Methylation profiling in gastric cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Myung Soon Kim
PROVIDER: E-GEOD-39532 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Early gastric cancers (EGC) precede advanced gastric cancers (AGC) with a favorable clinical outcome compared to advanced gastric cancers (AGC). To understand the progression mechanisms of EGC to AGC, it is required to disclose the EGC and AGC genomes in terms of the the mutational and evolutionary perspectives. In this study, we performed whole-exome sequencing and copy number profiling of nine microsatellite (MS)-unstable (MSI-H) (5 EGC and 4 AGC) and eight MS-stable (MSS) gastric cancers (4 EGC and 4 AGC). Unexpectedly, we observed no substantial differences in the number, sequence composition and functional consequences (potential driver mutations and affected pathways) of the mutations and CNAs between EGC and AGC genomes in both MSI-H and MSS cases. Gastrectomy tissues from 17 GC patients were used for this study. The hospital pathology department confirmed pathologic features of the GC (e.g., EGC vs. AGC, differentiation, lymph node metastasis and TNM stage). All of the picked areas from tumor and normal areas were frozen, cut, and stained with hematoxylin & eosin (H&E). Two pathologists selected cases with rich tumor cell population (at least 60%), which were subsequently used in the study. Copy number profiling was performed using Agilent 180K platform according to the manufacturer's protocol.
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Project description:Early gastric cancers (EGC) precede advanced gastric cancers (AGC) with a favorable clinical outcome compared to advanced gastric cancers (AGC). To understand the progression mechanisms of EGC to AGC, it is required to disclose the EGC and AGC genomes in terms of the the mutational and evolutionary perspectives. In this study, we performed whole-exome sequencing and copy number profiling of nine microsatellite (MS)-unstable (MSI-H) (5 EGC and 4 AGC) and eight MS-stable (MSS) gastric cancers (4 EGC and 4 AGC). Unexpectedly, we observed no substantial differences in the number, sequence composition and functional consequences (potential driver mutations and affected pathways) of the mutations and CNAs between EGC and AGC genomes in both MSI-H and MSS cases.
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Project description:Objective: Considerable evidence links dietary salt intake with the development of hypertension, left ventricular hypertrophy, and increased risk of stroke and coronary heart disease. Despite extensive epidemiological and basic science interrogation of the relationship between high salt (HS) intake and blood pressure, it remains unclear how HS impacts endothelial cell (EC) and vascular structure in vivo. This study aims to uncover the HS-induced vascular pathologies using a differential systemic decellularization in vivo (DISDIVO) approach.Approach and Results: We performed systematic molecular characterization of the endothelial glycocalyx (eGC) and EC proteomes in mice with HS (8%) diet-induced hypertension versus healthy control animals. Isolation of eGC and ECs compartments was achieved using the DISDIVO approach. Altered protein expression in hypertensive compared to normal mice was characterized by liquid chromatography tandem-mass spectrometry (LC-MS/MS). Proteomic results from eGC fractions revealed a significant downregulation of eGC and associated proteins in HS diet-induced hypertensive mice. Among 1696 proteins identified in this group, 723 were markedly downregulated while 168 were upregulated, bioinformatic analysis indicates critical damage and derangement of eGC layer. In the ECs fraction HS-induced hypertension significantly altered protein mediators of contractility, metabolism, mechanotransduction, renal functions, and coagulation cascades. In particular, we observed dysregulation of integrin subunits alpha2, alpha2b, and alpha5, which relay external signals to the actin cytoskeleton.Conclusion: These findings provide novel molecular insight on HS-induced structure changes in eGC and ECs that may increase cardiovascular risk and potentially guide the development of new diagnostics and therapeutic interventions.
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