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Clinical Trial News
Novel Therapy for Myelofibrosis
Myelofibrosis is an incurable blood disease characterized by symptoms related to lack of blood production and enlarged internal organs, especially the liver and spleen. Its hallmark is scarring (fibrosis) of the bone marrow (myelo-), hence the name “myelofibrosis”. As the disease progresses the marrow becomes obliterated by fibrosis seriously impairing its ability to produce blood. Paradoxically marrow elements appear in the liver and spleen, both of which enlarge greatly. The spleen may become especially massive compressing the stomach impairing eating, and also causing abdominal pain. The average survival of high risk cases is only 5-8 years, and there are no approved therapies. Surgical removal of the enlarged spleen is very problematic, and the disease can transform into acute leukemia in 5-20% of patients. Obviously, some sort of treatment besides supportive care is urgently needed.
A very exciting research development occurred in 2005. Four independent research groups almost simultaneously discovered a main molecular abnormality in myelofibrosis and two other closely related diseases, polycythemia vera and essential thrombocythemia. The same genetic mutation was found in all three conditions, providing confirmatory evidence that these diseases not only were related, but also may have the same fundamental genetic cause. This mutation was discovered in a gene called JAK2, which controls the production of a cell enzyme known as JAK kinase, important in regulating bone marrow and blood production. When the JAK2 gene is altered (mutated), it causes JAK kinase to be activated all the time sending unregulated signals to DNA, and promoting abnormal growth of bone marrow elements.
Abiraterone Acetate for Prostate Cancer
Most cases of prostate cancer are usually curable by surgery or radiation therapy. A small percentage of patients have recurrences after primary therapy, or are incurable from the beginning. In either of these situations tumor growth may vary from slow to intermediate to aggressive. Testosterone initially fuels this growth; therefore, standard treatment is to remove the main source of testosterone production by means of either medical or surgical treatment. This procedure very frequently halts the tumor’s progress, sometimes quite dramatically. Eventually, despite an initial favorable response and low levels of testosterone, cancer begins to grow again. This situation has been called “hormone-resistant prostate cancer”. One reason for relapse after castration is that too much residual testosterone remains in the body because the adrenal glands and the cancer itself may continue to produce hormones in small but significant amounts. In addition, the tumor also may develop increased numbers of hormone receptor proteins, which function to send more growth signals.
Hormone-resistant prostate cancer is an advanced stage of the disease with a three year survival potential of only 20%. Obviously, if there were some way to block residual hormone production it might be possible to create a total, or near total absence of testosterone. Although a drug that blocks hormone production has been available for years, it has many side effects and a low response rate. A new agent that blocks male hormone production, abiraterone acetate, was discovered at the Institute of Cancer Research in London, and the first reported Phase I study in 2007 seemed very promising. Further trials showed it to be more potent and less toxic than the previous alternative. Phase II trials showed a significant decline in the tumor marker PSA as well as tumor shrinkage in about half the treated patients. A large phase III trial of patients previously treated with chemotherapy proved that abiraterone acetate produced significantly longer responses and a 36% increase in median survival as compared to a placebo.
Clinical Trials for Cancer Patients-March 2011
Dear Colleagues:
We wish to make you aware of some selected clinical trials we offer at Tower Cancer Research Foundation (TCRF), which I believe to be especially interesting and important. Our Foundation, an independent non-profit clinical trials unit, has continued to grow. Besides a complete portfolio of clinical trials, you can find a full description of all Foundation activities, our staff, and also educational publications on our website at www.towercancerfoundation.org.
We invite you to contact us by phone or email to discuss potential patients you may wish to consider for the trials outlined below. We can be reached at 310-205-5707 or by e-mail. Marie Fuerst RN,MS, our Director of Clinical Research Operations, also can be reached at 310-285-7269 or by e-mail. We look forward to collaborate with you.
Aurora Kinase Inhibitor
Virtually all cells in the body divide and reproduce by a complex process known as mitosis. At first, DNA-containing chromosomes duplicate themselves into two identical copies. Then part of the cell structure known as microtubules form a spindle-like array displayed in a fiber-like configuration. These microtubules attach to the duplicated chromosomes and function to pull the chromosomes apart toward opposing poles of the cell. The spindle breaks down, and the cell membrane pinches off along the equator of the mother cell creating two identical daughter cells. (See illustration).