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  • 1
    Electronic Resource
    Electronic Resource
    Absence of p16 gene (CDKN2) deletions in microdissected primary breast carcinoma specimens (1997)
    Springer
    Annals of surgical oncology 4 (1997), S. 416-420 
    Details
    ISSN: 1534-4681
    Keywords: p16 ; (CDKN2) ; MTS1 ; Breast carcinoma ; Microdissection ; Genetic alterations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: The p16 gene (CDKN2), a tumor suppressor gene located on chromosome 9p21, has been demonstrated to be mutated or deleted with high frequency in a variety of tumor cell lines, including breast. While previous studies have not demonstratedCDKN2 mutations in primary breast carcinomas, it is possible that gene deletion in neoplastic DNA was masked by the presence of contaminating normal stromal DNA in breast carcinoma specimens. Methods: We investigated the incidence of homozygous deletion ofCDKN2 by analyzing 20 microdissected pure populations of primary breast carcinoma cells. Using polymerase chain reaction (PCR) techniques, the entire coding region and intervening introns ofCDKN2 were amplified. The PCR products were resolved by agarose gel electrophoresis and single-strand conformation polymorphism (SSCP) analysis. Results: We detected no deletions or mutations of the p16 gene. Conclusions: CDKN2 is not deleted with high frequency in primary breast carcinomas, and the p16 gene does not play a role in breast carcinogenesis via this mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02305555
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  • 2
    Electronic Resource
    Electronic Resource
    Sentinel Lymph Node Biopsy: Is It Indicated in Patients With High-Risk Ductal Carcinoma-In-Situ and Ductal Carcinoma-In-Situ With Microinvasion? (2000)
    Springer
    Annals of surgical oncology 7 (2000), S. 636-642 
    Details
    ISSN: 1534-4681
    Keywords: Breast carcinoma ; Ductal carcinoma-in-situ ; Microinvasion ; Sentinel lymph node biopsy ; Intraductal carcinoma ; Micrometastases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Axillary lymph node status is the strongest prognostic indicator of survival for women with breast cancer. The purpose of this study was to determine the incidence of sentinel node metastases in patients with high-risk ductal carcinoma-in-situ (DCIS) and DCIS with microinvasion (DCISM). Methods: From November 1997 to November 1999, all patients who underwent sentinel node biopsy for high-risk DCIS (n = 76) or DCISM (n = 31) were enrolled prospectively in our database. Patients with DCIS were considered high risk and were selected for sentinel lymph node biopsy if there was concern that an invasive component would be identified in the specimen obtained during the definitive surgery. Patients underwent intraoperative mapping that used both blue dye and radionuclide. Excised sentinel nodes were serially sectioned and were examined by hematoxylin and eosin and by immunohistochemistry. Results: Of 76 patients with high-risk DCIS, 9 (12%) had positive sentinel nodes; 7 of 9 patients were positive for micrometastases only. Of 31 patients with DCISM, 3 (10%) had positive sentinel nodes; 2 of 3 were positive for micrometastases only. Six of nine patients with DCIS and three of three with DCISM and positive sentinel nodes had completion axillary dissection; one patient with DCIS had an additional positive node detected by conventional histological analysis. Conclusions: This study documents a high incidence of lymph node micrometastases as detected by sentinel node biopsy in patients with high-risk DCIS and DCISM. Although the biological significance of breast cancer micrometastases remains unclear at this time, these findings suggest that sentinel node biopsy should be considered in patients with high-risk DCIS and DCISM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s10434-000-0636-2
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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