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

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

Nine endometrial carcinomas were examined for numerical aberrations of the chromosomes 1,7, and X by fluorescence in situ hybridization using highly repetitive chromosome-specific probes. In addition, a combination of a centromeric and a telomeric chromosome 1 probe was applied to detect structural chromosome 1 aberrations. Chromosome aberrations were found in six tumors. In four of these, an imbalance between 1q12 and 1p36 was detected, indicating the presence of an extra 1p- chromosome. In regard to the chromosomes 7 and X, monosomies and trisomies were found. Intratumoral genetic heterogeneity in endometrial carcinomas was detectable by FISH and flow cytometry. In conclusion, our findings confirm that chromosome 1 is frequently involved in structural chromosome changes, indicating chromosome 1 to be of importance in the evolution of endometrial carcinoma.
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PMID:Rearrangement of chromosome 1 is a frequent finding in endometrial carcinoma. An in situ hybridization study in nine endometrial carcinomas. 762 5

Hereditary nonpolyposis colon cancer (HNPCC) is an autosomal dominant trait responsible for approximately 6% of colorectal cancers. Linkage of the HNPCC trait to the D2S123 locus on 2p15-16 has previously been reported in two families. This HNPCC locus is now designated "COCA1." We have tested seven Canadian HNPCC families, who have a variety of clinical presentations, for linkage to a panel of microsatellite polymorphisms in the vicinity of D2S123. One family was clearly linked to the COCA1 locus (LOD = 4.21), and a second family is likely to be linked (LOD = 0.92). In three families linkage was excluded. In the remaining two families the data were inconclusive. In the linked family, individuals with cancer of the endometrium or ureter share a common haplotype with 12 family members with colorectal cancer. This supports the suspected association between these extracolonic neoplasms and the HNPCC syndrome. In addition, five of the six individuals with adenomatous polyps (but no colorectal cancer) have the same haplotype as the affected individuals, while the sixth carries a recombination. One individual with colorectal cancer carries a recombination that places the COCA1 locus telomeric to D2S123. This study localizes the COCA1 gene to an 8-cM region that is consistent with the location of the hMSH2 gene. We also confirm that families presently classified as HNPCC are genetically heterogeneous.
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PMID:Hereditary nonpolyposis colon cancer: analysis of linkage to 2p15-16 places the COCA1 locus telomeric to D2S123 and reveals genetic heterogeneity in seven Canadian families. 819 29

Chromosome 8 loss of heterozygosity (LOH) in cancer of the urinary bladder is associated with high tumour grade and stage. We have screened 193 cases of transitional cell carcinoma (TCC) of the bladder using 30 microsatellite polymorphisms on chromosome 8. Forty three cases (22%) showed LOH on 8p, the majority of which (72%) had lost the entire short arm. Using 12 tumours with partial deletions of 8p, we have defined a minimum telomeric region of deletion between D8S264 and D8S133 (8p2l.1-pter). We also found LOH in the region 8pl1.2-12, where we have defined at least one centromeric target for deletion within a 4 cM interval. Two tumours were identified with loss of the telomeric region only, whereas all cases with loss in the centromeric region also had telomeric deletion. Chromosome 8p deletions have also been described in prostate, colorectal, hepatocellular, lung and endometrial carcinoma and collecting duct carcinoma of the kidney. It has been postulated that loss or inactivation of at least 2 tumour suppressor genes on 8p may play an important role in progression of both prostate and colorectal carcinomas. The regions of deletion we have identified in bladder tumours are compatible with these, suggesting that at least two genes on 8p may play a role in the development of many common solid tumours. Our findings significantly refine the localisation of the more centromeric of these loci.
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PMID:Deletion mapping implicates two tumor suppressor genes on chromosome 8p in the development of bladder cancer. 864

Telomerase, a ribonucleoprotein associated with synthesis of telomeric DNA, is postulated to play a role in cellular senescence and immortalization. Telomerase adds a hexonucleotide telomeric sequence to the chromosomal ends during replication and is preferentially expressed in most malignant and germ-line tissues but is usually undetectable in normal somatic cells. In the current study, 34 human endometrial tissues (20 malignant and 14 benign) were analyzed for telomerase activity by a nonradioactive PCR-based method using the TRAP-eze telomeric repeat amplification detection kit (Oncor). Nineteen of 20 (95%) endometrial carcinomas and 8 of 8 (100%) benign endometrial tissues from premenopausal women exhibited strong telomerase activity, whereas 6 of 6 (100%) benign endometrial tissues from postmenopausal women showed only weak telomerase activity. There was no correlation of telomerase activity with tumor grade, depth of invasion, or DNA content. Benign cycling endometrium, a rapidly proliferating tissue, features positive telomerase activity, although expression in nonneoplastic tissues has only rarely been previously reported. Only weak activity is detected in endometrial tissues after menopause, but telomerase activity can be strongly reactivated in patients who develop endometrial cancer.
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PMID:Telomerase activity in benign endometrium and endometrial carcinoma. 920 88

Cowden disease, a dominantly inherited syndrome characterized by a variety of proliferative lesions and predisposition to breast and thyroid cancer, has recently been linked to the polymorphic marker D10S215 on chromosome segment 10q23. Loss of heterozygosity in prostate cancer is linked to the same marker, whereas loss of heterozygosity in glioblastoma, endometrial cancer, and other malignancies also localizes to this region. Most recently, a putative tumor suppressor gene (PTEN/MMAC1) has been identified in the region between D10S215 and an adjacent, more telomeric marker (D10S541) and was found to be altered in breast cancers, prostate cancers, and glioblastomas. We examined 22 invasive breast cancers for loss of heterozygosity in the 10q23 region and found loss in 41% (9/22). There were two distinct regions of loss, including one near the D10S541 marker, with an approximately equal frequency of deletion in each. The observed pattern of deletion is consistent with the presence of a tumor suppressor gene between D10S215 and D10S541. Most of the poorly differentiated carcinomas in the case collection showed loss of heterozygosity in the region near D10S215, suggesting that this loss correlates with a poor prognosis.
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PMID:Sporadic breast cancers exhibit loss of heterozygosity on chromosome segment 10q23 close to the Cowden disease locus. 949 29

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

Telomerase is a ribonucleoprotein that synthesizes telomeric DNA onto chromosomal ends using an RNA component as a template. Extension of telomeric repeats by telomerase prevents telomere shortening with cell divisions and contributes to chromosomal stability, possibly leading to immortalization of the cells. In the present study, we determined the telomerase activity of gynecological tumors and cell lines using a newly developed non-radioisotope telomeric repeat amplification protocol. A total of 21 cell lines derived from cervical cancer, endometrial cancer, ovarian cancer, and choriocarcinoma was examined, and all lines were found to be positive for telomerase activity, although the activity varied among cell types. A total of 50 gynecological malignant tumors was also examined, and 10 of 12 (83%) cervical cancers, 12 of 13 (92%) endometrial cancers, 18 of 21 (86%) ovarian cancers, 2 of 2 tubal cancers, and 1 of 1 vulvar cancer were found to be positive for telomerase activity. A total of 88% of gynecological tumors tested was thus found to be telomerase positive. However, no significant correlation was observed between telomerase activity and clinical features for any tumor type, although ovarian tumors expressing high telomerase activity tended to be more invasive. In contrast to that in malignant tumors, telomerase expression was weak and less common in premalignant lesions, with 5 of 7 cervical intraepithelial lesions and 4 of 6 borderline ovarian tumors exhibiting faint activity. Nine benign uterine lesions were also examined, and all were negative for telomerase activity except 1 uterine myoma, which had a weak signal. Three benign ovarian cysts examined had weak telomerase activity. These findings suggest that telomerase activation is common in gynecological malignant tumors and may be a critical step in their pathogenesis. However, premalignant lesions and some types of benign tumors also express weak telomerase activity.
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PMID:Telomerase activity in gynecological tumors. 981 62

Telomerase activity has been implicated in the progression of various human tumors. Our aim was to evaluate telomerase activity and to compare it with histo-pathological factors in uterine endometrial carcinoma, to look for possible correlations. Telomerase activity was measured by dilution analysis using a PCR-based telomeric repeat amplification method and detected in 31 of 35 primary endometrial carcinoma tumor specimens. High telomerase activity, detected after 100-fold dilution of extracts, was identified in 15 specimens. There was no significant correlation between the positive telomerase activity and tumor surgical stage or histo-pathological factors. However, high telomerase activity was significantly correlated with advanced surgical stage and with pelvic lymph node metastasis. Our findings suggest that an increase in telomerase activity may be associated with tumor progression and that its level may have a prognostic value in endometrial carcinoma.
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PMID:Telomerase activity correlates with histo-pathological factors in uterine endometrial carcinoma. 1050 33

Seventeen patients with endometrial cancer were studied. Tissues of primary (P) and metastatic (M) lesions were obtained from 8 patients and complete sets of P, M and Recurrent (R) lesions were obtained from 9 patients during a follow-up period of 1-10 years. Expressions of estrogen receptors, progesterone receptors, multidrug resistance protein-1, multidrug resistance-related protein, c-erbB-2, membrane-type metalloproteinase, human telomerase RNA, human telomerase reverse transcriptase RNA, E-cadherin and autocrine motility factor receptor were studied by RT-PCR. Also, telomeric restriction fragment length (TRFL) and microsatellite instability were determined between P, M and R. The results indicate that there are significant differences in the gene expression frequency during tumor progression. The mismatch rate ranged from 0 to 47.1% between P and M and from 14.3% to 66.7% between P and R, respectively. The TRFL analysis showed a marked reduction in P and M (P vs. M: 8.2 +/- 0.9 vs. 5.6 +/- 0.4 kb, mean +/-SEM, n = 9, p = 0.002 by paired Student's t test). The length further decreased in R (P vs. R: 8.2 +/- 0.9 vs. 3.2 +/- 0.7, p = 0.01, M vs. R: 5.6 +/- 0.4 vs. 3.2 +/- 0.7, p = 0.005). The genomic instability/replication error was tested by AluI arbitrary primed polymerase chain reaction (AP-PCR). Five out of 17 patients showed an altered replication error pattern (29.4%). The mean number of abnormal AluI AP-PCR patterns in M and R compared to the P was 1.5 (M) and 4 (R). The difference between the P and R was statistically significant (p < 0.04). The present data indicate that biological behavior of cancer cells in P, M and R may differ significantly.
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PMID:Gene expression in primary, metastatic and recurrent lesions of endometrial cancer. 1054 51


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