October 28, 2005

Medical News, part II

Again, some news that is encouraging but likely to have no short term effects. But it is good news none the less!

New prostate cancer clue

Fusion of genes, also seen in other types of cancer, may lead to better screening and treatment, study says


October 28, 2005

Prostate cancer may result when two genes accidentally combine within a cell, a research finding that may point to new ways to diagnose and treat the disease.

The fusion of normally separate genes in prostate cells was observed in more than half of cancer samples in a study released today in the journal Science. The combined genes cause the overproduction of proteins that spur cells to grow out of control, according to research led by Arul Chinnaiyan, a biologist at the University of Michigan in Ann Arbor.

"There is really intriguing evidence that this particular gene fusion is the causative agent of prostate cancer," Chinnaiyan, 35, said in an interview. What causes the genes to fuse isn't known, he said.

Newly diagnosed cases of prostate cancer in U.S. men will total about 232,000 this year, and deaths from the disease will top 30,000, according to the Atlanta-based American Cancer Society.

Gene rearrangements involve the movement of a gene fragment from one segment of DNA to another, often affecting whether the gene is turned on or off. Such rearrangements previously were found in leukemia, lymphoma and soft-tissue cancers.

Tests for the presence of the fused genes in blood or urine would be "far more accurate than current screening tests," according to Chinnaiyan. Doctors now test men for prostate- specific antigen, a substance released by the prostate gland.

PSA tests often are positive even when cancer isn't present, so biopsies are needed to confirm cancer. Better tests would reduce the need for biopsies.

Knowing that gene mutations can cause prostate cancer also gives drug companies targets at which to aim new medicines. The discovery that gene fusion is at the heart of chronic myelogenous leukemia, a disorder known as CML in which the body produces cancerous white blood cells, led to the development of a Novartis drug called Gleevec.

In the new study, the researchers found "overexpression" of two proteins in 95 of 167 cancer cases, and in none of 54 tissue samples with no cancer. Two genes involved, ETV1 and ERG, previously were implicated in cancer-causing genetic rearrangements in a rare bone cancer called Ewing's sarcoma, according to the National Cancer Institute in Bethesda, Md.

The gene fusion in prostate cancer "is likely to be the most common rearrangement yet identified in human malignancies," including the majority of prostate cancer cases, the researchers said in the journal.

Other gene fusions not yet identified may account for the remaining cases of prostate cancer, Chinnaiyan said.

The study provided the first evidence that "non-random, recurrent" genetic rearrangements can occur in cancers derived from so-called epithelial cells, which line the body's cavities, the National Cancer Institute said. Unlike the random scrambling of genes seen in some tumor cells, prostate cancer appears to involve a recurrent pattern that can be used to predict the disease.

Epithelial-cell diseases include breast, lung and colon cancers, Jacob Kagan, a program director at the National Cancer Institute, said in a statement today. The institute, part of the U.S. National Institutes of Health, was among sponsors of the study.

New drugs might be aimed at inactivating ERG or ETV1 or at inhibiting their expression in the first place, Chinnaiyan said. The study results must be verified in a larger number of tissue samples before new detection techniques or therapies can be developed, the National Cancer Institute said.
Copyright 2005 Newsday Inc.

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