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)

The aim of this study was to identify amplified oncogenes in endometrial cancer using array-based comparative genomic hybridization (array CGH). Despite its prevalence, the molecular mechanisms of endometrial carcinogenesis are still poorly understood. The selected array CGH allows the simultaneous examination of 58 oncogenes commonly amplified in human cancers and is capable of achieving increased mapping resolution compared with conventional CGH. A subset of 8 specimens from a bank of 60 malignant and normal specimens was selected for array analysis to identify potential genes of interest. TaqMan polymerase chain reaction was carried out on the 60 specimens to examine if aberrations at the genomic level correlated with gene expression and to compare expression in normal and malignant samples. Oncogenes amplified in the endometrial cancers included AR, PIK3CA, MET, HRAS, NRAS, D17S1670, FGFR1, CTSB, RPS6KB1, LAMC2, MYC, PDGFRA, FGF4/FGF3, PAKI, and FGR. Three genes were examined at the messenger RNA level. AR and PIK3CA were higher in normal specimens, and MET was higher in malignant samples, suggesting a role for MET in endometrial cancer. Newer arrays examining more genes and larger sample numbers are necessary to elucidate the carcinogenic pathway in endometrial cancer.
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PMID:Genome-wide analysis of deoxyribonucleic acid in endometrial cancer using comparative genomic hybridization microarrays. 1668 70

Many genetic factors play important roles in the development of endometrial cancer. The aim of this study was to investigate genetic alterations in the Taiwanese population with endometrial cancer. DNA was extracted from 10 cases of fresh-frozen endometrial cancer tissue. The exomes of cancer-related genes were captured using the NimbleGen Comprehensive Cancer Panel (578 cancer-related genes) and sequenced using the Illumina Genomic Sequencing Platform. Our results revealed 120 variants in 99 genes, 21 of which were included in the Oncomine Cancer Research Panel used in the National Cancer Institute Match Trial. The 21 genes comprised 8 tumor suppressor candidates (ATM, MSH2, PIK3R1, PTCH1, PTEN, TET2, TP53, and TSC1) and 13 oncogene candidates (ALK, BCL9, CTNNB1, ERBB2, FGFR2, FLT3, HNF1A, KIT, MTOR, PDGFRA, PPP2R1A, PTPN11, and SF3B1). We identified a high frequency of mutations in PTEN (50%) and genes involved in the endometrial cancer-related molecular pathway, which involves the IL-7 signaling pathway (PIK3R1, n=1; AKT2, n=1; FOXO1, n=1). We report the mutational landscape of endometrial cancer in the Taiwanese population. We believe that this study will shed new light on fundamental aspects for understanding the molecular pathogenesis of endometrial cancer and may aid in the development of new targeted therapies.
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PMID:Genetic alterations in endometrial cancer by targeted next-generation sequencing. 2662 1

Immunotherapy has provided a promising therapeutic strategy for endometrial cancer (EC). The present study aims to develop a prognostic classifier based on immune-related genes (IRGs) to stratify EC patients. A total of 15 prognosis-related IRGs were further filtrated by multivariate Cox regression: LTA, TMSB15A, S100A14, PLA2G2A, PDGFRA, CLDN4, CTF1, PRLH, PTN, SST, HTR3E, NRP1, RORA, THRA and CBLC. A prognostic signature was constructed to split EC patients into the high-risk and low-risk group with statistically different survival outcomes, indicating good potential for the prognostic signature in survival surveillance. Furthermore, five compounds with potential anti-tumor effects were selected, including ciclopirox, ikarugamycin, vincamine, mevalolactone, and thiamazole. The abundance of follicular helper T cells, regulatory T cells and M0 macrophages were significantly enhanced in the high-risk group while resting memory CD4+ T cells, gamma delta T cells, M2 macrophages and resting mast cells were markedly elevated in the low-risk group. Memory activated CD4+ T cells, CD8+ T cells and activated mast cells were three most correlative with riskscore. An immunophenoscore (IPS) analysis revealed that patients of the low-risk group had a higher IPS and more inclined to respond to immune checkpoint inhibitors. Mutation analysis showed that patients of the low-risk group represented more tumor mutation burden but low riskscore, thus getting better prognosis. Patients of the low-risk group were more sensitive for gemcitabine, bleomycin, vinblastine, vinorelbine and methotrexate by prediction. We constructed a potential prognostic model and might offer new insight on the identification of new immune-related biomarkers and target therapy in EC.
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PMID:Development of an immune gene prognostic classifier for survival prediction and respond to immunocheckpoint inhibitor therapy/chemotherapy in endometrial cancer. 3261 57