia Chromosome. She determined that they looked odd because two large pieces of two different chromosomes had changed places. But the significance of that translocation wasn’t immediately apparent.

At the Massachusetts Institute of Technology in the 1980s, Nobel Laureate Dr. David Baltimore followed up on Dr. Rowley’s observations to make a critical discovery about what causes CML. His laboratory was able to show that one of the results of the exchange of chromosomal material was the creation of a completely new gene, BCR-Abl, which was only found in CML cells. Dr. Baltimore went on to show that the BCR-Abl protein causes CML in laboratory and animal models. Knowing what causes CML provided the platform for the next major discovery in the treatment of this form of leukemia, which is most commonly found in older adults.

Dr. Brian Druker at Oregon Health and Science University combined perseverance, innovation, and personal commitment to cancer patients to make the next major breakthrough in the 1990s. One of the most critical challenges that he faced was not scientific, but economic.

At the time, the number of patients afflicted with CML in the U.S. was thought to be too small to entice major pharmaceutical companies to develop a drug. Regardless, Dr. Druker was able to convince Novartis (then called Ciba-Geigy) to allow him to screen some of the compounds in their huge chemical collections. Remarkably, he discovered a drug that blocked the activity of the BCR-Abl protein.

After another decade of testing and clinical trials,  Gleevec (imatinib mesylate) was approved by the Food and Drug Administration for treatment of CML in 2001. Together with other, later drugs which target the BCR-Abl protein, Gleevec has transformed CML from a lethal diagnosis to a manageable disease for more than 90 percent of patients.

Effective treatment of CML has undoubtedly saved thousands of lives, but it took four decades of discovery in four different parts of the country to make this possible. No matter how much we want a cure for cancer tomorrow, the history of science has taught us that it takes time. Even a brief examination of the major breakthroughs in cancer medicine reveals that the major discoveries were only possible because of a series of advances, painstakingly accumulated over many decades.

In every case, success results from the marriage of hard work and innovation nurtured by the element of time. (Money is crucial, too, of course. Without it, research can’t happen at all, and cutting funding only slows the development of new treatments.)

Discoveries made in the 1990s set the stage for the advances in targeted therapies against a broad range of cancers, including melanoma, lung cancer, and leukemia, for which we’ve seen major advancements during just the past year. These promising paths need the time — and dollars, of course — to find their greatest benefits for cancer patients during the next decade. It really is about time.

>> Link to original article

A retinoid called all-trans retinoic acid (ATRA), which is a vitamin A-derivative, is already used successfully to treat a rare sub-type of acute myeloid leukemia (AML)*, however this drug has not been effective for the more common types of AMLs.

Team leader Dr Arthur Zelent and colleagues at the ICR have been working to unlock the potential of retinoids to treat other patients with AML. In a paper recently published in Nature Medicine, they show that the key could be an antidepressant called tranylcypromine (TCP).

“Retinoids have already transformed one rare type of fatal leukemia into a curable disease. We’ve now found a way to harness these powerful drugs to treat far more common types of leukemia,” senior author Dr Zelent, from the ICR, said. “Until now, it’s been a mystery why the other forms of AML don’t respond to this drug. Our study revealed that there was a molecular block that could be reversed with a second drug that is already commonly used as an antidepressant. We think this is a very promising strategy, and if these findings can be replicated in patients the potential benefits are enormous.”

ATRA works by encouraging the leukemia cells to mature and die naturally. The team thinks the failure of AML to respond to this drug may be due to genes that ATRA normally targets becoming switched off. In their search for a drug that could be used to reboot the activity of ATRA, the team looked to an emerging area of research called epigenetics. Epigenetic drugs do not target genes directly but instead target whether genes are switched on or off. They discovered that inhibiting an enzyme called LSD1, using TCP, could switch these genes on again and make the cancer cells susceptible to ATRA.

Along with collaborators at the University of Münster in Germany, the team have already started a Phase II clinical trial of the drug combination in acute myeloid leukemia patients.

Co-author Dr Kevin Petrie from the ICR says: “Both the retinoid ATRA and the antidepressant TCP are already available in the UK and off-patent, so these drugs should not be expensive for the health service. AML remains very difficult to treat and sadly is often fatal, with rates of the disease projected to increase significantly as the population ages, so it is particularly pleasing to have identified this new treatment approach. Importantly, we believe these drugs are targeting only the cancer cells and leaving normal healthy cells largely untouched, so we are hopeful that they would have fewer side-effects for patients than standard drugs. We look forward to seeing the results of the clinical trials.”

Each year, more than 2,200 people in the UK are diagnosed with acute myeloid leukemia, a type of cancer characterised by the uncontrolled growth of immature white blood cells in the bone marrow.

Professor Chris Bunce, Research Director at leukemia & Lymphoma Research, said: “These results are extremely significant. Current drugs for AML are very aggressive and many older patients have a poor outlook as they cannot tolerate treatment. ATRA has been a major success story in recent years in treating a particular subtype of AML. In finding a way to expand its use, we would have the potential to save thousands of lives a year.”

The study was a collaboration between scientists at the ICR, Cardiff University and Queen’s University, Belfast, in the UK; Johns Hopkins University, Baltimore, Progen Pharmaceuticals and Medical University of South Carolina in the US; the University Health Network and the University of Toronto in Canada; and the University of Münster in Germany. It was funded in the UK by leukemia & Lymphoma Research along with the Samuel Waxman Cancer Research Foundation.

* Retinoids are already licensed to treat a type of AML called acute promyelocytic leukaemia (APL).

The researchers found five-year survival rates among children with acute lymphoblastic leukemia (ALL) increased from about 84 percent to 90 percent from 1990 to 2005. Surviving for five years is considered a cure because so few deaths occur past that timeframe.

“We’re talking about a disease that was incurable 50 years ago,” said study author Dr. Stephen Hunger. “Now we see a 90 percent cure rate. That’s pretty remarkable.”

The study is published in the March 12 online issue of the Journal of Clinical Oncology.

Hunger, a professor of pediatrics at the University of Colorado School of Medicine and director of the Center for Cancer and Blood Disorders at Children’s Hospital Colorado, said the clinical trials have helped doctors refine their use and dosage of drugs, resulting in greater survival rates. For example, one type of corticosteroid was found to be more effective than another drug in the same class, he said.

ALL is a rare blood or bone-marrow cancer, but it still is the most common form of childhood leukemia. Between 2,800 and 3,000 new cases are diagnosed every year in the United States, Hunger said.

Leukemia, the most common childhood cancer, occurs when the body produces too many abnormal white blood cells, resulting in harm to the immune system and symptoms such as bruising, frequent infections and diarrhea. The acute form progresses quickly if not treated with chemotherapy.

The cause of ALL is not known, but risk factors include having a sibling with leukemia or having had chemotherapy or radiation treatment for some other condition.

The study, done at the University of Colorado, found that the increased survival rate held for all racial and ethnic groups, both sexes, and for all age groups except infants younger than 1 year old. Survival rates improved as the study proceeded.

Death rates fell between 30 percent and 50 percent during the study period, except for among infants, according to the research. Infant survival rates stayed about the same because improvements in drug usage were offset by more deaths from infections and side effects, the study found.

More than 21,000 children with ALL — more than half of all cases in the United States — from age 0 to 22,  were included in the research. Participants came from the Children’s Oncology Group clinical trials funded by the U.S. National Cancer Institute.

Another expert noted that the study shows just how much progress has been made.

“It’s amazing, really, that even not knowing why the disease occurs, we can do so well at curing it,” said Dr. Arlene Redner, associate chief of oncology in the division of pediatric hematology, oncology and stem-cell transplantation at Cohen Children’s  Medical Center in New Hyde Park, N.Y.

The study is also important because it shows that effective treatment is widely available, Redner said.

“One of the important things about this study is that it shows that children anywhere in the United States can get this therapy,” she said. “It’s not just at national treatment centers, but also at small centers.”

The future for children with leukemia continues to brighten, Hunger said.

“It’s fantastic that now 90 percent of patients can expect to be cured,” he said. “However, if your child is part of the 10 percent that isn’t cured, it is small consolation.”

Efforts now need to focus on that 10 percent, he said, adding: “The goal is to cure everyone.”

SOURCES: Stephen Hunger, M.D., professor, pediatrics, University of Colorado Medical School, Aurora; Arlene Redner, M.D., associate chief, oncology, division of pediatric hematology, oncology and stem cell transplantation, Cohen Children’s Medical Center, New Hyde Park, N.Y.; March 12, 2012, Journal of Clinical Oncology

The results suggest that bexarotene could possibly help the approximately 5.4 million Americans with Alzheimer’s disease, according to the neuroscientists at Case Western Reserve University School of Medicine.

However, while studies involving animals can be useful, they often fail to produce similar results in humans.

Bexarotene is approved in the United States to treat skin problems caused by cutaneous T-cell lymphoma.

The body’s inability to clear amyloid beta from the brain is a major factor in the development of Alzheimer’s disease, according to a university news release. Previous research showed that the main cholesterol carrier in the brain, apolipoprotein E (ApeE), plays an important role in clearing amyloid beta proteins.

In this study, the researchers found that bexarotene increased ApoE expression, and the elevated levels of ApoE boosted clearance of amyloid beta from the brain. Bexarotene stimulates retinoid X receptors (RXR), which are proteins that control the production of ApoE.

Within six hours of receiving bexarotene, soluble amyloid levels in the mice fell by 25 percent and the effect lasted for three days. This decrease was associated with rapid improvement in a wide number of behaviors in mice with Alzheimer’s, according to the release.

In addition, bexarotene treatment also rapidly stimulated the removal of amyloid plaques from the brain, the researchers said. The plaques are accumulations of amyloid that form in the brain and are a hallmark of Alzheimer’s disease.

“This is a particularly exciting and rewarding study because of the new science we have discovered and the potential promise of a therapy for Alzheimer’s disease,” study senior author Gary Landreth, a professor of neurosciences, said in a university news release.

“We need to be clear; the drug works quite well in mouse models of the disease. Our next objective is to ascertain if it acts similarly in humans. We are at an early stage in translating this basic science discovery into a treatment,” he added.

The study appeared Feb. 9 in the journal Science.

SOURCE: Case Western Reserve University, news release, Feb. 7, 2012

The researchers identified two mutations in an important gene known as the histone H3.3. This gene is key in modulating genetic expression. “These mutations prevent the cells from differentiating normally and help protect the genetic information of the tumor, making it less sensitive to radiotherapy and chemotherapy,” says Dr. Nada Jabado, hematologist-oncologist at The Montreal Children’s Hospital of the McGill University Health Centre and principal investigator of the study.

“This research helps explain the ineffectiveness of conventional treatments against cancer in children and adolescents — we’ve been failing to hit the right spot,” says Dr. Jabado. “It is clear now that glioblastoma in children is due to different molecular mechanisms than those in adults, and should not be treated in the same way. Importantly, we now know where to start focusing our efforts and treatments instead of working in the dark.”

Inappropriate regulation of this gene has been observed in other cancers such as colon, pancreatic, lymphoma, leukemia and pancreatic neuroendocrine cancer, and future research could therefore reveal improved treatments for these diseases.

Brain tumours are the primary cause of death for children with cancer in Europe and North America. The diagnosis of glioblastoma in a child or adolescent remains a death sentence and about 200 children in Canada die every year of this cancer. Most children will die within the two years of their diagnosis regardless of treatment.

Erivedge, reviewed under the agency’s priority review program, is the first FDA-approved drug for metastatic basal cell carcinoma. Erivedge was reviewed under the FDA’s priority review program that provides for an expedited six-month review of drugs that may offer major advances in treatment.

Basal cell carcinoma is generally a slow growing and painless form of skin cancer that starts in the top layer of the skin (epidermis). The cancer develops on areas of skin that are regularly exposed to sunlight or other ultraviolet radiation.

Erivedge is a pill taken once a day and works by inhibiting the Hedgehog pathway, a pathway that is active in most basal cell cancers and only a few normal tissues, such as hair follicles.

“Our understanding of molecular pathways involved in cancer, such as the Hedgehog pathway, has enabled the development of targeted drugs for specific diseases,” said Richard Pazdur, M.D., director of the Office of Hematology and Oncology Products in the FDA’s Center for Drug Evaluation and Research. “This approach is becoming more common and will potentially allow cancer drugs to be developed more quickly. This is important for patients who will have access to more effective therapies with potentially fewer side effects.”

The safety and effectiveness of Erivedge was evaluated in a single, multi-center clinical study in 96 patients with locally advanced or metastatic basal cell carcinoma. The clinical study’s primary endpoint was objective response rate (ORR) or the percentage of patients who experienced complete and partial shrinkage or disappearance of the cancerous lesions after treatment. Of the patients with metastatic disease receiving Erivedge, 30 percent experienced a partial response and 43 percent of patients with locally advanced disease experienced a complete or partial response.

The most common side effects observed in patients treated with Erivedge were muscle spasms, hair loss, weight loss, nausea, diarrhea, fatigue, distorted sense of taste, decreased appetite, constipation, vomiting, and loss of taste function in the tongue.

Erivedge is being approved with a BOXED WARNING alerting patients and health care professionals of the potential risk of death or severe birth effects to a fetus (unborn baby). Pregnancy status must be verified prior to the start of Erivedge treatment. Male and female patients should be warned about these risks and the need for birth control. Erivedge is marketed by South San Francisco based-Genentech, a member of the Roche Group.