ISSN:
1573-7217
Keywords:
chemosensitivity pattern
;
cytogenetics
;
hormone receptors
;
human breast cancer cell line
;
oncogenes
;
tumor markers
;
ultrastructural analysis
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Two human cancer cell lines (MA 2 and MA 3) were established from pleural effusions of infiltrating ductal carcinomas of the breast.The lines were maintained in continuous monolayer culture withdoubling times of 70 (MA 2) and 78 (MA 3) hr for more than two years and possessed extensively rearranged abnormal karyotypeswith modal chromosome number of 83 (MA 2) and 81 (MA 3) and DNA index values of 1.65 and 1.77, respectively. No amplifications or rearrangements were evident in the c-myc, int-2, c-erb B2, c-Ha-ras, or hst 1 genes in MA 2 and MA 3 cell lines. The clinical histories of the patients from whom the cell lines were derived are reported and compared with the results observed inthe cell lines in vitro. The presence of CEA, CA 15-3, and MCA tumormarkers observed in the primary tumor tissues was retained by the established cell lines. While the primary tumor tissueswere ER+/PgR borderline + (MA 2) and ER−/PgR+(MA 3), the MA 2 line was ER+/PgR− and the MA 3 line remained ER−/PgR+. The MDR P-glycoprotein was not expressed either in primary tumor tissues or in the respective cell lines. High expression of cytokeratins7, 18, and 19 was evident by immunohistochemical analysis in each cell line, whereas cytokeratins 8 and 17 were poorly or not at allexpressed. The treatment history of the patients fromwhom the cell lines were derived involved CMF followed six monthslater by novantrone and cisplatin plus VP 16 (MA 2) and FEC followedfour years later by CMF (MA 3). The chemosensitivitypattern assay of the cell lines indicated that the MA 2 linewas sensitive to doxorubicin, cisplatin, and vinblastine, whereas theMA 3 line was sensitive to doxorubicin and cisplatin. The characteristics of these cell lines indicate them to be a goodexperimental model to investigate breast cancer biology and anticancerdrug response.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1005740813216
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