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Periodic
Updates
02/01/2002
For five years researchers have known that a familial
prostate cancer gene is located on chromosome 1q 24-25,
but have struggled to identify the individual gene(s) in
this region associated with increased prostate cancer
risk. In this week's issue of the journal Nature
Genetics, a broad international team of researchers,
headed by Dr Jeffery Trent from the NIH have reported that
"mutations in the gene encoding
2'-5'-oligoadenylate(2-5A)-dependent RNase L (RNASEL)
segregate in prostate cancer families that show linkage to
the HPC1." RNASEL functions to regulate cell growth
and division and has been suspected to function as a tumor
suppressor gene, encoding for a protein whose loss of
function allows cells to transform into cancer.
While hereditary prostate cancer accounts for a relatively
small percentage (less than 5%) of all cases, researchers
have long suspected that the genetic alterations in
familial forms of the disease might also be present in the
much more common sporadic cases of prostate cancer.
Providing evidence for the loss of RNASEL in sporadic
prostate cancer will be an important next step.
The investigators conclude that these findings may indeed
lead to new therapeutic approaches for prostate cancer.
Some therapies work by inhibiting functions that cause
disease by becoming overactive. In this case, the
scientific finding is the opposite: the loss of function
of tumor suppressor genes represent a loss of function
that is difficult to restore. However, a broader
understanding into the role of RNASEL in prostate cancer
may lead to other related proteins which can be
effectively inhibited to restore the function of this
suddenly interesting gene in prostate cancer biology.
Reference
Carpten J et al. Germline mutations in the
ribonuclease L gene in families showing linkage with HPC1.
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