Cytogenetic studies of endometrial malignancies

Milatovich, Athena; Heerema, Nyla A.; Palmer, Catherine G.

doi:10.1016/0165-4608(90)90007-w

Cited by 40 publications

(28 citation statements)

References 12 publications

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“…Previous studies also frequently found gain of or from the long arm of chromosome 1 in endometrial carcinomas, and this finding is registered in 39 of 111 cases (35%) in the Mitelman database (2003), in six of which it is the sole abnormality. Milatovich et al (1990) suggested that aberrations of chromosome 1 represent a primary change in endometrial cancer because they are sometimes seen as the sole abnormality. As we now have confirmed that such changes indeed do occur nonrandomly in endometrial carcinomas, sometimes in the absence of other abnormalities, they undoubtedly meet the criteria for acceptance as primary chromosomal aberrations of this tumor type.…”

Section: Discussionmentioning

confidence: 98%

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: 98%

Genomic aberrations in carcinomas of the uterine corpus

Micci

Teixeira

Haugom

et al. 2004

Genes Chromosomes & Cancer

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“…The predominant abnormality was trisomy or tetrasomy 1q, which occurred in about 72% of the tumors examined, and the second most frequent was trisomy 10, found in 40% of the tumors (Sandberg, 1990). Only a few cytogenetic studies of human uterine carcinosarcomas have been reported (Emoto et al, 1992;Fujita et al, 1985;Harker et al, 1983;Milatovich et al, 1990). Among solid tumors, one had a modal number of 56 with many rearranged chromosomes, including i (14q) and ϩ16p (Fujita et al, 1985), and 3 of 6 homologous endometrial carcinosarcomas had structural abnormalities of chromosomes 1, 3 and 5 (Milatovich et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Only a few cytogenetic studies of human uterine carcinosarcomas have been reported (Emoto et al, 1992;Fujita et al, 1985;Harker et al, 1983;Milatovich et al, 1990). Among solid tumors, one had a modal number of 56 with many rearranged chromosomes, including i (14q) and ϩ16p (Fujita et al, 1985), and 3 of 6 homologous endometrial carcinosarcomas had structural abnormalities of chromosomes 1, 3 and 5 (Milatovich et al, 1990). Studies on uterine-carcinosarcoma cell lines in culture showed that one cell line had 45, XX, Ϫ5, Ϫ6, Ϫ7 ϩt(5q,6p) and ϩmar1 (Harker et al, 1983) and 2 others had different chromosomal abnormalities.…”

Section: Discussionmentioning

confidence: 99%

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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“…The presence of this alteration has been the subject of varyingly satisfactory explanations. Suzuki et al (1997) discussed the formerly known cytogenetic alterations in endometrial carcinomas, in which chromosome 1 often showed isochromosome formation (Milatovich et al, 1990). Furthermore, Sonoda et al (1997) discussed proto-oncogenes such as SKI and TRK which are located in 1q.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal alterations in 98 endometrioid adenocarcinomas analyzed with comparative genomic hybridization

Levan

Partheen

Österberg

et al. 2006

Cytogenet Genome Res

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The aim of the present study was to investigate chromosomal alterations in a large set of homogeneous tumors, 98 endometrioid adenocarcinomas. We also wanted to evaluate differences in chromosomal alterations in the different groups of tumors in relation to stage, survival and invasive or metastatic properties of the tumors. Comparative genomic hybridization (CGH) was used to detect chromosomal alterations in tissue samples from 98 endometrioid adenocarcinomas. All chromosomes were involved in DNA copy number variations at least once in the tumor material, but certain changes were recurrent and rather specific. Among the specific changes, it was possible to identify 39 chromosomal regions displaying frequent DNA copy number alterations. The most frequent alteration was detected at 1q25→q42, in which gains were found in 30 cases (30%). Gains at 19pter→p13.1 were detected in 26 tumors (26%) and at 19q13.1→q13.3 in 19 tumors (19%). Increased copy numbers were also detected at 8q (8q21→q22 and 8q22→qter), at a relatively high rate, in 17 cases (17%). Furthermore, gains at 10q21→q23 and 10p were found in 14 (14%) and 13 cases (13%), respectively. The most common losses were found in the three regions 4q22→qter, 16q21→qter and 18q21→qter, all of which were detected in eight of the 98 tumors (8%). We also detected differences between the tumors from deceased patients and from survivors. Gain at 1q25→q42 was more commonly detected in the tumors from patients who died of cancer. We noted that the regions most affected differed in the different surgical stages (I–IV). The results of the CGH analysis identify specific chromosomal regions affected by copy number changes, appropriate objects for further genetic studies.

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Cytogenetic studies of endometrial malignancies

Cited by 40 publications

References 12 publications

Genomic aberrations in carcinomas of the uterine corpus

Genomic aberrations in carcinomas of the uterine corpus

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

Chromosomal alterations in 98 endometrioid adenocarcinomas analyzed with comparative genomic hybridization

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