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Department of Genetic Oncology, Institut National de la Santé et de la Recherche Médicale CRI 9703 [F. E., J. J., R. S., T. N., H. S.], Laboratory of Tumor Biology [R. S., T. N. D. B., H. S.], and Department of Pathology [J. J.], Paoli-Calmettes Institute, 13273 Marseille Cedex 9; Department of Pathology, University of Marseille "La Timone," 13385 Marseille Cedex 5 [C. C.]; Unit of Genetic Oncology, Curie Institute, 75321 Paris Cedex 05 [D. S-L.]; Departments of Clinical Biology [B. B-d. P.] and Pathology [J-M. G.], Gustave Roussy Institute, 94805 Villejuif Cedex; Laboratory of Human Molecular Oncology, Oscar Lambret Institute, 59020 Lille Cedex [J-P. P.]; Laboratory of Pathology and Molecular Oncology, Bergonié Institute, 33076 Bordeaux Cedex [M. L.]; and Institut National de la Santé et de la Recherche Médicale Unité 119, 13009 Marseille [D. B.], France
BRCA1-associated breast cancers (BRCA1-BCs) frequently harbor a high histoprognostic grade, p53 alterations, and estrogen receptor negativity. Although these parameters predict a poor outlook, the overall survival in BRCA1-BCs is equivalent to or even better than that in sporadic cases. These features are reminiscent of what is observed for breast carcinoma of the medullary type, a high-grade tumor with a particular favorable course. To explore a possible relationship between this phenotype and BRCA1 mutations, we first compared 32 BRCA1-BCs and 200 consecutive cases of breast cancer without familial history for the prevalence of typical medullary breast carcinoma (TMC) using the criteria given by Ridolfi et al. [R. Ridolfi et al., Cancer (Phila.), 40: 1365–1385, 1977]. Second, we searched for BRCA1 mutations in a set of 18 cases of TMC, using denaturing gradient gel electrophoresis and Cleavase fragment length polymorphism scanning.
Six of 32 (19%) BRCA1-BCs were of the TMC type, compared to 0 of 200 controls (P < 0.0001). Among the 18 TMCs, 2 BRCA1 nonsense mutations were found. This corresponds to almost 7 times the contribution of BRCA1 mutations in the general population. Two additional missense mutations were identified. Together, these results suggest that, although TMC and BRCA1-BCs are not strictly coincidental, an important connection between the two populations does exist.
1 This work was supported by the Paoli-Calmettes Institute, Institut National de la Santé et de la Recherche Médicale, Université de la Mediterranée, Assistance Publique Marseille (APM), and grants from La Ligue Nationale Contre le Cancer (the National Office and the District committees of Alpes de Haute Provence, Hautes Alpes, Bouches du Rhône, Corse du Sud, Haute Corse, Var), Association pour la Recherche sur le Cancer, Fédération Nationale des Centres de Lutte Contre le Cancer, and FEGEFLUC.
2 To whom requests for reprints should be addressed, at Department of Genetic Oncology, Institut National de la Santé et de la Recherche Médicale CRI 9703, Paoli-Calmettes Institute, 232 Boulevard Sainte Marguerite, 13273 Marseille Cedex 9, France. Phone: 33-491-22-35-40; Fax: 33-491-22-35-04; E-mail: sobol@marseille.inserm.fr.
Received 1/14/98. Accepted 3/ 2/98.
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