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The CancerWeb Report, What's New In Cancer
Cancer Genes: October 1995
Last modified on:
Tuesday, April 20, 1999 12:03:10
Copyright © 1994-2008, Information Ventures, Inc.
DD96, a novel cancer gene -
Successive genetic alterations represent critical steps in the
development of cancer. However, distinguishing which alterations
are critical for making a cell cancerous is difficult since the
cancer cell genome is very flexible, exhibiting increasing
numbers of alterations as the disease progresses. To date,
alterations in the ras oncogene and the p53 tumor suppressor gene
are the best candidates for a critical role. A report in the
October, 1995 issue of Clinical Cancer Research by a group at the Beth
Israel Hospital in Boston describes a novel gene, DD96, isolated
from renal cell carcinoma, which may turn out to be a another
widespread cancer gene. Only rarely expressed in certain normal
epithelial cells, such as those lining parts of the kidney
tubules, but not in those of the breast, bladder or skin, it was
detected in carcinomas of the breast, colon, kidney, and lung.
It is also expressed in breast ductal epithelial cell lines that
have been immortalized (halfway to a true cancer state in that
they can divide indefinitely), and in premaligant conditions such
as adenoma of the colon and ductal carcinoma in situ (DCIS) of
the breast. The gene encodes for a protein of molecular weight
about 13,500 whose function is not known.
A mutation predisposing to breast, colon, ovarian and prostate
cancers - A study that received major news media attention was published in
the October, 1995 issue of Nature Genetics. It described an
approximately 1% incidence of a mutation (called 185delAG) of the
BRCA 1 gene in 858 DNA samples from Ashkenazi Jews, but no such
mutation in 815 samples from controls who were not selected for
ethnic origin. The mutation may predispose these men and women
of Eastern European origin to breast, colon, ovarian and prostate
cancers. However, mutations in BRCA 1 have only been studied and
clearly related to cancer in families with a history of high
cancer rates. For this reason it is not known whether mutated
BRCA 1 alone is sufficient to cause cancer, or whether other
factors present in the particular families at risk, but not in
the general population, are necessary. While it is certainly
premature to talk of screening for this particular mutation, the
high-profile study has served to highlight potential problems
associated with screening for genetic changes with possible
adverse health implications. Information of this sort could be
used to make critical decisions on matters of wide social and
economic impact, including life and medical insurance, credit
rating, and employment. This issue is only likely to grow in
significance as more genes, both cancer- and non-cancer-related,
are identified.
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