15 Common Myths About Cervical Cancer

About 9,700 women in the United States will be diagnosed with cervical cancer this year. It may seem like a small number, until you consider that another 1.2 million women will develop a pre-cancerous condition called dysplasia. And if left untreated, dysplasia will become cervical cancer.

"Because of Pap smears, a huge number of women are no longer dying of cervical cancer in this country, but this is a disease that can be almost entirely prevented," says Carolyn Johnston, M.D., clinical associate professor of obstetrics and gynecology at the University of Michigan Medical School and a gynecologic oncologist at the U-M Comprehensive Cancer Center.

In addition to early detection through screening, a new vaccine now available could help prevent cervical cancer. In honor of Cervical Cancer Awareness Month, which is January, U-M experts respond to common myths and misconceptions about this disease.

Myth 1: Cervical cancer cannot be prevented.

Truth: Infection with the human papillomavirus, or HPV, is an absolute requirement for cervical cancer to develop. This virus is transmitted sexually, but the majority of the most worrisome types of infection can be prevented with a newly available vaccine. Preventing HPV infection dramatically reduces a woman's risk of cervical cancer. In addition, cervical cancer usually develops slowly after persistent infection with HPV and will first appear as a precancerous condition called dysplasia. If detected at this stage, it can be effectively treated to prevent cervical cancer from developing. Screening with Pap smears and tests for HPV detect these pre-cancerous conditions so patients are treated early.

Behavioral issues can also influence cervical cancer. "A woman can reduce her risk of these problems by limiting the number of sexual partners over a lifetime, by not smoking cigarettes and by following accepted screening guidelines. Each of these behaviors relates to known risk factors for this disease," says Anthony Opipari, M.D., Ph.D., associate professor of obstetrics and gynecology at the U-M Medical School.

Myth 2: I'm too young to worry about cervical cancer.

Truth: The average age of cervical cancer patients is 48. While it's not common, women can be diagnosed in their 20s. HPV infection and the precancerous condition dysplasia are common in younger women.

Myth 3: I don't have intercourse, so I don't need the HPV vaccine.

Truth: HPV can be passed from one partner to another through intercourse, as well as orally and through touching. In 2006, the Food and Drug Administration a vaccine, Gardasil, to protect against four types of HPV, two of which are commonly linked to cervical cancer and two linked to genital warts. A CDC advisory committee recommended that Gardasil be given routinely to girls age 11-13. Until everyone is vaccinated, girls and women ages 13-26 are also candidates for the vaccine. Experts believe the vaccine should be given at a young age before a woman becomes sexually active.

Myth 4: I had the HPV vaccine, so I don't need to use condoms during sex.

Truth: The HPV vaccine will protect you from infection with four types of HPV but there are other strains of this virus and many other sexually transmitted diseases that it does not protect against. Continue using condoms to protect against STDs.

Myth 5: I don't need a Pap test.

Truth: A woman's first Pap test should be given when she turns 21 or three years after she begins having intercourse, whichever comes first. Recommendations differ for how often a woman should receive a Pap test. Ask your doctor how often you should be screened. Even if you have the HPV vaccine, you still need a regular Pap test. The vaccine targets four types of HPV but it will not protect against all the types of HPV that can cause cervical cancer, so it's still important to continue regular screenings.

Myth 6: I'm too old to need a Pap test any longer.

Truth: "We have seen an increase in cervical cancer and HIV in older populations," says Lauren Zoschnick, M.D., clinical assistant professor of obstetrics and gynecology at the U-M Medical School. "Women can have new sexual partners, which puts them at risk of cervical cancer and other STDs." Talk to your health care provider about the need to have Pap smears even if you have gone through menopause, have had a hysterectomy, or are over the age of 65.

Myth 7: My doctor gave me a pelvic exam, which is the same as a Pap test.

Truth: The Pap test collects cells from the cervix, which are sent to a lab to be evaluated. In a pelvic exam, your doctor physically examines the cervix and other parts of a woman's anatomy. Both are important to detect problems early.

Myth 8: My Pap test was abnormal, which means I must have cancer.

Truth: Not necessarily. You'll likely need follow-up tests, possibly a test for HPV, colposcopy or a biopsy to test for cancerous cells. An abnormal Pap test could indicate a precancerous condition that can be treated. Conversely, a negative Pap test does not always mean a woman is cancer-free. About 10 percent of all Pap tests return a false negative result, meaning the test did not identify a problem that is there. If you have problems such as bleeding or pain, seek further care even if your last Pap test was normal.

Myth 9: Cervical cancer has no symptoms.

Truth: Bleeding after intercourse, bleeding between menstrual periods or bleeding after menopause may indicate cervical cancer. Other symptoms include an abnormal discharge or pain in the pelvic region.

Myth 10: If I am diagnosed with cervical cancer, I am going to die.

Truth: Survival after cervical cancer caught in its earliest stage is 92 percent. The later it is diagnosed, the lower the chance of survival. Survival is lower in developing countries because of inadequate screening. Regular screening will help ensure cervical cancer is caught at an early, treatable stage.

Myth 11: After I finish treatment, I will live the rest of my life worried about cancer returning.

Truth: If cervical cancer is going to recur, it is most likely to happen in the first two years after treatment. Most patients are followed for five years, after which the risk of recurrence is extremely low.

Myth 12: I must have a hysterectomy to treat cervical cancer.

Truth: Early cervical cancer is typically treated with a hysterectomy, surgery that removes the cervix and uterus. But it's not the only option. Radiation and chemotherapy are used to treat more advanced disease and may also be options for women with early stage disease who cannot have surgery. Some women with early cervical cancer can also avoid hysterectomy with procedures such as a cone biopsy that removes only the cancerous tissue and a small margin of surrounding healthy tissue, or a procedure called radical trachelectomy, which removes the cervix but not the uterus.

Myth 13: I won't be able to conceive a child after cervical cancer treatment.

Truth: If you have a hysterectomy or radiation to treat cervical cancer, you will not be able to conceive. But newer surgical procedures help preserve a woman's fertility without compromising survival. A radical trachelectomy removes the cervix but not the uterus so that a woman can still conceive. For small, early cancers, a cone biopsy may be appropriate and will also preserve fertility.

Myth 14: A hysterectomy to treat cervical cancer will put me in menopause afterward.

Truth: Hysterectomy to treat cervical cancer does not remove the ovaries, which are what determines whether a person is menopausal. Cervical cancer very rarely spreads to the ovaries. Women who receive pelvic radiation to treat cervical cancer will likely experience menopause because the radiation will affect the ovaries.

Myth 15: Taking hormone replacement therapy will increase my risk of cervical cancer.

Truth: Cervical cancer does not respond to hormones like breast or ovarian cancers. Low doses of hormone replacement therapy can treat menopausal symptoms without increasing the risk of cervical cancer.

For more information about cervical cancer and the HPV vaccine, visit the following resources:

-- U-M Cancer Center: http://www.mcancer.org

-- U-M Cancer AnswerLine: 800-865-1125

-- Michigan Cancer Consortium: http://www.michigancancer.org/

-- National Cancer Institute: http://www.cancer.gov

-- HPV Questions and Answers: http://www.cdc.gov/std/hpv/STDFact-HPV-vaccine.htm

University of Michigan Health System
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http://www.med.umich.edu/

Destructive Enzyme Shows A Benevolent Side

New research shows that a recently discovered enzyme that destroys the messenger RNA (mRNA) for some proteins can also help to protect the mRNA during times of stress. The response might help cancer cells survive chemotherapy and radiation therapy.

The study examined a recently discovered enzyme called PMR1. That enzyme attaches to certain mRNA molecules and remains there like a hand grenade with its pin in place.

These mRNAs carry the information for making highly potent proteins, proteins that cells must stop making suddenly. When that 'stop' command arrives, the pin is pulled and the enzyme destroys the mRNA, quickly halting production of that protein.

This new study found, however, that under stress conditions, the same enzyme - while attached to the mRNA - helps form temporary shelters within the cell called stress granules. There, the mRNA can be protected so that production of the protein can quickly resume whenever the stress ends, perhaps insuring that the cell survives.

Stress granules are short-lived aggregates of mRNA and proteins, and they accumulate when cells are subjected to conditions such as starvation, low oxygen (which can occur within large tumors), chemotherapy or radiation therapy.

The study, led by researchers at Ohio State University's Comprehensive Cancer Center, is published in the December issue of the journal Molecular and Cellular Biology.

"The stress response protects cells from these conditions by sequestering mRNAs for those proteins not specifically involved in the stress response itself," says principal investigator Daniel R. Schoenberg, professor of molecular and cellular biochemistry and a researcher with Ohio State's Comprehensive Cancer Center.

"By understanding how PMR1 and similar enzymes are incorporated into stress granules and inactivated, we may be able to learn how to block this protective mechanism and make it harder for cancer cells to survive cancer therapies."

Schoenberg first discovered the PMR1 enzyme in 1995, and his lab has been actively studying it since that time.

For this study, Schoenberg and a group of colleagues wanted to learn if the enzyme also destroys its mRNA during periods of stress.

To answer the question, they used cultured cells to which they'd added active and mutant forms of the enzyme. They then stressed the cells using the chemical arsenite, a relative of arsenic.

The investigators found that during stress, the enzyme interacts directly with another protein called TIA-1, a key protein involved in assembling stress granules. This interaction draws the enzyme-mRNA complex into stress granules.

But the researchers were unable to detect any sign that the message was destroyed.

"The fact that we don't see an acceleration of mRNA decay suggests that something in the stress response protects these mRNAs from being degraded, even though the degrading enzyme PMR1 is there in the stress granules with its target mRNA."

Schoenberg and his colleagues will next study the other proteins within stress granules to try to learn how PMR1-mRNA complex is preserved.

Funding from the National Institute of General Medical Sciences supported this research.

Schoenberg collaborated on this study with Nancy Kedersha at Brigham and Women's Hospital and Harvard Medical School.

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Contact: Darrell E. Ward
Ohio State University

Designer Hens Lay Anti-Cancer Eggs

Scientists at Scotland's Roslin Institute that produced Dolly the Sheep have genetically modified "designer" hens to lay eggs containing proteins that can fight human forms of cancer and other diseases. It is thought this will make a range of existing drugs easier and cheaper to produce.

The hens are producing proteins that have the potential to treat arthritis, multiple sclerosis, and malignant melanoma, or skin cancer.

The results of this research are to be published in today's issue of the Proceedings of the National Academy of Sciences.

The Roslin team genetically engineered the hens by inserting the gene for the desired proteins into the ovalbumin gene, a protein in egg white. They chose two proteins: human interferon b-1a, which is used to treat a range of tumours and virus infections, and miR24, a monclonal antibody used in the treatment of skin cancer.

They started by using a virus to insert the protein DNA into the DNA of chick embryos. The chicks were hatched and the researchers found that the male ones had DNA in their semen. These were bred with normal hens and the female chicks that carried the new genes then went on to produce the eggs containing the desired proteins. Some 500 genetically modified, or "transgenic" hens have now been created in this way.

The news was welcomed by the UK's leading cancer charity, Cancer Research UK, at the weekend. Herbie Newell, director of translational research at the charity said that anything that speeds up the number of new treatments available and reduces their cost "must be welcomed".

Dr Helen Sang of the Roslin Institute and lead scientist on the project has been working on this for 15 years. It could still be another 15 years before drugs become available because of the long development cycle of such innovative treatments. First the patent trials have to be completed, that takes about 5 years, and then the drug development and approval takes another 10 years.

The idea is to produce the protein-based drugs in flocks of birds reared as "biofactories" much in the same way as chickens are for normal eggs. The proteins are quite straightforward to harvest from the egg-white.

Using genetically modified organisms to create drugs for treating humans is not new. Insulin for treating diabetes is produced in genetically modified bacteria. Other more complex proteins have been produced in the milk of sheep, goats, cows and rabbits. However this is the first time that birds have been used and the researchers think this method could lead to cheaper and faster drug production because of the shorter life cycle of hens and eggs.

This latest Roslin work forms part of the Avian Transgenic Project, which includes the biotechnology firms Viragen and Oxford BioMedica.

Proceedings of the National Academy of Sciences of the United States of America.

Use of biotechnology in pharmaceutical manufacturing (wikipedia)

Written by: Catharine Paddock
Writer: Medical News Today

Scripps Research Combination Therapy Obliterates New Vessel Growth In Tumors And Retinopathy

The paper is being published online in the Proceedings of the National Academy of Sciences.

"While a number of new drugs that inhibit new blood vessel growth are now available in the clinics, no one so far has been cured with available anti-angiogenic agents," said Professor Martin Friedlander, a Scripps Research scientist and retina specialist at Scripps Clinic who led the study. "Our study shows that combining anti-angiogenic agents that target multiple angiogenic pathways can significantly increase the effectiveness of such a therapeutic approach. Such combination angiostatic therapy provides a whole new range of treatment options for patients with neovascular diseases, where complete inhibition of new blood vessel growth is the desired result."

While new blood vessel growth from preexisting capillaries ("angiogenesis") is fundamental to survival, the abnormal formation of new blood vessels ("neovascularization") contributes to the pathogenesis of tumor growth and metastasis as well as the vast majority of diseases that lead to catastrophic loss of vision. A number of angiostatic molecules have been used to impair blood vessel formation as clinical adjuncts to conventional radio- and chemotherapy. Others have proven to be modestly effective in treating neovascular eye diseases.

The new study combined the actions of three classes of angiostatic compounds, each targeting different angiogenic pathways, and showed striking results in the treatment of an animal model of glioblastoma, a highly malignant brain cancer, and ischemic retinopathy, excessive blood vessel growth in the eye that is a major cause of blindness worldwide.

"Our combination therapy reduced tumor mass and increased survival in the glioblastoma model," Friedlander said. "In models of neovascular eye diseases, the therapy resulted in complete inhibition of pathological neovascularization in more than 60 percent of the eyes; over 90 percent had greater than 75 percent inhibition of new vessel growth with no adverse affects on normal tissue vasculature. In contrast, individual therapies with comparable doses of individual drugs were minimally effective, if at all."

Importantly, Friedlander notes that the use of single therapies can result in the activation of alternative compensatory pro-angiogenic pathways designed to stimulate new vessel growth, while the combination approach significantly reduced such compensatory upregulation.

"The fact that multiple angiogenic pathways are activated in response to single therapies, but not to combination treatment, supports the hypothesis that compensatory mechanisms might prevent single angiostatics from inhibiting neovascularization," he said. "These results suggest that combination therapy prevents this natural compensation, enhancing the overall anti-angiogenesis effect."

In combination, the angiostatic therapies were effective at much lower concentrations than when used as individual monotherapies. Even when diluted up to 100-fold, the triple combination inhibited angiogenesis at levels comparable to optimal doses of any single therapy. A ten-fold dilution of the triple combination demonstrated extensive neovascular inhibition with complete inhibition observed in 44 percent of the treated retinas. At these same concentrations, the angiostatic activity of each monotherapy was negligible, indicating that combining multiple angiostatic drugs was synergistic rather than additive.

The effectiveness of combination therapies at relatively low doses may be a distinct advantage in therapy, the study noted. In the elderly or diabetic patients, high levels of circulating angiostatics could precipitate stroke or heart attack due to the fact that such patients make collateral blood vessels in hearts and brains that are starved for oxygen from vascular diseases such as arteriosclerosis, hypertension, and diabetes. For these and other patients, the use of lower doses of angiostatic therapies could minimize potential adverse side effects.

"The point of the study was to show proof-of-concept that targeting multiple angiogenic pathways will be more effective than inhibiting single ones due to potential compensatory upregulation," Friedlander said. "As more and more anti-angiogenic agents reach the market, there will be even more combinations to choose from. In our laboratory, we're now looking at new combinations of approved angiostatic drugs to see if we can achieve similar promising results that can have immediate translation into the clinic."

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Other authors of the study, Combination Angiostatic Therapy Completely Inhibits Ocular and Tumor Angiogenesis, were Michael I. Dorrell, Edith Aguilar, Lea Scheppke, and Faith H. Barnett of The Scripps Research Institute. See: Proceedings of the National Academy of Sciences of the United States of America

The study was supported by the National Eye Institute, the Scripps Fonseca/Mericos Fund, the V. Kann Rasmussen and MacTel Foundations, and the Skaggs Scholars in Clinical Science.

About The Scripps Research Institute

The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations, at the forefront of basic biomedical science that seeks to comprehend the most fundamental processes of life. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune, cardiovascular, and infectious diseases, and synthetic vaccine development. Established in its current configuration in 1961, it employs approximately 3,000 scientists, postdoctoral fellows, scientific and other technicians, doctoral degree graduate students, and administrative and technical support personnel. Scripps Research is headquartered in La Jolla, California. It also includes Scripps Florida, whose researchers focus on basic biomedical science, drug discovery, and technology development. Currently operating from temporary facilities in Jupiter, Scripps Florida will move to its permanent campus in 2009.

Contact: Marisela Chevez
Scripps Research Institute

Poniard Pharmaceuticals And The Scripps Research Institute Broaden Research Collaboration

The expanded collaboration will include the discovery of focal adhesion kinase (FAK) inhibitors to treat cancer and will be co-led by David Schlaepfer, Ph.D., associate professor in the Department of Immunology at The Scripps Research Institute in La Jolla, Calif., and Chris Liang, Ph.D., director of medicinal chemistry at Scripps Florida.

Poniard and Scripps' initial scientific collaboration represented the first major biotech collaboration for Scripps Florida, a division of The Scripps Research Institute in Palm Beach County. In addition to FAK inhibitors, the research initiative is focusing on discovering novel, small-molecule protein kinase inhibitors as therapeutic agents, including cancer treatments.

"We are pleased to have negotiated this broadened research collaboration with The Scripps Research Institute under the terms of our existing agreement, which enables us to access scientific expertise at both the Scripps La Jolla and Palm Beach County sites," said Jerry McMahon, Ph.D., chairman, president and CEO of Poniard. "Dr. Schlaepfer is an international expert in the study of FAK, and we believe that he will be an invaluable resource in our drug discovery efforts on this exciting and promising new cancer target."

Dr. Schlaepfer's research at Scripps focuses on molecular signaling that regulates cell motility and invasion. During cancer progression, tumor cells can acquire a highly motile and invasive phenotype. These properties directly promote tumor spread and metastasis. As FAK is commonly overexpressed in malignant human tumors, Dr. Schlaepfer is employing multiple strategies to inhibit FAK activity within tumor cells. He is the author of several papers on this topic, including those published in the Journal of Cell Biology, Cancer Research, Nature Cell Biology and Oncogene.

"FAK is associated with the invasion and metastasis of tumor cells and has recently been implicated in chemoresistance," added Dr. McMahon. "It is possible that inhibitors of FAK may enhance the activity of picoplatin in the treatment of solid tumors. We are looking forward to collaborating with Dr. Schlaepfer on this critical research."

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About The Scripps Research Institute

The Scripps Research Institute is one of the world's largest independent, non-profit biomedical research organizations, at the forefront of basic biomedical science that seeks to comprehend the most fundamental processes of life. Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune, cardiovascular, and infectious diseases, and synthetic vaccine development. Established in its current configuration in 1961, it employs approximately 3,000 scientists, postdoctoral fellows, scientific and other technicians, doctoral degree graduate students, and administrative and technical support personnel. Scripps Research is headquartered in La Jolla, California. It also includes Scripps Florida, whose researchers focus on basic biomedical science, drug discovery, and technology development. Currently operating from temporary facilities in Jupiter, Scripps Florida will move to its permanent campus in 2009.

About Poniard Pharmaceuticals

Poniard Pharmaceuticals, Inc. is a specialty pharmaceutical company focused on the discovery, development and commercialization of innovative oncology products to impact the lives of people with cancer. Picoplatin, the Company's lead product candidate, is a new generation platinum therapy with an improved safety profile. An intravenous chemotherapeutic agent, it is designed to overcome and prevent platinum resistance associated with chemotherapy in solid tumors. Picoplatin is currently being studied in clinical trials for the treatment of small cell lung, colorectal and hormone-refractory prostate cancers. As part of the Company's strategic goal of building a diverse oncology pipeline, the Company is collaborating with The Scripps Research Institute on the discovery of novel, small-molecule, multi-targeted protein kinase inhibitors and focal adhesion kinase (FAK) inhibitors. For additional information please visit http://www.poniard.com/.

This release contains forward-looking statements, including statements regarding the Company's business model, drug development program and strategic collaborations and goals. The Company's actual results may differ materially from those indicated in these forward looking statements based on a number of factors, including anticipated operating losses, uncertainties associated with research, development, clinical trials, the results of later clinical testing and related regulatory approvals, future capital needs and uncertainty of additional financing, competition, uncertainties associated with intellectual property, dependence on third-party manufacturers, suppliers and collaborators, lack of sales and marketing experience, loss of key personnel, uncertainties associated with market acceptance, technology change and government regulation, general market conditions and the other risks and uncertainties described in the Company's current and periodic reports filed with the Securities and Exchange Commission, including the Company's Annual Report on Form 10-K for the year ended December 31, 2005, and its Quarterly Report on Form 10-Q for the quarter ended September 30, 2006. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this release. The Company undertakes no obligation to update any forward-looking statement to reflect new information, events or circumstances after the date of this release or to reflect the occurrence of unanticipated events.

© 2007 Poniard Pharmaceuticals, Inc. All Rights Reserved.

Poniard and Poniard Pharmaceuticals are trademarks of Poniard Pharmaceuticals, Inc.

For Further Information:

Poniard Pharmaceuticals

Julie Rathbun
Corporate Communications

Contact: Keith McKeown
Scripps Research Institute

Washington, D.C., Bill Requiring HPV Vaccine Would Save 'Thousands' Of Women's Lives, Editorial Says

"Emotion and ignorance shouldn't thwart" a Washington, D.C., City Council bill that would require girls entering the sixth grade to receive Merck's human papillomavirus vaccine Gardasil and would "save the lives of thousands of women," a Washington Post editorial says (Washington Post, 1/11). Gardasil in clinical trials has been shown to be 100% effective in preventing infection with HPV strains 16 and 18, which together cause about 70% of cervical cancer cases. FDA in July 2006 approved the vaccine for sale and marketing to girls and women ages nine to 26, and CDC's Advisory Committee on Immunization Practices later that month voted unanimously to recommend that girls ages 11 and 12 receive the vaccine. According to the legislation, sponsored by City Council Members Mary Cheh (D) and independent David Catania, female students would be required to show proof of vaccination before enrolling in the sixth grade in District of Columbia Public Schools, unless their parent or legal guardian chose to "opt out" of the requirement. The bill does not specify the circumstances under which girls would be allowed an exemption (Kaiser Daily Women's Health Policy Report, 1/10). According to the editorial, the bill gives parents the "right" to "have a say in the health management" of their children and "would mandate that parents get the data needed to make informed choices." Opposition to the measure because of "the misguided belief that the virus doesn't pose the same kind of threat to the public as other transmissible pathogens" or the belief that "receiving the vaccine will encourage promiscuity" do not "square with the fact[s]," the Post says. "If common sense wins out here, the [d]istrict will lead the nation in an important area of public health -- and will save some lives," the editorial concludes (Washington Post, 1/11).

Related Opinion Piece
If you have a daughter entering the sixth grade of a public school in the district next year, "your daughter is 11 and probably black, so the assumption" made by the bill is "she'll be having unprotected sex in no time -- but don't take offense," Washington Post columnist Courtland Milloy writes in an opinion piece. According to Milloy, Catania and Cheh, who he calls "two nice white people," proposed a program to vaccinate "girls under 13 in a predominantly black school system" against HPV. "After all, if the girls' parents can't protect them -- and, God knows, they can't protect themselves -- then somebody's got to do it." Milloy writes, "Forget about taking time to educate the public about HPV or exploring any adverse side effects of the vaccination. ... And please don't bring up that old paranoia about government agencies conducting medical experiments on black people. ... That practice was found to be unconstitutional -- eventually." He adds, "Let's just go right at these presumed-to-be promiscuous, 11-year-old black girls" (Milloy, Washington Post, 1/10).

"Reprinted with permission from http://www.kaisernetwork.org. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at http://www.kaisernetwork.org/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork.org, a free service of The Henry J. Kaiser Family Foundation . © 2005 Advisory Board Company and Kaiser Family Foundation. All rights reserved.

Bayer And Onyx Announce Pivotal Nexavar Kidney Cancer Study Published In NEJM

Bayer Pharmaceuticals Corporation (NYSE: BAY) and Onyx Pharmaceuticals, Inc. (Nasdaq: ONXX) has announced that the New England Journal of Medicine has published their pivotal Phase III trial demonstrating that Nexavar® (sorafenib) tablets doubled median progression-free survival (PFS) in patients with advanced renal cell carcinoma (RCC), or kidney cancer. The data, as assessed by independent radiologic review, are from the Treatment Approaches in Renal Cancer Global Evaluation Trial (TARGET) - the largest randomized controlled trial ever conducted in advanced RCC.

"Historically, patients with kidney cancer have had limited treatment options and there has been a particularly critical need for new therapies to help patients with advanced disease," said co-principal investigator Ronald Bukowski, M.D., Director of the Experimental Therapeutics Program of The Cleveland Clinic Taussig Cancer Center in Cleveland, OH. "This landmark study demonstrated the efficacy, tolerability and clinical benefit of Nexavar, which has rapidly become a valuable weapon against this devastating disease."

Based on these data, Nexavar was granted U.S. Food and Drug Administration (FDA) approval for the treatment of patients with advanced RCC, or kidney cancer, on December 20, 2005. Since then, Nexavar has been approved in nearly 50 countries.

"Nexavar was the first new drug approved for patients with advanced kidney cancer in over a decade," said Bill Bro, President and Chief Executive Officer of the Kidney Cancer Association (KCA). "With the advent of targeted therapies such as Nexavar, there has been remarkable change - patients are experiencing improved outcomes without the toxic effects traditionally associated with chemotherapy."

Phase III Summary

More than 900 patients with advanced RCC were randomized one-to-one to receive either 400 mg Nexavar or placebo orally twice a day in this randomized, multi-national, placebo-controlled Phase III study. The endpoints of the study are overall survival (OS), PFS, overall response rate and safety. PFS measures the length of time that a patient lives without evident tumor growth or death.

PFS doubled to a median of 5.5 months in patients receiving Nexavar compared to 2.8 months for patients receiving placebo (p < 0.001). This represented a 56% reduction in the risk of progression (hazard ratio 0.44; 95% CI, 0.35 to 0.55) for patients on Nexavar versus placebo. All patient subgroups examined benefited regardless of performance status or risk group, including patients who had not received conventional treatment with biologics, such as interleukin-2 or interferon-alpha.

In May 2005, due to the clinical and statistical significance of the PFS data, the companies unblinded the trial and announced that patients who were receiving placebo were allowed to "cross over" to drug treatment. The first OS analysis conducted immediately before cross-over found a 39% improvement in OS for Nexavar patients (hazard ratio 0.72, p=0.018). A further OS analysis performed six months following cross over was based on 367 survival events (patient deaths) that had occurred by November 30, 2005. Results showed a continued trend toward improved survival, with a 23% reduction in the risk of death (19.3 months for Nexavar patients versus 15.9 months for placebo patients; hazard ratio 0.77, p=0.02), despite the fact that nearly half of placebo patients had "crossed over" to Nexavar. Patients continue to be followed and a final survival analysis will be available in the first half of 2007. The Phase III data published in NEJM have previously been communicated at international scientific congresses.

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About Nexavar

Nexavar is an oral multi-kinase inhibitor that targets both the tumor cell and tumor vasculature. In preclinical models, Nexavar targeted members of two classes of kinases known to be involved in both cell proliferation (growth) and angiogenesis (blood supply) - two important processes that enable cancer growth. These kinases included RAF kinase, VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-B, KIT, FLT-3 and RET.

Nexavar is currently approved in nearly 50 countries, including the United States and in the European Union, for the treatment of patients with advanced kidney cancer. In addition, Nexavar is being evaluated by the companies, international study groups, government agencies or individual investigators as a single agent or combination treatment in a wide range of cancers, including adjuvant RCC, advanced liver cancer, metastatic melanoma, non-small cell lung cancer and breast cancer.

About Kidney Cancer

Renal cell carcinoma is the most common form of kidney cancer. Nearly 208,000 people worldwide are diagnosed (about 37,000 Americans) with renal cell carcinoma each year and more than 102,000 of them die (about 12,000 Americans) from the disease annually. For more information on renal cell carcinoma, visit the Kidney Cancer Association (KCA) web site at: http://www.curekidneycancer.org/.

Important Safety Considerations for U.S. Patients Taking Nexavar

Based on the currently approved package insert for the treatment of patients with advanced kidney cancer, hypertension may occur early in the course of therapy and blood pressure should be monitored weekly during the first six weeks of therapy and treated as needed. Incidence of bleeding regardless of causality was 15% for Nexavar vs. 8% for placebo and the incidence of treatment-emergent cardiac ischemia/infarction was 2.9% for Nexavar vs. 0.4% for placebo. Most common treatment-emergent adverse events with Nexavar were diarrhea, rash/desquamation, fatigue, hand-foot skin reaction, alopecia, and nausea. Grade 3/4 adverse events were 38% for Nexavar vs. 28% for placebo. Women of child-bearing potential should be advised to avoid becoming pregnant and advised against breast-feeding. In cases of any severe or persistent side effects, temporary treatment interruption, dose modification or permanent discontinuation should be considered.

For U.S. Nexavar prescribing information, visit http://www.nexavar.com/.

About Onyx Pharmaceuticals, Inc.

Onyx Pharmaceuticals, Inc. is engaged in the development of novel cancer therapies that target the molecular basis of cancer. With its collaborators, the company is developing small molecule drugs, including Nexavar with Bayer Pharmaceuticals Corporation. For more information about Onyx's pipeline and activities, visit the company's web site at: http://www.onyx-pharm.com/.

About Bayer Pharmaceuticals Corporation

Bayer Pharmaceuticals Corporation (http://www.bayerpharma.com/) is part of the worldwide operations of Bayer HealthCare AG, a subsidiary of Bayer AG. Bayer HealthCare is one of the world's leading, innovative companies in the healthcare and medical products industry and is based in Leverkusen, Germany. Bayer HealthCare generated sales amounting to some 9.4 billion euros and employed 33,800 people worldwide in 2005.

The company combines the global activities of the Animal Health, Consumer Care, Diabetes Care, and Pharmaceuticals divisions. The new Pharmaceuticals division was established on January 1, 2006, and comprises the former Biological Products and Pharmaceutical divisions. Bayer HealthCare Pharmaceuticals now has three business units: Hematology/Cardiology, Oncology and Primary Care.

Bayer HealthCare's aim is to discover and manufacture products that will improve human and animal health worldwide. The products enhance well-being and quality of life by diagnosing, preventing and treating diseases.

Forward Looking Statements

This news release contains forward-looking statements based on current assumptions and forecasts made by Bayer Group management. Various known and unknown risks, uncertainties and other factors could lead to material differences between the actual future results, financial situation, development or performance of the company and the estimates given here. These factors include those discussed in Bayer's public reports filed with the Frankfurt Stock Exchange and with the U.S. Securities and Exchange Commission (including its Form 20-F). Bayer assumes no liability whatsoever to update these forward-looking statements or to conform them to future events or developments.

This news release also contains "forward-looking statements" of Onyx within the meaning of the federal securities laws. These forward-looking statements include without limitation, statements regarding the timing, progress and results of the clinical development, regulatory processes, and commercialization efforts of Nexavar. These statements are subject to risks and uncertainties that could cause actual results and events to differ materially from those anticipated. Reference should be made to Onyx's Annual Report on Form 10-K for the year ended December 31, 2005, filed with the Securities and Exchange Commission under the heading " Risk Factors" and Onyx's Quarterly Reports on Form 10-Q for a more detailed description of such factors. Readers are cautioned not to place undue reliance on these forward-looking statements that speak only as of the date of this release. Onyx undertakes no obligation to update publicly any forward-looking statements to reflect new information, events, or circumstances after the date of this release except as required by law.

NEXAVAR® is a registered trademark of Bayer AG, Germany.

Mark Bennett
Bayer HealthCare

A New Target For The Treatment Of Breast Cancer:

The active ingredient in a drug currently being tested to treat rheumatoid arthritis might also one day serve as an effective means of treating one of the deadliest forms of breast cancer. Researchers with the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) have demonstrated that inhibiting the activity of the protease enzyme known as TACE can deprive tumor cells of a key factor needed for their proliferation. TACE is strongly present in a form of breast cancer which responds poorly to current therapies.

We have shown that inhibition of the TACE protease in breast cancer cells blocks the shedding of two critical growth factor proteins and results in an inhibition of a key signaling pathway that controls cell division," said Paraic Kenny, a post-doctoral cell biologist with the research group of Mina Bissell in Berkeley Lab's Life Sciences Division. "Based on analysis of cells grown in three-dimensional cultures, the inhibition of this protease results in the reversion of the malignant phenotype of these breast cancer cells and switches their behavior back to a phenotype very reminiscent of non-malignant breast epithelial cells."

Kenny is the co-author along with Bissell of a paper published in the Journal of Clinical Investigation entitled: Targeting TACE-Dependent EGFR-ligand Shedding in Breast Cancer. This paper presents the latest experimental results from an on-going investigation led by Bissell into the ecology of tumors.

It has long been Bissell's contention that "no tumor is an island." Tumor cells, she maintains, exist in the same microenvironment as healthy cells and must therefore appropriate normal physiological processes to facilitate their growth and spread. As she and her colleagues have repeatedly demonstrated, this idea can open up potential new avenues and targets for diagnostic and therapeutic applications.

For this latest paper, Kenny and Bissell looked into the pathway by which the EGFR signal is carried. EGFR, which stands for Epidermal Growth Factor Receptor, is the protein on the outer surface of a cell that is activated by EGF and related growth factors and signals for the cell to divide. Given that one of the hallmarks of cancer is cell division run amok, the reduction of high levels of EGFR activity has long been a primary target for anti-cancer drug development. So far, however, drugs aimed at directly inhibiting EGFR activity have met with only limited success in the cancer clinic, primarily in a small number of lung cancers.

"Because of this, we turned our attention to the processes that regulate the production of the ligands which bind and activate EGFR," Kenny said. "We reasoned that this binding and activation is essential for EGFR activation and that finding a way to block this interaction might prove to be an important additional approach to explore for inhibition of this pathway."

Earlier studies had indicated that TACE (tumor necrosis factor-alpha-converting enzyme) acts like a "molecular scissors" that releases from the cell surface a pair of ligands, called Amphiregulin and TGF-alpha, which activate EGFR. Bissell and Kenny found that by targeting TACE (also known as ADAM17) with either molecular inhibitors or short interfering RNAs (siRNAs) that silence the TACE gene, they could effectively block the shedding of Amphiregulin and TGF-alpha ligands. This resulted in the inhibition of EGFR signaling and the reversion of malignant characteristics in tumor cells. It is the first reported use of protease inhibitors to stop breast cancer cell proliferation and restore the normal breast tissue structure.

"We have designed an entirely new way of targeting EGFR signaling in breast cancer," said Kenny. "Almost all the work to date has involved the use of antibodies that stick to kinases or drugs that block kinase activities."

These newest results are very much in keeping with Bissell's contention that cancer growth and spread is not solely a tumor cell-autonomous process brought on by a genetic mutation. Bissell is one of the leading proponents of the idea that a cell's genetic information is supplemented by contextual information encoded within the microenvironment that surrounds the cell.

"It is becoming increasingly apparent that, as with other organs, the biogenesis of the tumor represents an interaction between the tumor cell, other types of cells and the rest of the microenvironment," she said.

Kenny and Bissell successfully tested their protease blocking approach on several different breast cancer cell lines. In addition, they examined the data from 295 breast cancer patients and found that tumors which produced the highest levels of TACE and the TGF-alpha ligand posed the greatest risk to women.

"Women with those types of tumors would seem to be poorly served by existing treatments and may stand to benefit from therapies that are based on the inhibition of TACE activity," said Kenny. "We would like to see some of the companies who have developed the new generation TACE inhibitors for treatment of rheumatoid arthritis also consider evaluating them in cancer patients."

Kenny stressed that the importance of EGFR to so many different tumor types, including lung, head and neck, bladder, colorectal and kidney, makes it likely that "TACE inhibition has the potential to be an effective means of stopping tumor growth for EGFR-dependent cancers outside the breast as well."

This research was supported by grants and a Distinguished Fellowship Award from the U.S. Department of Energy's Office of Biological and Environmental Research, the National Cancer Institute,and an Innovator award from the U.S. Department of Defense's Breast Cancer Research Program to Bissell, and by a Susan G. Komen Breast Cancer Foundation fellowship to Kenny.

Berkeley Lab is a U.S. Department of Energy national laboratory located in Berkeley, California. It conducts unclassified scientific research and is managed by the University of California. Visit our Website at http://www.lbl.gov/.

* For more information on the research of Mina Bissell and Paraic Kenny, please visit the Website at http://www.lbl.gov/lifesciences/BissellLab/main.html

Contact: Lynn Yarris
DOE/Lawrence Berkeley National Laboratory

YM BioSciences Provides Update On Tesmilifene Pivotal Trial

YM BioSciences Inc. (AMEX:YMI, TSX:YM, AIM:YMBA), an oncology company that identifies, develops and commercializes differentiated products for patients worldwide, today announced that the independent Data Safety Monitoring Board (DSMB) for the pivotal Phase III trial of tesmilifene in patients with metastatic or recurrent breast cancer has notified the Company that the milestone of 320 events required for the third interim analysis in its pivotal Phase III trial has occurred.

Since the last "data sweep" was completed in November 2006, the DSMB advised the Company to conduct a further data sweep to bring the survival data current prior to performing the third interim analysis. This data sweep is ongoing and the Company expects this work to be completed and to have a formal recommendation from the DSMB in February 2007. A data sweep is conducted on a periodic basis prior to each interim analysis.

"Although we are eager to learn the outcome of this third interim analysis, a meticulous review by the DSMB of any new data is entirely in keeping with the rigor of this trial," said David Allan, Chairman and CEO of YM BioSciences. "Because of the interest in this third analysis and expectations that it might occur this month, we decided to confirm that the threshold number of events has been reached. We have no additional information from this trial at this time."

The pivotal Phase III trial compares the survival of patients treated with tesmilifene combined with epirubicin/cyclophosphamide to epirubicin/cyclophosphamide alone in women with rapidly progressing metastatic and/or recurrent breast cancer. The trial, which completed enrollment of 723 patients in September 2005, is the subject of a Special Protocol Assessment and a Fast Track designation for advanced breast cancer by the FDA.

The trial is being conducted according to a sequential design that permits a number of planned interim analyses and the trial will continue until one of two specific statistical conditions is satisfied. At each analysis, the hazard ratio between the tesmilifene-containing treatment arm and the control arm is calculated and then reviewed by the DSMB. The trial may be concluded if either the tesmilifene-containing treatment arm is superior to the control by a specified margin or it is determined that such evidence is not going to be found. If the evidence is insufficient for either conclusion to be drawn, then the trial continues until the next analysis. At the first and second interim analyses, the DSMB recommended that the trial continue as planned.

About Tesmilifene

Tesmilifene is a novel, small molecule that selectively targets multiple-drug resistant (MDR) tumor cells, sensitizing them to chemotherapy. Tesmilifene may offer clinical benefit in a number of tumor types and is being tested with a variety of chemotherapeutic regimens. In addition to the current pivotal trial, a Phase III trial of tesmilifene with doxorubicin in metastatic or recurrent breast cancer has been completed and a Phase II study to evaluate tesmilifene plus docetaxel (Taxotere(R)) in patients with metastatic breast cancer is being conducted in collaboration with Sanofi-Aventis. In hormone-refractory prostate cancer (HRPC), two single-arm Phase II trials of tesmilifene in combination with chemotherapy (one with mitoxantrone plus prednisone; the other with cyclophosphamide) and a randomized Phase II trial comparing cyclophosphamide alone to cyclophosphamide plus tesmilifene have been conducted. Based on the clinical data generated from these three studies, the Company is currently evaluating additional clinical work in patients with HRPC. Clinical studies in other tumor types, including gastric and hepatic cancer, are also being planned.

About YM BioSciences

YM BioSciences Inc. is an oncology company that identifies, develops and commercializes differentiated products for patients worldwide. In addition to tesmilifene, the Company has two other late-stage products: nimotuzumab, a humanized monoclonal antibody that targets the epidermal growth factor receptor (EGFR) and is approved in several countries for treatment of various types of head and neck cancer, and is in clinical trials in numerous tumor types including glioma (pediatric and adult), pancreatic cancer, prostate cancer, non-small cell lung cancer, esophageal cancer, cervical cancer and breast cancer; and AeroLEF(TM), a unique, inhaled-delivery composition of free and liposome-encapsulated fentanyl in development for the treatment of moderate to severe pain.

This press release may contain forward-looking statements, which reflect the Company's current expectation regarding future events. These forward-looking statements involve risks and uncertainties that may cause actual results, events or developments to be materially different from any future results, events or developments expressed or implied by such forward-looking statements. Such factors include, but are not limited to, changing market conditions, the successful and timely completion of clinical studies, the establishment of corporate alliances, the impact of competitive products and pricing, new product development, uncertainties related to the regulatory approval process and other risks detailed from time to time in the Company's ongoing quarterly and annual reporting. Certain of the assumptions made in preparing forward-looking statements include but are not limited to the following: that the pivotal tesmilifene Phase III trial will be completed on schedule and yield mature data in calendar 2007; that the DSMB's recommendations to continue the pivotal trial for tesmilifene based on three planned interim analyses implies that the trial continues to have the prospect of meeting its primary endpoint; that nimotuzumab will continue to demonstrate a competitive safety profile in ongoing and future clinical trials; that YM and its various partners will complete their respective clinical trials within the timelines communicated in this release. We undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

YM BioSciences Inc.
http://www.ymbiosciences.com/

EU Red Tape Hampers International Cancer Trials

European bureaucracy has made running large clinical trials for new cancer drugs more difficult, according to a Cancer Research UK report published in the European Journal of Cancer*.

The European Union Clinical Trials Directive was intended to harmonise standards across the continent, making it easier for international groups to collaborate. But because every member state implements European laws in a slightly different way, the effect has, in fact, been to increase costs, delay trials starting, and make collaboration more difficult.

Large-scale, multinational trials are the only way to prove the effectiveness of many anticancer drugs, especially those being developed for rare diseases, because of the large numbers of patients needed.

Dr Richard Sullivan, director of clinical programmes at Cancer Research UK and co-author of the report, said: "Our research confirms concerns that the introduction of the 2004 EU Clinical Trials Directive would delay and significantly increase the cost of cancer clinical trials in the UK. Critically, the legislation has also prevented the running of co-ordinated international trials by some trials units due to uncertainty over how each country in the EU is implementing the new rules - the very situation the Directive was intended to resolve. It is essential to provide proper funding for the academic trials community. A review of how the Directive is being implemented across member states is urgently needed."

* J. Hearn, R. Sullivan, The impact of the 'Clinical Trials' directive on the cost …, Eur J Cancer(2006), doi:10.1016/j.ejca.2006.09.016. For further information click here.

About Cancer Research UK

Together with its partners and supporters, Cancer Research UK's vision is to beat cancer.

-- Cancer Research UK carries out world-class research to improve understanding of the disease and find out how to prevent, diagnose and treat different kinds of cancer.

-- Cancer Research UK ensures that its findings are used to improve the lives of all cancer patients.

-- Cancer Research UK helps people to understand cancer, the progress that is being made and the choices each person can make.

-- Cancer Research UK works in partnership with others to achieve the greatest impact in the global fight against cancer.

http://www.cancerresearchuk.org