"...one of the commonest cancers in men has the potential to be corrected without using typical gene therapy."
Nearly 90 percent of prostate cancers -- "the typical, garden varieties," according to Johns Hopkins scientists -- are linked to a previously unsuspected but common genetic process that could be reversible. The process looks to be a fundamental one in cancer and appears in other common forms of the disease, like breast cancer.
Unlike cancers due to mutations that make structural changes in a gene, such as the colon cancers that run in families, most prostate cancer may involve a process called "gene switching," the researchers say. Switching occurs when certain members of a family of genes are switched on while others in the family shut down. "It's a process common during embryonic development," says molecular pathologist Shrihari S. Kadkol, M.D., Ph.D., one of the researchers in a study appearing today in Nature Medicine, "but we believe this is the first time anyone's definitively linked gene switching within a family of genes, with cancer."
"Most important is that someday, it's likely we can reverse switching with drugs," says molecular pathologist Gary R. Pasternack, M.D., Ph.D., who led the Hopkins research team. "This means one of the commonest cancers in men has the potential of being corrected without using typical gene therapy."
In their work, the scientists used molecular probes to highlight and
compare the gene activity in cancer patients' normal prostate tissue with that
of their tumors. The investigators found clear evidence that a gene called pp32
was switched on in normal cells but generally switched off in cancer cells.
Earlier studies by the team showed pp32 acts as a suppressor and keeps cells
from turning malignant. Yet close relatives of the gene, to theresearchers' surprise,
act like pp32's genetic evil twins and encourage tumor growth. The pp32r1 and pp32r2
genes are present and turned on
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Contact: Marjorie Centofanti
mcentofanti@jhmi.edu
410-955-8725
Johns Hopkins Medical Institutions
2-Mar-1999