Marker chromosomes of the long arm of chromosome 1 in endometrial carcinoma

Fujita, Hiromasa; Wake, Norio; Kutsuzawa, T; Ichinoe, K; Hreshchyshyn, Myroslaw M.; Sandberg, Avery A.

doi:10.1016/0165-4608(85)90149-9

Cited by 54 publications

(17 citation statements)

References 15 publications

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“…Abnormalities of chromosome 2 were never seen alone in the present series, indicating they are secondary events, possibly playing a role in cell differentiation. Trisomy 2 has also previously been reported in 12 endometrial carcinomas (Fujita et al, 1985;Couturier et al, 1986Couturier et al, , 1988Dutrillaux and Couturier, 1986;Horgas et al, 1988;Bardi et al, 1995;Sirchia et al, 1997;Tibiletti et al, 1997) but again never as the sole abnormality. Trisomy 12 was found as the sole abnormality in case 38 from the present series and in another tumor reported by Couturier et al (1986), whereas in another eight tumors (three from this series and five from previous publications), it occurred together with other aberrations.…”

Section: Discussionmentioning

confidence: 53%

“…This does not preclude the possibility that the same change may also be of pathogenetic consequence in some tumors, however. That the loss always occurred together with other abnormalities, as well as in nine tumors previously characterized (Kusyk et al, 1982;Fujita et al, 1985;Dutrillaux and Couturier, 1986;Musilova and Michalova, 1986;Nilbert et al, 1990;Shah et al, 1994;Gil-Benso et al, 1997;Tibiletti et al, 1997;Iliszko et al, 1998), is indicative of a secondary neoplastic role, if any.…”

Section: Discussionmentioning

confidence: 69%

“…The essential gene or genes might be in this segment. Other abnormalities of chromosome 1 may also be of interest, especially chromosomal segment 1p13p22, which was involved in rearrangements in four cases from the present series and in 12 cases previously examined (Fujita et al, 1985;Musilova and Michalova, 1986;Couturier et al, 1988;Horgas et al, 1988;Fletcher et al, 1989;Milatovich et al, 1990;Laxman et al, 1993;Shah et al, 1994;Bardi et al, 1995). As for the 1q abnormalities, the putative gene loci of pathogenetic importance remain unknown.…”

Section: Discussionmentioning

confidence: 80%

“…As pointed out above, trisomy 7 is a nonrandom change in endometrial carcinomas, as indicated by its occurrence in 16 previously examined tumors (Fujita et al, 1985;Dutrillaux and Couturier, 1986;Yoshida et al, 1986;Couturier et al, 1988;Milatovich et al, 1990;Tharapel et al, 1991;Sreekantaiah et al, 1992;Shah et al, 1994;Bardi et al, 1995;Sirchia et al, 1997), in all but one (Shah et al, 1994) of which it occurred together with other abnormalities. Here we present the first case in which an isochromosome of the long arm was found to be the sole abnormality (case 7), suggesting that genes in 7q might be pathogenetically important in this tumor type.…”

Section: Discussionmentioning

confidence: 83%

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Genomic aberrations in carcinomas of the uterine corpus

Micci

Teixeira

Haugom

et al. 2004

Genes Chromosomes & Cancer

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Endometrial carcinoma, the most common invasive neoplasm of the female genital tract, occurs either in a hormone-related, less virulent form (type I) or in a hormone-independent, more aggressive form (type II). Another cancer of the uterine corpus is carcinosarcoma, a biphasic or mixed epithelial-mesenchymal tumor, now classified as metaplastic carcinoma. We examined by karyotyping and comparative genomic hybridization a consecutive series of 67 endometrial carcinomas and 15 carcinosarcomas and compared the cytogenetic features of the different carcinoma subtypes. All three subtypes of uterine carcinoma had in common a nonrandom gain of material from 1q and 8q but differed from one another in other respects. Endometrial carcinomas of type I mostly presented gains from chromosome arms 1q and 8q and losses from Xp, 9p, 9q, 17p, 19p, and 19q, whereas endometrial carcinomas of type II showed a more complex imbalance picture, with gains from chromosome arms 1q, 2p, 3q, 5p, 6p, 7p, 8q, 10q, and 20q and losses from Xq, 5q, and 17p. The carcinosarcomas mostly showed gains of or from 1q, 5p, 8q, and 12q but losses from 9q, that is, they were much more similar to endometrial carcinomas in their pattern of acquired genomic changes than to sarcomas of the uterine corpus. It was also possible to identify different copy number changes among the different grades of type I carcinomas, between serous papillary and clear-cell carcinomas of type II, as well as between homologous and heterologous carcinosarcomas. Specifically, type I adenocarcinomas that were highly differentiated mostly showed gains from 1q and 10p; those that were moderately differentiated showed gains from 1q, 7p, 7q, and 10q as well as losses from Xp, 9p, 9q, 17p, 19p, and 19q; whereas those poorly differentiated showed gains from 1q, 2p, 2q, 3q, 6p, 8q, and 20q but losses from Xp, Xq, 5q, 9p, 9q, 17p, and 17q. The serous papillary carcinomas showed gains from 1q, 2p, 2q, 3q, 5p, 6p, 6q, 7p, 8q, 18q, 20p, and 20q but losses from 17p, whereas the clear-cell carcinomas showed gains from 3q, 7p, 8q, 10q, 16p, and 20q but losses from 6q. Finally, the homologous carcinosarcomas presented gains from 1p, 1q, 8q, 12q, and 17q as well as losses from 9q and 13q, whereas the heterologous tumors showed gains from 1q, 8p, and 8q. The reproducibility of the observed correlations between karyotypic aberration patterns and histological differentiation was underscored by the fact that those carcinosarcomas whose epithelial component resembled type I endometrial carcinomas also exhibiting a type I aberration profile, whereas carcinosarcomas with a type II carcinoma differentiation had karyotypic abnormalities similar to those of type II endometrial carcinomas.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 83%

See 2 more Smart Citations

Genomic aberrations in carcinomas of the uterine corpus

Micci

Teixeira

Haugom

et al. 2004

Genes Chromosomes & Cancer

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“…This view is supported by the fact that gain of lq material was the most frequent imbalance in our series (Figure 3). Isochromosome lq has, as the only abnormality, otherwise been described in an endometrial carcinoma (Fujita et al, 1985), in an ovarian tumour (Pejovic et al, 1993), and in cancers of the breast (Pandis et al, 1992b). As one of several changes, on the other hand, + i(lq) is a frequent finding (Mitelman, 1991).…”

Section: Discussionmentioning

confidence: 99%

Karyotypic abnormalities in tumours of the pancreas

et al. 1993

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Summary Short-term cultures from 20 pancreatic tumours, three endocrine and 17 exocrine, were cytogenetically analysed. All three endocrine tumours had a normal chromosome complement. Clonal chromosome aberrations were detected in 13 of the 17 exocrine tumours: simple karyotypic changes were found in five carcinomas and numerous numerical and/or structural changes in eight. When the present findings and those previously reported by our group were viewed in conjunction, the most common numerical imbalances among the 22 karyotypically abnormal pancreatic carcinomas thus available for evaluation turned out to be, in order of falling frequency, -18, -Y, + 20, + 7, + 11 and -12. Imbalances brought about by structural changes most frequently affected chromosomes I (losses in lp but especially gains of lq), 8 (in particular 8q gains but also 8p losses), and 17 (mostly 17q gain but also loss of 17p). Chromosomal bands lp32, 1q1O, 6q21, 7p22, 8p2l, 8ql 1, 14pl 1, l5q10-1 1, and 17qll were the most common breakpoint sites affected by the structural rearrangements. Abnormal karyotypes were detected more frequently in poorly differentiated and anaplastic carcinomas than in moderately and well differentiated tumours.Pancreatic carcinoma accounts for about 10% of malignancies of the digestive organs and the outcome is fatal in more than 95% of the cases.

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Uterine carcinosarcoma is derived from a single stem cell: Anin vitro study

et al. 1997

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Expression of intermediate filaments (IFs) has been suggested to be a reliable marker for differentiating epithelial and non‐epithelial tumors. Moreover, the c‐erbB‐2 and p53 genes are considered to be involved relatively early in the process of human carcinogenesis. In order to elucidate the origin of uterine carcinosarcomas, we analyzed IF, c‐erbB‐2 and p53 expression in and the ultrastructural characteristics of clones derived from a human uterine‐carcinosarcoma cell line, EMTOKA. The expression of IFs and other proteins in the EMTOKA clones was identical to that in the EMTOKA cell line. It and its 7 clones all expressed cytokeratins 8, 17, 18 and 19, vimentin, epithelial membrane antigen, S‐100, myoglobin, type‐II collagen, α‐smooth‐muscle actin, placental alkaline phosphatase and epidermal‐growth‐factor receptor. The c‐erbB‐2 and p53 expression levels of all the cell types of the EMTOKA cell line and its clones were the same. Interestingly, an ultrastructural study showed that the EMTOKA cell line and its clones at early and late passages possessed the characteristics of epithelial cell types without either transitional forms between the epithelial and stromal components or differentiation into sarcomatous components. The results of this study lend particular support to the combination tumor hypothesis that a precursor (stem) cell gives rise both to epithelial and to mesenchymal components during the histogenesis of uterine carcinosarcoma, the epithelial component of which appears to be dominant, suggesting that the established cell lines derived from a common stem cell. Int. J. Cancer 72:821–827, 1997. © 1997 Wiley‐Liss, Inc.

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Marker chromosomes of the long arm of chromosome 1 in endometrial carcinoma

Cited by 54 publications

References 15 publications

Genomic aberrations in carcinomas of the uterine corpus

Genomic aberrations in carcinomas of the uterine corpus

Karyotypic abnormalities in tumours of the pancreas

Uterine carcinosarcoma is derived from a single stem cell: Anin vitro study

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