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1360
CANCER October 1, 1997 / Volume 80 / Number 7
10. Hoang JM, Cottu PH, Thuille B, Salmon RJ, Thomas G, Hamelin
R. BAT-26 an indicator of the replication error phenotype in
colorectal cancers and cell lines. Cancer Res 1997;15:300–3.
4.
Raquel Seruca, M.D.
Institute of Molecular Pathology and Immunology of
the University of Porto (IPATIMUP)
Porto, Portugal
Manuel Sobrinho-Simões, M.D.
Institute of Molecular Pathology and Immunology of
the University of Porto (IPATIMUP)
Department of Pathology
Medical Faculty
University of Porto
Porto, Portugal
Author Reply
W
e welcome the correspondence from Dr. Seruca
and Dr. Sobrinho-Simões confirming our observation of a paucity of microsatellite instability in young
patients with gastric adenocarcinoma.1 We recently
studied gastric adenocarcinomas in 17 more young
patients younger than 40 years from Braga, Portugal
(unpublished data). A mutator phenotype suggestive
of the hereditary nonpolyposis colorectal carcinoma
syndrome2 was found in only one case (6%). However,
low level microsatellite instability occurring in less
than 29% of markers analyzed3 was detected in 6 more
cases (35%). Although the significance of low frequency microsatellite instability is as yet undetermined, there may be subtle differences in the molecular pathology of gastric carcinoma occurring in young
patients from relatively high and low risk populations
that require exploration. The data reported so far suggest that the prevalence of a hereditary nonpolyposis
colorectal carcinoma – associated mutator phenotype
is lower in early onset gastric carcinoma than in early
onset colorectal carcinoma.4 It remains to be determined whether or not the few early onset gastric carcinomas with a mutator phenotype harbor underlying
DNA mismatch repair gene mutations.
REFERENCES
1.
2.
3.
Hayden JD, Cawkwell L, Sue-Ling H, Johnston D, Dixon MF,
Quirke P, et al. Assessment of microsatellite alterations in
young patients with gastric adenocarcinoma. Cancer 1997;
79:684–7.
Aaltonen LA, Peltomäki P, Leach FS, Sistonen P, Pylkkanen
L, Mecklin J-P, et al. Clues to the pathogenesis of familial
colorectal cancer. Science 1993;260:812–6.
Gleeson CM, Sloan JM, McGuigan JA, Ritchie AJ, Weber JL,
Russell SEH. Widespread microsatellite instability occurs in-
/ 7b71$$1349
09-10-97 13:20:26
cana
frequently in adenocarcinoma of the gastric cardia. Oncogene 1996;12:1653–62.
Liu B, Farrington SM, Petersen GM, Hamilton SR, Parsons
R, Vogelstein B, et al. Genetic instability occurs in the majority of young patients with colorectal cancer. Nat Med
1995;1:348–52.
Jeremy D. Hayden, B.Sc., M.B., Ch.B.
Iain G. Martin, M.D., F.R.C.S.
Division of Surgery and Molecular Oncology
University of Leeds
Leeds, United Kingdom
Association of Stein–Leventhal
Syndrome with the Incidence of
Postmenopausal Breast Carcinoma
in a Large Prospective Study of
Women in Iowa
A
recent article by Anderson et al.1 published in Cancer reported the results from a cohort study including 472 women with a history of Stein – Leventhal syndrome (SLS). No association emerged between SLS
and risk of breast carcinoma (14 cases overall).
SLS is characterized by menstrual irregularities,
infertility, a high level of androgens, and obesity,
which are clinical and hormonal conditions associated
with the risk of breast carcinoma. Other studies have
shown inconsistent data regarding the association between SLS and the risk of breast carcinoma.2,3 Thus,
it is also important to examine further the issue in
consideration of the recent hypothesis of an association between SLS and insulin resistance and hyperinsulinemia4 (i.e., possible risk factors for breast carcinoma). Therefore, we analyzed data from a large case –
control study on breast carcinoma conducted between
June 1991 and February 1994 in six Italian areas: the
provinces of Pordenone and Gorizia, the urban areas
of Milan and Genoa, the province of Forlı̀ in northern
Italy, the province of Latina near Rome in central Italy,
and the urban area of Naples in southern Italy. Study
methods have been described previously.5,6
The cases studied were 2569 women (median age
55 years; range, 23 – 74 years) with incident (i.e., diagnosed within 1 year before the interview), histologically confirmed breast carcinoma who were admitted
to the major teaching and general hospitals in the
areas under surveillance. The controls were 2588
women (median age, 56 years; range, 20 – 74 years)
who were admitted for acute conditions (22% for traumas, 33% for other orthopedic disorders, 16% for acute
W: Cancer
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