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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytogenetic studies were performed on endometrial specimens of four patients with hyperplasia, six with adenocarcinoma, and one with a mixed mesodermal tumor. Except for one cell, all 65 cells from the hyperplastic specimens had a normal female karyotype. However, a total of 92 cells from the five adenocarcinoma specimens had chromosome abnormalities, though all 20 cells from a specimen of a well differentiated adenocarcinoma showed a normal karyotype. The chromosome number and morphology of the aneuploid cells had minimal changes. The modal number of chromosomes was pseudodiploid in one case and hyperdiploid in four cases. Three kinds of structural abnormalities involving chromosomes #1 were identified to be of clonal origin: del(1p21) in two cases, tdic(1;16)(p21;q24) in one case, and i(1q) markers in two cases. Because the carcinoma cells had two chromosomes #1 of normal morphology, the presence of the marker chromosome led to partial trisomy or tetrasomy of the long arm of chromosome #1. This involvement may be assumed to represent a karyotypic change characteristic of some adenocarcinomas of the endometrium. Complex karyotypes with many rearranged chromosomes were observed in cells from the mixed mesodermal tumor. The karyotypic differences between endometrial carcinoma and the mixed medodermal tumor suggest that the genesis (and its mechanism) of the former may differ from that of the latter.
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PMID:Marker chromosomes of the long arm of chromosome 1 in endometrial carcinoma. 299 83

Cytogenetic studies were performed on endometrial specimens of four patients with hyperplasia. Six with adenocarcinoma and one with mixed mesodermal tumor. All 65 cells obtained from hyperplasia specimens excluding one cell, had a normal female karyotype. However, cells from five adenocarcinoma specimens had chromosomal abnormalities, though a specimen of a well differentiated adenocarcinoma showed a normal karyotype. A few numerical abnormalities which were clonal in origin, were noted in one case each. Three kinds of structural abnormalities involving chromosomes 1 were identified as clonal in origin; del (1) (p21), t. dic(1; 16) (p21; q24), and i (lq). Since carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to the partial trisomy or tetrasomy of the long arm of a chromosome 1, being characteristic of cells from adenocarcinoma of the endometrium. A successively transplantable tumor has been produced from a poorly differentiated carcinoma cells with the t. dic (1; 16) (p21; q24) marker chromosome. Histological and chromosomal examinations were performed in cells from the passage 1, 4 and 5 tumors in order to explore the role of this marker played in the formation of the endometrial carcinoma. Though the degree of differentiation status of tumor cells had been changed during transplantations, the t. dic (1; 16) (p21; q24) marker were observed consistently among these cells. This suggested that the rearrangement of chromosome 1 was not produced as a result of genetic instability due to tumor progression, but rather specifically associated with the endometrial carcinogenesis. None of karyotypic changes excluding the marker and the tetraploid was responsible for these phenotypic changes.
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PMID:[Cytogenetic study of endometrial carcinoma]. 301 54

Despite the fact that adenocarcinoma of the endometrium is currently the most common gynecologic malignancy in the United States, few chromosomal studies have been done to date characterizing this disease. HEC-1A, a cell line used by many laboratories as a reference cell line for endometrial carcinoma, has never been subjected to definitive karyotyping. For this reason, with the use of improved banding techniques, this has now been accomplished, and several consistent abnormalities have been identified. There was a marker chromosome formed from an insertion of 2q21, probably representing an insertion of the lacking chromosome 14. In addition, there was a translocation to the telomeric region of 1p; and trisomies of 3, 7, and 17. Many of these abnormalities are known to consistently be associated with other primary malignancies. In addition, the chromosomes in which trisomy is noted carry genes associated with epidermal growth factor and estrogen receptors, which also bear marked homology to known oncogenes. It would appear that further detailed studies of various grades and stages of endometrial carcinoma, as well as histologic types and "precursor lesions," may lead to an understanding of those chromosomal changes associated with disease initiation and progression.
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PMID:Cytogenetics of an endometrial adenocarcinoma cell line and its implications. 341 Mar 49

Cytogenetic studies were performed on endometrial specimens from four patients with hyperplasia, six with adenocarcinoma and one with mixed mesodermal tumor. Except for one cell, all 65 cells from the hyperplastic specimens had a normal female karyotype. However, a total of 92 cells from the 5 adenocarcinoma specimens had chromosomal abnormalities, though all 20 cells from a specimen of a well differentiated adenocarcinoma showed a normal karyotype. The chromosome number and morphology of the aneuploid cells had minimal changes. The modal number of chromosomes was pseudodiploid in one case and hyperdiploid in four. Three kinds of structural abnormalities involving chromosomes 1q were identified as of clonal origin: del. 1 (p21) in 2 cases, t. dic (1;16) (p21;q24) in one case and i (1q) markers in 2 cases. Since the carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to a partial trisomy or tetrasomy of the long arm of a chromosome 1. This involvement of the long arm of chromosome 1, therefore, may be assumed to represent a karyotypic change in the characteristics of adenocarcinoma of the endometrium. Complex karyotypes with many rearranged chromosomes were observed in cells from the mixed mesodermal tumor. The karyotypic differences between endometrial carcinoma and the mixed mesodermal tumor suggest that the genesis (and its mechanism) of the former may differ from that of the latter.
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PMID:[Abnormalities of chromosome involving 1q in uterine endometrial carcinomas]. 345 90

A cytogenetic study of 71 malignant effusions caused by different histopathologic types of cancer was performed by a direct technique. Abnormal metaphases were present in 50 effusions (70.4%); a detailed analysis of banded karyotypes was possible in 20 of these. Trisomies and monosomies were present in 18 of 20 cases. The most common trisomies were +19, +3, +5, +8, +9, +10, +16 and +22; the most frequent monosomies were -X, -2, -5, -7, and -21. Clonal structural abnormalities were identified in 18 of 20 cases. In most instances, they were extensive, and some chromosomes were involved in a nonrandom fashion. Chromosomes #1, #13, and #6 were the most frequently involved in these rearrangements. A common marker chromosome, t(7;9)(p11;q12), was observed in two patients with cancer of the endometrium. Double minutes (DMs) were present in two patients, and there was a homogeneously stained region (HSR) in one.
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PMID:Cytogenetic study of cancer cells in effusions. 394 48

A chromosome study was performed in a recurrent endometrial cancer. The cytogenetic analysis performed with a quinacrine-Hoechst banding technique revealed rearrangements of chromosomes #1 and #11 [i.e.: der(11),t(1;11)(q21;q23)], which was found in all metaphases. In addition, a deletion of chromosome 6(q21), trisomy of chromosomes #7 and #10, monosomy X, and -4 as the clonal changes. Partial trisomy for a long arm of chromosome #1 also was observed in almost all analyzed metaphases (11 of 12 cells). These data showed the association of rearrangement of 1q in endometrial cancer and/or redevelopment of tumor, and also suggest the possible participation of chromosome #11 on which the human proto-oncogene c-ets was mapped.
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PMID:Recurrent endometrial adenocarcinoma with rearrangement of chromosomes 1 and 11. 394 58

Endometrial cancer is a common gynecologic tumor, yet reports of cytogenetic studies are few. We studied chromosomes from seven primary specimens of endometrial cancer. Six had abnormal chromosomes; five had a diploid-hyperdiploid modal number and one was triploid. One specimen had a normal karyotype. Chromosome 1 was frequently involved in abnormalities (five tumors) with i(1q) in two tumors, and one tumor each had der(7)t(1;7)(q12;p11) and +add (1)(p13). One additional tumor had trisomy 1 in the single cell which could be fully analyzed. Trisomy 7 was noted in two tumors, and trisomy 10 in one. Because trisomies of these chromosomes have been reported in other cases of endometrial cancer, we used fluorescent in situ hybridization (FISH) with centromere probes to determine the prevalence of trisomies 7 and 10 in these specimens. No additional tumors were found to have trisomies 7 or 10 by FISH. Our data, in combination with published literature, suggest that additional copies of 1q or portions of 1q constitute the primary change in this tumor. Extra copies of genes in this region may play an important role in tumorigenesis in endometrial carcinoma.
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PMID:Cytogenetic and FISH analysis of endometrial carcinoma. 817 89

Recently various authors described a new mechanism involved in the genesis of some tumors, which is characterized by a tendency for replication mistakes and by genomic instability of microsatellite repeats. This instability can be revealed through the shift in the electrophoretic mobility of the analyzed fragments, which is due to a different number of repeat units. This phenomenon is widely documented in colorectal tumors of patients affected by hereditary nonpolyposis colorectal carcinoma (HNPCC). We performed a cytogenetic and molecular study of 23 endometrial adenocarcinomas to investigate the presence of genomic instability and to evaluate the possibility of a positive correlation with specific chromosomal changes. The study of genomic instability was performed using 23 microsatellites localized over 8 chromosomes. Genomic instability of microsatellites was observed in 3 cases over all 8 analyzed chromosomes. The tumoral stage of cases with microsatellite instability does not differ significantly from the remaining tumors. As a matter of fact several cases showing no evidence of instability were more advanced (II B, III A) than tumors with instability. In ten cases we observed trisomy of chromosome 10, in some as a sole anomaly. The 3 cases with genomic instability revealed a near-diploid karyotype and all showed the presence of a supernumerary marker derived from chromosome 1 rearrangements. A derivative chromosome 1 was revealed in 4 cases without evidence of microsatellite instability. It should be noted that the presence of many unidentified markers and the small number of tumors with instability do not allow us to give a definitive significance to this observation. Our results indicate that there is not an apparent correlation between microsatellite instability and specific chromosomal abnormalities. Moreover, we did not find any correlation between pathological characteristics of the tumor and genomic instability. Microsatellite instability appears to be a relatively rare event in endometrial carcinoma.
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PMID:Cytogenetic abnormalities and microsatellite instability in endometrial adenocarcinoma. 910 39

Retrospective analysis of chromosomal changes in endometrial carcinoma was performed by fluorescence in situ hybridization on free nuclei isolated from formalin-fixed paraffin-embedded tissue. We examined 23 archival samples for numerical aberrations of chromosomes 1 and 10 with the use of specific DNA probes for the pericentromeric and centromeric regions of these two chromosomes. Numerical aberrations of chromosomes 1 and 10 were detected in 39% of the case analyzed, and the frequency of trisomy 10 tended to increase as the histological grade worsened. Our findings confirm the association of cytogenetic anomalies involving chromosomes 1 and 10 with endometrial carcinoma, as reported by other studies, and suggest that changes in centromere 10 copy number may correlate with the degree of tumor differentiation.
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PMID:Numerical abnormalities of chromosomes 1 and 10 in endometrial adenocarcinoma: fluorescence in situ hybridization analysis of 23 archival paraffin-embedded samples. 980 32