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Genetic alterations in ductal carcinoma in situ and invasive carcinoma of the breast

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Several histological classifications propose a subdivision of ductal carcinoma in situ (DCIS) into well-, intermediately, and poorly differentiated subtypes. The use of biological parameters (extent of immunopositivity, proliferation rate, and aneuploidy) facilitates such subdivision. Moreover, determination of genetic alterations can contribute to the identification of the different DCIS subtypes. Our recent data indicate that inactivation of an unidentified tumor suppressor gene on chromosome 16q is involved in the development of most well and intermediately differentiated DCIS. Moreover, amplification and inactivation of various genes on chromosome 17 are implicated in the development of poorly differentiated DCIS. These data show that there is a genetic basis for the classification of DCIS in a well and poorly differentiated type, and support the evidence of independent genetic routes to develop a specific type of carcinoma in situ of the breast.

Our study has revealed that the spectrum of genetic alterations in the in situ tumors is comparable to that of the invasive carcinomas. However, the frequencies of the individual genetic alterations differ significantly between the two tumor categories. As most invasive carcinomas also contain an in situ component, we want to compare the genetic alterations in both components of the same tumor and, in this way, identify the genetic alterations that are involved in the progression from the in situ to the invasive stage. We have microdissected the invasive and adjacent in situ component of paraffin-embedded invasive breast carcinomas with a relatively large in situ component, isolated DNA, and performed comparative genomic hybridization (CGH).

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Robanus-Maandag, E., Bosch, C., Vos, C. et al. Genetic alterations in ductal carcinoma in situ and invasive carcinoma of the breast. Breast Cancer Res 2 (Suppl 1), P8.07 (2000).

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