92 Chromosomal aberration patterns of mammary carcinoma cells in vivo and in vitro

92 Chromosomal aberration patterns of mammary carcinoma cells in vivo and in vitro

Abstracts 18 7 9 9 " CHROMOSOMAL ABERRATION PATTERNS OF MAMMARY CARCINOMA CELLS IN VIVO AND IN VITRO. Fritz H61zel and Regina Kunzmann. Departments ...

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Abstracts

18 7

9 9 " CHROMOSOMAL ABERRATION PATTERNS OF MAMMARY CARCINOMA CELLS IN VIVO AND IN VITRO. Fritz H61zel and Regina Kunzmann. Departments of Physiol. Chemistry and Obstet./Gynecol., University of Hamburg-Eppendorf, F.R.G. In advanced mammary cancer multiple chromosomal abnormalities have been described, which are due to clonal evolution of the tumor cell populations. At present, specific structural aberrations indicative of mammary carcinoma have not been generally accepted. Cytogenetic analyses show aberration patterns characteristic of the tumor cell populations derived from individual patients, which are useful for the identification of established cell lines. Alterations of the chromosomal aberration patterns may occur in rive and during extended in vitro cultivation. In this investigation, the chromosomal aberrations of cells derived from three different explants obtained from the same patient were explored by G-banding analyses, and by Cbanding for the identification of markers with complex chromosomal rearrangements. The markers were compared with the chromosomal aberration patterns found after long-term in vitro cultivation. The karyotype of cells derived from the 2nd and 3rd explant contained multiple alterations which had occurred in vivo. The results show that some of the marker chromosomes were based on stable rearrangements, whereas other markers were subject to further structural alteration giving rise to deviated patterns of chromosomal aberrations. The study allowed us to monitor the evolution of the chromosomal aberration patterns exemplifying the instability of the genome of human mammary carcinoma cells.

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CYTOGENETIC ANALYSIS OF FIVE HUMAN BREAST CARCINOMAS. C. L6pez-Gin6s, R. Gil, R. Noguera, M. Gregori, A. Pellin, and A. Llombart-Bosch. Department of Pathology, University of Valencia, 46010 Valencia, Spain.

Tissues from 5 breast tumors have been processed for chromosome analysis by the direct method and by short term culture. Four of the tumors were classified as infiltrating ductal carcinomas and one as medullary carcinoma. Four of the cases were derived from primary tumors, and one from biopsies of histopathologically positive lymph nodes. The cytogenetic results were obtained by the direct method and analyzed using trypsin G.banding method. In the medullary carcinoma 66 metaphases were counted, six of them with a normal karyotype. The tumor presented a modal number of 41 chromosomes and 9 structural rearrangements. In the infiltrating ductal carcinomas were counted between 23 and 32 metaphases. One tumor had a modal number of 62 chromosomes and four markers. The remaining 3 tumors presented modal numbers of 46, 74 and 62 chromosomes and 17-18 markers. One case exhibited greater normal diploid population. Additionally one case contained double minute chromosomes (1-2 in some metaphases). In conclusion all of the cases presented numerous numeric and structural aberrations. The chromosome 1 is the most frequently involved in the structural rearrangements. The most common site of structural alterations was lq21 band. Other chromosomes involved included: #3, #9, #15, #16, #17, #18 and #21. Processing, culture and chromosome rearrangements are discussed, and further studies are in progress to correlate these cytogenetic data and other biological and clinical variables.

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CYTOGENETICFINDINGS IN PRIMARY BREAST CANCER. Ch. Verellen.Dumoulin, C. Hamer, R. De Meyer, B. de Hemptinne, C. Fievet, and H. Maisin. Center of Human Genetics, Departments of Surgery, Pathology and Radiotherapy, Catholic University of Louvain, 1200 Bruxelles, Belgique.

Cytogenetic analysis by G.banding was undertaken on five female patients with breast cancer, using direct and short term culture tumor preparations. The patients were 34, 59, 60, 62 and 76 years old. All the cases were duct type infiltrating tumors and the hormonal receptors were negative in 3 cases and positive in 2. The karyotype was obtained from the primary tumor in 4 cases and from a controlateral breast tumor discovered several months after the first tumor in the youngest patient. The number of metaphases analysed in each case ranged from 15 to 35. The chromosome number is in the near triploid level. There is a very high number {1-20) of structurally abnormal chromosomes identified or unidentified. The only constant cytogenetic anomaly is a structurally abnormal chromosome I seen in nearly normal karyotypes as well as in complex ones.