Confocal Laser Endomicroscopy for the Diagnosis of Gastric Intestinal Metaplasia, Intraepithelial Neoplasia, and Carcinoma
Ontology highlight
ABSTRACT:
DISEASE(S): Metaplasia,Gastric Carcinoma,Carcinoma,Gastric Intestinal Metaplasia,Gastric Intraepithelial Neoplasia,Stomach Neoplasms,Carcinoma In Situ,Neoplasms
PROVIDER: 2128739 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:The requirement of goblet cells (intestinal metaplasia; IM) to define BarrettM-bM-^@M-^Ys esophagus (BE) remains controversial as some studies have shown that the risk of progression to esophageal adenocarcinoma (EAC) is similar for non-goblet cell metaplasia (NGM) and IM. IM harbors genomic aberrations in known cancer-associated genes and these have been linked to increased EAC risk. No detailed studies have explored DNA alterations in NGM. We hypothesized that a comparison of DNA alterations in cancer-associated genes in IM and NGM samples would provide insight into their relative risks for progression to EAC. Patient biopsies were analyzed using Affymetrix SNP 6.0 arrays, FISH, and targeted resequencing of 20 frequently mutated EAC genes. Frequent CNAM-bM-^@M-^Ys targeting cancer-associated genes were found in IM whereas no such changes were observed in NGM. In one subject, FISH confirmed loss of CDKN2A and amplification of chromosome 8 in IM but not in a nearby NGM biopsy. Targeted sequencing in a subset of metaplasia tissues revealed 11 non-synonymous mutations in 16 IM samples and 2 mutations in 19 NGM samples. Our results show that IM has a much higher frequency of cancer-associated mutations than NGM and is therefore likely to pose a higher risk for development of EAC. 57 non-goblet metaplasia, intestinal metaplasias, and composite specimens from 45 subjects were studied. DNA copy number abnormalities (CNAM-bM-^@M-^Ys) were identified using Affymetrix arrays and fluorescence in situ hybridization (FISH). Data was processed in Nexus 6.0 (BioDiscovery, CA). Targeted sequencing of all exons from twenty genes found to be frequently mutated in EAC was performed on metaplasia samples using Ion AmpliSeqM-bM-^DM-" DNA sequencing.
2012-12-15 | E-GEOD-40769 | biostudies-arrayexpress
Project description:Background: Gastric intestinal metaplasia (IM) is a pre-cancerous stage spanning a morphological spectrum that is poorly represented by human cell line models.
Objective: We aim to establish and characterize human IM cell models to better understand IM progression along the cancer spectrum.
Design: A large human gastric IM organoid (IMO) cohort (n=28), their clonal derivatives and normal gastric organoids (n=42) for comparison were established. Comprehensive multi-omics profiling and functional characterization were performed.
Results: Single-cell transcriptomes revealed IMO cells spanning a spectrum from hybrid gastric/intestinal to advanced intestinal differentiation. Their lineage trajectories connected different cycling and quiescent stem and progenitors, highlighting differences in gastric to IM transition and the potential origin of IM from STMN1 cycling isthmus stem cells. Hybrid IMOs showed impaired differentiation potential, high lineage plasticity beyond gastric or intestinal fates, and reactivation of a fetal gene program.
Cell populations in gastric IM and cancer tissues were highly similar to those derived from IMOs and exhibited a fetal signature. Genomically, IMOs showed elevated mutation burden, frequent chromosome 20 gain, and epigenetic de-regulation of many intestinal and gastric genes. Functionally, IMOs were FGF10 independent and showed downregulated FGFR2. Several IMOs exhibited a cell-matrix adhesion independent (CMi) subpopulation that displayed chromosome 20 gain but lacked key cancer driver mutations, potentially representing the earliest neoplastic precursor of IM-induced gastric cancer.
Conclusions: Overall, our IM organoid biobank captured the heterogeneous nature of IM, revealing mechanistic insights on IM pathogenesis and progression, offering an ideal platform for studying early gastric neoplastic transformation and chemoprevention.
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Project description:Metaplasia of the gastric epithelia (intestinal metaplasia, IM) is a pre-malignant lesion associated with increased gastric cancer (GC) risk.
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