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  Her2 Immunotherapy For Prostate Cancer Looks Promising
May 16, 1999 A new technique that links immune cells to Her2-positive prostate cancer cells shows the first documented responses to immunotherapy in prostate cancer. Her2 is a protein that tells cells to divide, making the cancer particularly aggressive and unresponsive to hormone therapy. Some prostate cancer cells produce too much Her2.
     Dr. Nicholas James and his team at the University of Birmingham, England, designed a trial to test whether two different therapies can work together to rev up a patient's immune system so as to destroy Her2-positive prostate cancer cells. Patients were given a Her2 antibody intravenously as well as subcutaneous injections of a drug called GM-CSF (granulocyte-macrophage colony-stimulating factor). GM-CSF is a growth factor that boosts the body's production of immune system cells. The antibody was designed to attach to the Her2-positive cancer and also to the immune cells, which could then kill the cancer cells.
     Dr. James has tested versions of the therapy with 111 patient participants in two separate trials. This study reports only on 25 patients, those who have taken the drug for the longest period of time in the second trial. In 70 percent of patients who showed a response, either the PSA level fell or its rise slowed down. One-third of the patients reported less pain. Patients also reported very little toxicity, according to James. This is an initial step in a strategy which, as a result of this study, will undergo further examination.

Replacing P53 Gene in Prostate Cancer Helps Shrink Tumors
May 16, 1999 Dr. Christopher Logothetis and his team of investigators at M.D. Anderson Cancer Center in Texas have demonstrated evidence that replacing the p53 gene may shrink prostate cancers.
     Normally, the p53 gene performs the task of triggering damaged cells go into apoptosis, or "programmed cell death." But as cancer progresses and spreads, the gene loses the power to do this.
     Logothetis was testing to find out if replacing p53 in a prostate cancer patient would increase production of its normal protein, and restore the process of cancer cell death. This could reduce the size of prostate tumors, Logothetis said. This strategy, Logthetis said, has been shown to be feasible in other cancer types, such as lung and head and neck cancer.
     The gene was delivered by injection into the prostate, and the patients had a prostatectomy (removal of the prostate gland) performed following therapy. The investigators were able to demonstrate on serial examination before the prostatectomy that seven of the 26 treated cancers reduced in size.
     Thirty patients in all are being treated, but some have not completed the therapy schedule. Logothetis and his research colleagues view the results of the study as encouraging evidence in support of the original hypothesis. He says these findings will serve as the foundation for combination therapy incorporating p53 gene therapy in the treatment of prostate cancer.

 
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May 16, 1999
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