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Harvard Medical
School researchers report that a gene-activating protein may be
the factor that explains why the drug tamoxifen fights cancer
in the breast but increases the risk of cancer in the uterus.
Drs. Yongfeng
Shang and Myles brown, reporting in the journal Science, said
the presence of a protein called steroid receptor coactivator
1 (SRC-1) may be key to why tamoxifen effects some tissues differently
than others.
Tamoxifen,
widely prescribed for women who have breast cancer that is sensitive
to the effects of the hormone estrogen, is a selective estrogen
receptor modulator (SERM) that "recruits" molecules
that repress genes that promote cancer growth in breast cancer
cells, but help recruit molecules that promote cancer in uterine
cancer cells.
The explanation,
the researchers said, may lie in the fact that the SRC-1 protein
is more abundant in the uterus than in the breast.
A newer SERM,
raloxifene, works the same way as tamoxifen in breast cancer cells,
but does not recruit the cancer-promoting molecules in uterine
cancer cells.
Drs. Benita
S. Katzenellenbogen and John A. Katzenellenbogen of the University
of Illinois at Urbana-Champaign, in a related editorial, say the
understanding of how these molecules work "provides a foundation
for the development of SERMs that are optimized for breast cancer
prevention and treatment, and menopausal hormone replacement."
Other
Sources: Science
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