Cytogenetic Findings in Malignant Mixed Mesodermal Tumors of the Uterus

Gil-Benso, Rosario; López‐Ginés, Concha; Cardá, Carmen; Monteagudo-Crespo, Carlos; Torres, J.V.; Llombart‐Bosch, Antonio

doi:10.1016/s0165-4608(97)00201-x

Cited by 8 publications

(7 citation statements)

References 12 publications

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“…This speculation is based solely on frequency data, however, and therefore is fraught with all the uncertainties and caveats mentioned above for chromosome 1. Trisomy 20 was present in three tumors with complex karyotypes and therefore probably represents a secondary and relatively nonspecific change, a conclusion also supported by having been reported in only four previously examined tumors (Couturier et al, 1988;Gil-Benso et al, 1997;Sirchia et al, 1997;Tibiletti et al, 1997) and was part of a simple karyotype only in the case described by Sirchia et al (1997).…”

Section: Discussionsupporting

confidence: 65%

“…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: 68%

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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: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 68%

Genomic aberrations in carcinomas of the uterine corpus

Micci

Teixeira

Haugom

et al. 2004

Genes Chromosomes & Cancer

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“…Deletion of chromosome 1 at p32 and deletion of chromosome 11 at q13 are common markers in anomalous cases. Double minutes, homogeneously staining regions, and telomeric associations were also seen 20 . Rearrangements of chromosome 1, leading to loss of distal 1p, and homogeneously staining regions have so far been the most frequent cytogenetic changes in this tumor type.…”

Section: Discussionmentioning

confidence: 95%

Primary Peritoneal Malignant Mixed Mesodermal (Müllerian) Tumor

Hussein¹,

Hussein

Abd-Elwahed

2009

Tumori

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“…Del 1p was also seen in a case of LG-ESS [4] and is common in malignant mixed mesodermal tumours (MMMT) of the uterus [11], as well as in many other tumour types [17], supporting the hypothesis that a suppressor gene whose loss or inactivation could be a common event in the progression of many solid tumours may be located here [12]. Chromosome 19 at q13 band is often involved in MMMT of the uterus [11], arising mostly through the addition of material of unknown origin to 19q13. Aberrations of chromosome 19 have already been demonstrated in other LG-ESS, even if the chromosomal change was different [4].…”

Section: Discussionmentioning

confidence: 99%

Endometrial stromal sarcomas: immunohistochemical, electron microscopical and cytogenetic findings in two cases

et al. 1999

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Uterine sarcomas are approximately 3% of all malignant uterine corpus tumours. Of these, the tumours that originate solely in the stromal elements of the uterine wall are infrequent and have not been well characterized cytogenetically. We report two cases of endometrial stromal sarcomas (ESS), one low grade and one high grade, diagnosed by conventional histology, immunocytochemistry, electron microscopy and cytogenetics. Morphologically clear-cut differential structures were seen at optical, immunohistochemical, and electron microscopic levels, permitting a clear differential diagnosis. The low-grade ESS expressed hormonal receptors and vimentin, whereas the high-grade ESS showed no hormone receptors, high Ki-67 activity, and occasional cytokeratin-positive cells. Ultrastructurally, no malignant epithelial differentiation was seen in the tumour cells, but cilia were found in both cases. Cytogenetic study of the low-grade ESS showed pseudodiploid karyotype with chromosomes 6 and 20 rearranged. The high-grade ESS showed a complex karyotype with clonal numerical and structural anomalies. The chromosomes involved in the structural rearrangements were 1, 3, 6, 7, 13, 14, 15, 17, 19, and 21.

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Cytogenetic Findings in Malignant Mixed Mesodermal Tumors of the Uterus

Cited by 8 publications

References 12 publications

Genomic aberrations in carcinomas of the uterine corpus

Genomic aberrations in carcinomas of the uterine corpus

Primary Peritoneal Malignant Mixed Mesodermal (Müllerian) Tumor

Endometrial stromal sarcomas: immunohistochemical, electron microscopical and cytogenetic findings in two cases

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