endometrial neoplasms/proline

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Deregulation of estrogen receptor coactivator proline-, glutamic acid-, and leucine-rich protein-1/modulator of nongenomic activity of estrogen receptor in human endometrial tumors.

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Proline-, glutamic acid-, and leucine-rich protein-1)PELP1/MNAR [modulator of nongenomic activity of estrogen receptor (ER)], a novel coregulatory protein, modulates genomic as well as nongenomic activity of ERs. We characterized the expression and localization of PELP1 in both benign and cancerous

Downregulation of Proline Hydroxylase 2 and Upregulation of Hypoxia-Inducible Factor 1α are Associated with Endometrial Cancer Aggressiveness.

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Proline hydroxylase 2 (PHD2) is involved in tumorigenesis. This study aimed to examine PHD2 and hypoxia-inducible factor 1α (HIF-1α) expression in different endometrial tissues and explore the correlations between PHD2 and HIF-1α expression with clinicopathological characteristics of

cis-4-[(18)F]-Fluoro-l-proline fails to detect peripheral tumors in humans.

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System A amino acid transport is increased in transformed and malignant cells. The amino acid 4-cis[(18)F]fluoro-l-proline (cis-[(18)F]FPro) has been shown to be a substrate of the System A amino acid carrier. In this pilot study, we investigated the diagnostic potential of cis-[(18)F]FPro in

p53 and p21 genetic polymorphisms and susceptibility to endometrial cancer.

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OBJECTIVE Recently, there has been considerable interest in the association of specific cancers with single nucleotide polymorphisms (SNPs). In this regard, genetic polymorphism at codon 72 (CCC/proline to CGC/arginine [Pro(72)Arg]) of the p53 gene is one of the most frequently studied subjects. An

Models including plasma levels of sphingomyelins and phosphatidylcholines as diagnostic and prognostic biomarkers of endometrial cancer.

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In endometrial cancer, biomarkers for preoperative identification of patients with low risk for disease progression would enable stratification according to the extent of surgery needed, and would avoid the complications that can be associated with radical surgery. A panel of proteins, amino acids,

Genotype misclassification in genetic association studies of the rs1042522 TP53 (Arg72Pro) polymorphism: a systematic review of studies of breast, lung, colorectal, ovarian, and endometrial cancer.

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Preferential loss of heterozygosity at the rs1042522 locus of the tumor protein 53 gene (TP53) (Arg72Pro) is observed in several tumors. Genetic association studies in oncology often use tumor tissue rather than unaffected tissue for genotyping; in such cases, loss of heterozygosity at the TP53

Evaluation of the frequency of TP53 gene codon 72 polymorphisms in Iranian patients with endometrial cancer.

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Polymorphisms of the TP53 gene codon 72 exhibit less effective function in tumor suppression and usually are associated with human cancer. To investigate the frequency of proline and arginine alleles of TP53 codon 72, the present study analyzed the DNA from blood samples of 30 Iranian women with

Cyclin D1 gene (CCND1) mutations in endometrial cancer.

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Cyclin D1 is frequently overexpressed in human neoplasias by gene rearrangement and amplification, but no mutations in the CCND1 gene have so far been reported. However, in vitro mutagenesis of CCND1 has shown that substitutions affecting threonine 286 residue produced cyclin D1 nuclear

PELP1/MNAR suppression inhibits proliferation and metastasis of endometrial carcinoma cells.

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Proline-, glutamic acid- and leucine-rich protein-1/modulator of non-genomic activity of estrogen receptor (ER) (PELP1/MNAR) is a novel nuclear receptor (NR) co-activator that plays an essential role in the actions of ER. Emerging findings suggest that PELP1/MNAR is a novel proto-oncogene, whose

An upstream estrogen response element linked to exogenous p53 tumor suppressor gene expression differentiates effects of the codon 72 polymorphism.

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The objective of this study was to assess the effects of an upstream estrogen response element (ERE) on exogenous p53 tumor suppressor gene with a codon 72 polymorphism about which there have been controversial reports in relation to cancer risk. The p53 gene (bases 166-1143 from start codon) with

Peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 as a molecular target in breast cancer: a therapeutic perspective of gynecological cancer.

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Peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (PIN1) induces conformational and functional changes to numerous key signaling molecules following proline-directed phosphorylation and its deregulation contributes to disease, particularly cancer. PIN1 is overexpressed in breast cancer,

Human Papillomavirus E6 Knockdown Restores Adenovirus Mediated-estrogen Response Element Linked p53 Gene Transfer in HeLa Cells.

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The p53 gene is inactivated by the human papillomavirus (HPV) E6 protein in the majority of cervical cancers. Treatment of HeLa S3 cells with siRNA for HPV E6 permitted adenovirus-mediated transduction of a p53 gene linked to an upstream estrogen response element (ERE). Our previous study in

The founder mutation MSH2*1906G-->C is an important cause of hereditary nonpolyposis colorectal cancer in the Ashkenazi Jewish population.

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Hereditary nonpolyposis colorectal cancer (HNPCC) is caused by mutations in the mismatch-repair genes. We report here the identification and characterization of a founder mutation in MSH2 in the Ashkenazi Jewish population. We identified a nucleotide substitution, MSH2*1906G-->C, which results in a

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