Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differential display methodology was employed to examine and compare the mRNA species derived from normal endometrial tissue and endometrial carcinoma (grade 3, stage III) tissue biopsies. Two cDNA sequences, one expressed in the tumour group only (T19) and the other expressed only in the normal group (N22), were selected for verification of differential expression by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The expression of N22 was restricted to the normal group, suggesting a possible tumour suppressing function. Sequence analysis of this fragment revealed a high degree of similarity to a human cDNA sequence of unknown function. The expression of T19 mRNA was observed in both normal and neoplastic tissues, however the relative abundance was significantly higher in endometrial carcinomas. Expression of T19 mRNA was further examined in a larger clinical sample set and was significantly increased in the tumours (n = 16), with a three-fold increase when compared with the normal endometria, n = 5 (Kruskal-Wallis analysis of variance, P<0.05). Subsequent sequence analysis of T19 revealed a high degree of similarity to the 3' untranslated region of a rat growth factor responsive gene, SM-20. Further characterization of these mRNA transcripts may lead to the identification of novel genes involved in endometrial tumourogenesis.
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PMID:Identification and partial characterization of differentially expressed mRNAs in normal human endometria and endometrial carcinomas by differential display RT-PCR. 1090 81

Previous observations indicate that transfer of human chromosome (chr.) 1 induces senescence of endometrial cancer cells. To identify the gene(s) responsible for the senescence, we first analyzed the structural integrity of the introduced chr. 1 in immortal revertant from chr.1-transferred HHUA cells. The data demonstrated a correlation between nonrandom deletions within the 1q31-qter region and reversion to immortality. Next, by using a panel of 12 microsatellite markers, we found high frequencies of loss of heterozygosity in the particular 1q region (1q41-42), in surgically removed samples. Then, we screened the genetic mutation of the genes involved in this region, with endometrial cancer panel. Among them, EGLN1, that is a member of prolyl hydroxylase and can facilitate HIF-1 degradation by ubiquitination through the hydroxylation of HIF-1, was mutated at significantly higher frequencies (12/20, 60%). Introduction of wild-type EGLN1 into endometrial cancer cell lines (HHUA, Ishikawa and HWCA), that carry EGLN1 gene mutations induced senescence. This was invoked through the negative regulation of HIF-1 expression. In addition, alternative way of negative regulation of HIF-1 by Factor inhibiting HIF-1(FIH), SiRNA against HIF-1, and HIF-1 inhibitor, YC-1, could also induce senescence. Thus, EGLN1 can be considered as a candidate tumor suppressor on chr. 1q, and our observation could open the new aspect in exploring the machinery of senescence induction associated with HIF-1 signal transduction. These results also suggested the availability of negative regulation of HIF-1 signals for uterine cancer treatment, especially for uterine sarcomas that have worse prognosis and show a high frequency of EGLN1 gene abnormality.
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PMID:Induction of human endometrial cancer cell senescence through modulation of HIF-1alpha activity by EGLN1. 1616 Oct 47

Gynecological cancer is the leading cause of cancer mortality in women. However, the mechanisms underlying gynecological cancer progression have remained largely unclear. In the present study, 799 dysregulated genes were identified in ovarian serous cystadenocarcinoma (OV), 488 dysregulated genes in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), and 621 dysregulated genes in uterine corpus endometrial carcinoma (UCEC). Bioinformatics analysis revealed that mRNA splicing and cell proliferation-associated biological processes served important roles in OV progression. Metabolism-associated biological processes played important roles in CESC progression, and protein phosphorylation and small GTPase-mediated signal transduction served important roles in UCEC progression. The present study also constructed OV, CESC and UCEC progression-associated protein-protein interaction networks to reveal the associations among these genes. Furthermore, Kaplan-Meier curve analysis showed that progression-related genes were associated with the duration of overall survival. Finally, NARS2 and TPT1 in OV, SMYD2, EGLN1, TNFRSF10D, FUT11, SYTL3, MMP8 and EREG in CESC, and SLC5A1, TXN, KDM4B, TXNDC11, HSDL2, COX16, MGAT4A, DAGLA, ELOVL7, THRB and PCOLCE2 in UCEC were identified as hub genes in cancer progression. Therefore, this study may assist in the identification of novel mechanisms underlying cancer progression and new biomarkers for gynecological cancer prognosis and therapy.
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PMID:Identification of hub genes and key pathways associated with the progression of gynecological cancer. 3178 13