esophageal neoplasms/proline

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Small proline-rich repeat protein 3 enhances the sensitivity of esophageal cancer cells in response to DNA damage-induced apoptosis.

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Small proline-rich repeat protein 3 (SPRR3) has been linked with the altered chemoradiosensitivity, however the underlying molecular mechanisms remain elusive. Here, we report that ectopic overexpression of SPRR3 enhanced the sensitivity of cells in response to DNA damage-induced apoptosis via loss

Determination of proline in human serum by a robust LC-MS/MS method: application to identification of human metabolites as candidate biomarkers for esophageal cancer early detection and risk stratification.

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Altered serum proline levels are related to cancer metabolism. This study developed and validated a LC-MS/MS method to analyze proline in human serum. Surrogate blank serum, coupled with stable isotope l-proline-(13) C5 ,(15) N as internal standard, was used for generating standard curves ranging

Esophagin cDNA cloning and characterization: a tissue-specific member of the small proline-rich protein family that is not expressed in esophageal tumors.

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Cancer may be understood as the net effect of differences in gene expression between normal and transformed cells. In a novel direct approach applying this principle, complete genes expressed at altered mRNA levels in malignant versus normal esophageal epithelium were identified and isolated from

Estimation of the potential for nitrosation and its inhibition in subjects from high- and low-risk areas for esophageal cancer in southern China.

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We studied 2 counties in southern China, which are close to each other but show very different mortality rates from esophageal cancer. We collected 12 hr urine samples and analyzed them for NPRO, other nitrosamino acids, nitrate and ASC. The potential for forming NPRO and the effect on inhibition by

Urinary excretion of N-nitrosamino acids and nitrate by inhabitants of high- and low-risk areas for esophageal cancer in Northern China: endogenous formation of nitrosoproline and its inhibition by vitamin C.

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A total of 238 samples of 24-h urine were collected from inhabitants of high-risk (Lin-xian) and low-risk (Fan-xian) areas for esophageal cancer in northern China, according to three protocols: (a) from undosed subjects; (b) from subjects who had ingested 100 mg L-proline three times a day 1 h after

[Study on N-nitroso compound in food and its relevant risk factors for esophageal cancer].

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OBJECTIVE To study multiple risk factors of N-nitroso compounds (NOC) in high- and low-risk areas for esophageal cancer in southern China. METHODS The samples of 24-hr diets and 12-hr overnight urine were collected from 120 male healthy subjects (35-64 years old) selected by a 3-stage random cluster

The prolyl isomerase Pin1 is overexpressed in human esophageal cancer.

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Peptidyl-prolyl isomerase Pin1 specifically catalyzes the cis/trans-isomerization of proline in the target sequence of phosphorylated Ser/Thr-Pro in over 50 critical regulatory proteins. Pin1 is abnormally overexpressed in a range of human cancers, including lung, breast, colon and prostate cancers.

A chalcone inhibits the growth and metastasis of KYSE-4 esophageal cancer cells

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Objective: To investigate the in vitro and in vivo anticancer effects of a chalcone against KYSE-4 esophageal cancer cells. Methods: A chalcone was synthesized

p53 polymorphism in human papillomavirus-associated esophageal cancer.

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Human papillomavirus type 16/18 (HPV-16/18) is implicated in the pathogenesis of squamous cell carcinoma (SCC) of the cervix and esophagus. The arginine allele at codon 72 of p53 was found to be more susceptible to degradation by HPV E6 protein than is the proline allele in vivo, thus resulting in a

p53 Codon 72 arginine/proline polymorphism and cancer in Sudan.

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The aim of this report is to determine frequencies and associations of p53 codon 72 arg/pro polymorphism with different types of cancer in Sudan. p53 codon72 arg/pro polymorphism distribution and allele frequencies in 264 samples of different types of cancers were investigated using PCR. The results

Modeling gene-environment interactions in oral cavity and esophageal cancers demonstrates a role for the p53 R72P polymorphism in modulating susceptibility.

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A large number of epidemiological studies have linked a common single-nucleotide polymorphism (SNP) in the human p53 gene to risk for developing a variety of cancers. This SNP encodes either an arginine or proline at position 72 (R72P) of the p53 protein, which can alter the apoptotic activity of

Nuclear Localization of DNAJB6 Is Associated With Survival of Patients With Esophageal Cancer and Reduces AKT Signaling and Proliferation of Cancer Cells.

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OBJECTIVE The DnaJ (Hsp40) homolog, subfamily B, member 6 (DNAJB6) is part of a family of proteins that regulates chaperone activities. One of its isoforms, DNAJB6a, contains a nuclear localization signal and regulates β-catenin signaling during breast cancer development. We investigated the role of

Novel nonphosphorylated peptides with conserved sequences selectively bind to Grb7 SH2 domain with affinity comparable to its phosphorylated ligand.

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The Grb7 (growth factor receptor-bound 7) protein, a member of the Grb7 protein family, is found to be highly expressed in such metastatic tumors as breast cancer, esophageal cancer, liver cancer, etc. The src-homology 2 (SH2) domain in the C-terminus is reported to be mainly involved in Grb7

Fasting plasma amino acid levels in cancer patients.

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The concentration in plasma of 15 fasting amino acids were measured in 14 control volunteers and 55 cancer patients. In addition, 16 patients (7 with, 9 without total parenteral nutrition [TPN] ) with metastatic sarcoma had sequential amino acid profiles measured during 6 weeks of ablative

Upregulation of SPRR3 promotes colorectal tumorigenesis.

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Hereditary colorectal cancer develops through a series of well-defined genetic and histological changes. However, elucidation of the canonical pathway based on hereditary colorectal cancer has not provided a clear explanation of the molecular mechanisms of sporadic colorectal cancer. To identify the

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