Chromosome aberrations in 35 primary ovarian carcinomas
(1992) In Genes, Chromosomes and Cancer 4(1). p.58-68- Abstract
- Cytogenetic analysis was performed on short-term cultures of primary ovarian carcinomas from 62 patients. Cytogenetic analysis was successful in 59 cases. Clonal chromosome aberrations were detected in 35 tumors. Only numerical changes or a single structural change were found in five carcinomas: trisomy 12 was the sole anomaly in two tumors, one tumor had the karyotype 50,XX, + 5, + 7, + 12, + 14, a fourth tumor had a balanced t(1;5), and the fifth tumor had an unbalanced t(8;15). The fact that four of these five carcinomas were well differentiated suggests that simple karyotypic changes are generally characteristic of these less aggressive ovarian tumors. The majority of the cytogenetically abnormal tumors (n = 30) had complex karyotypes,... (More)
- Cytogenetic analysis was performed on short-term cultures of primary ovarian carcinomas from 62 patients. Cytogenetic analysis was successful in 59 cases. Clonal chromosome aberrations were detected in 35 tumors. Only numerical changes or a single structural change were found in five carcinomas: trisomy 12 was the sole anomaly in two tumors, one tumor had the karyotype 50,XX, + 5, + 7, + 12, + 14, a fourth tumor had a balanced t(1;5), and the fifth tumor had an unbalanced t(8;15). The fact that four of these five carcinomas were well differentiated suggests that simple karyotypic changes are generally characteristic of these less aggressive ovarian tumors. The majority of the cytogenetically abnormal tumors (n = 30) had complex karyotypes, with both numerical and structural aberrations and often hypodiploid or near-triploid stemlines. The numerical imbalances (comparison with the nearest euploid number) were mostly losses, in order of decreasing frequency -17, -22, -13, -8, -X, and -14. The structural aberrations were mostly deletions and unbalanced translocations. Recurrent loss of genetic material affected chromosome arms 1p, 3p, 6q, and 11p. The breakpoints of the clonal structural abnormalities clustered to several chromosome bands and segments: 19p13, 11p13-15, 1q21-23, 1p36, 19q13, 3p12-13, and 6q21-23. The most consistent change (16 tumors) was a 19p + marker, and in 12 of the tumors the 19p + markers looked alike. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1106322
- author
- Pejovic, Tanja
; Heim, Sverre
; Mandahl, Nils
; Baldetorp, Bo
LU
; Elmfors, Bengt
; Floderus, Ulla-Maria
; Furgyik, Stefan
; Helm, Göran
; Himmelmann, Anna
; Willen, Helena
and Mitelman, Felix
LU
(Less) - organization
- publishing date
- 1992
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Genes, Chromosomes and Cancer
- volume
- 4
- issue
- 1
- pages
- 58 - 68
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- pmid:1377010
- scopus:0026579241
- ISSN
- 1045-2257
- DOI
- 10.1002/gcc.2870040108
- language
- English
- LU publication?
- yes
- id
- a4684433-04a3-48da-a68b-ef6d64289c5c (old id 1106322)
- date added to LUP
- 2016-04-01 12:36:07
- date last changed
- 2021-09-19 05:11:05
@article{a4684433-04a3-48da-a68b-ef6d64289c5c,
abstract = {{Cytogenetic analysis was performed on short-term cultures of primary ovarian carcinomas from 62 patients. Cytogenetic analysis was successful in 59 cases. Clonal chromosome aberrations were detected in 35 tumors. Only numerical changes or a single structural change were found in five carcinomas: trisomy 12 was the sole anomaly in two tumors, one tumor had the karyotype 50,XX, + 5, + 7, + 12, + 14, a fourth tumor had a balanced t(1;5), and the fifth tumor had an unbalanced t(8;15). The fact that four of these five carcinomas were well differentiated suggests that simple karyotypic changes are generally characteristic of these less aggressive ovarian tumors. The majority of the cytogenetically abnormal tumors (n = 30) had complex karyotypes, with both numerical and structural aberrations and often hypodiploid or near-triploid stemlines. The numerical imbalances (comparison with the nearest euploid number) were mostly losses, in order of decreasing frequency -17, -22, -13, -8, -X, and -14. The structural aberrations were mostly deletions and unbalanced translocations. Recurrent loss of genetic material affected chromosome arms 1p, 3p, 6q, and 11p. The breakpoints of the clonal structural abnormalities clustered to several chromosome bands and segments: 19p13, 11p13-15, 1q21-23, 1p36, 19q13, 3p12-13, and 6q21-23. The most consistent change (16 tumors) was a 19p + marker, and in 12 of the tumors the 19p + markers looked alike.}},
author = {{Pejovic, Tanja and Heim, Sverre and Mandahl, Nils and Baldetorp, Bo and Elmfors, Bengt and Floderus, Ulla-Maria and Furgyik, Stefan and Helm, Göran and Himmelmann, Anna and Willen, Helena and Mitelman, Felix}},
issn = {{1045-2257}},
language = {{eng}},
number = {{1}},
pages = {{58--68}},
publisher = {{John Wiley & Sons Inc.}},
series = {{Genes, Chromosomes and Cancer}},
title = {{Chromosome aberrations in 35 primary ovarian carcinomas}},
url = {{http://dx.doi.org/10.1002/gcc.2870040108}},
doi = {{10.1002/gcc.2870040108}},
volume = {{4}},
year = {{1992}},
}