Chromosome analysis of 97 primary breast carcinomas: Identification of eight karyotypic subgroups

Genes Chromosomes and Cancer - Tập 12 Số 3 - Trang 173-185 - 1995
Nikos Pandis1,2, Yuesheng Jin1,3, Ludmila Gorunova1, Catarina Petersson1, Georgia Bardi1,2, Ingrid Idvall4, Björn Johansson1, Christian Ingvar5, Nils Mandahl1, Felix Mitelman1, S Heim1,3,2
1Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
2Department of Medical Genetics, Odense University, Odense, Denmark
3Department of Genetics, The Norwegian Radium Hospital and Institute for Cancer Research, Oslo, Norway
4Department of Clinical Pathology, Lund University Hospital, Lund, Sweden.
5Department of Surgery, Lund University Hospital, Lund, Sweden

Tóm tắt

AbstractChromosome banding analysis of 97 short‐term cultured primary breast carcinomas revealed clonal aberrations in 79 tumors, whereas 18 were karyotypically normal. In 34 of the 79 tumors with abnormalities, two to eight clones per case were detected; unrelated clones were present in 27 (34%) cases, whereas only related clones were found in seven. These findings indicate that a substantial proportion of breast carcinomas are of polyclonal origin. Altogether eight abnormalities were repeatedly identified both as sole chromosomal anomalies and as part of more complex karyotypes: the structural rearrangements i(1)(q10), der(1;16)(q10;p10), del(1)(q11–12), del(3)(p12–13p14–21), and del(6)(q21–22) and the numerical aberrations +7, +18, and +20. At least one of these changes was found in 41 (52%) of the karyotypically abnormal tumors. They identify a minimum number of cytogenetic subgroups in breast cancer and are likely to represent primary chromosome anomalies in this type of neoplasia. Other candidates for such a role are translocations of 3p12–13 and 4q21 with various partner chromosomes and inversions of chromosome 7, which also were seen repeatedly. Additional chromosomal aberrations that give the impression of occurring nonrandomly in breast carcinomas include structural rearrangements leading to partial monosomies for 1p, 8p, 11p, 11q, 15p, 17p, 19p, and 19q and losses of one copy of chromosomes X, 8, 9, 13, 14, 17, and 22. The latter changes were seen consistently only in complex karyotypes, however, and we therefore interpret them as being secondary anomalies acquired during clonal evolution.

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Genes Chromosomes and Cancer

Tập 12 Số 3

173-185

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