Cytogenetic analysis of four human ovarian carcinoma cell lines

Sheer, Denise; Sheppard, David M.; Gorman, Patricia; Ward, Bruce G.; Whelan, Richard D. H.; Hill, Bridget T.

doi:10.1016/0165-4608(87)90068-9

Cited by 46 publications

(19 citation statements)

References 18 publications

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“…Augustus et al (1986), studying effusions derived from ovarian tumors, also indicated band q21 as the most frequent breakpoint. These findings have been confirmed by Sheer et al (1987) on permanent cell lines. Eleven of the 14 markers derived from chromosome 1 in our series showed breakpoints in the above regions, generally q32, implying the genesis of markers lq -.…”

Section: Lpf-277-2 67supporting

confidence: 82%

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Chromosome aberrations in metastatic ovarian cancer: Relationship with abnormalities in primary tumors

Bello

Rey

1990

Intl Journal of Cancer

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Twenty malignant effusions secondary to ovarian cancer have been cytogenetically analyzed directly and after short in vitro culture. With the exception of one sample characterized by trisomy 3, all cases displayed clonal structural rearrangements. Chromosomes 1 and 3 were most frequently involved in the genesis of markers. Abnormalities of chromosomes 5, 6, 9, 11 and 12 were also recurrently found, and double minutes (DM) were observed in 2 samples. Our results agree with previous findings on the preferential involvement of chromosomes 1, 3 and 6 in ovarian carcinomas, and suggest that rearrangements of certain chromosomes are non-random but are secondary to the malignant progression of these tumors.

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Section: Lpf-277-2 67supporting

confidence: 82%

“…Usually, deletions in 3p13-21 are found (Van der Riet Fox Whang-Peng et al, 1984;Panani and Ferti, 1985;Hill et al, 1984;Trent and Salmon, 1981;Trent et al, 1985;Sheer et al, 1987). In our series, only 3 of the 10 markers derived from chromosome 3 involved the short arm, one of them at p13.…”

Section: Lpf-277-2 67mentioning

confidence: 72%

Chromosome aberrations in metastatic ovarian cancer: Relationship with abnormalities in primary tumors

Bello

Rey

1990

Intl Journal of Cancer

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“…Cytogenetic manifestations of gene amplification, hsr and dmin chromosomes, have repeatedly been reported in ovarian tumor cell lines (Sheer et al, 1987), in malignant effusions secondary to ovarian carcinoma (Whang-Peng et al, 1984;Bullerdiek et al, 1985;Augustus et al, 1986 MusilovA andMichalovA, 1986), and also in primary tumor specimens from untreated patients with ovarian cancer (Atkin et al, 1983;Bullerdiek et al, 1985;Tanaka et al, 1989). We have found hsr in seven patients, but no dmin.…”

Section: Discussionmentioning

confidence: 94%

Chromosome aberrations in 35 primary ovarian carcinomas

Pejović¹,

Heim²,

Mitelman³

et al. 1992

Genes Chromosomes & Cancer

123

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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.

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“…Wake et al (1980) ®rst demonstrated a translocation between chromosomes 6 and 14 in the papillary serous subtype of ovarian tumors. Deletions and translocations involving di erent portions of chromosome 6q were subsequently reported by cytogenetic analyses of primary ovarian carcinomas and ovarian cancer cell lines (Buick et al, 1985;Deger et al, 1997;Sheer et al, 1987;Tibiletti et al, 1996;Trent and Salmon, 1981;Whang-Peng et al, 1984). Frequent losses of heterozygosity (LOH) on this chromosome were also observed in primary ovarian tumors (Cliby et al, 1993;Ehlen and Dubeau, 1990;Foulkes et al, 1993;Lee et al, 1990).…”

Section: Introductionmentioning

confidence: 96%