Human-derived proteome characterization of tongue coating in colorectal cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Qubo Chen
PROVIDER: PXD055725 | iProX | Sat Sep 07 00:00:00 GMT+01:00 2024
REPOSITORIES: iProX
Similar Datasets
Project description:Background: The change of cellular energy metabolism in colorectal carcinogenesis is poorly understood. It is widely accepted tht most, if not all, colorectal cancers (CRCs) arise from adenomatous polyps (APs). Our aim was to characterize the mitochondrial and bioenergetic alternations in the adenoma-carcinoma sequence. Results: Two glycolysis-related genes, aldolase B (ALDOB) and solute carrier family 16 member 4 (SLC16A4), were upregulated in polyps. This result was further confirmed by the real-time PCR analysis showing that the both ALDOB and SLC16A4 mRNA expressions were higher in the polyps with villous component compared with their adjacent normal mucosa.
2017-05-23 | GSE81804 | GEO
Project description:Colorectal cancer (CRC) is the third most common cancer worldwide. Colorectal polyps are recognised pre-cursors of CRC, however hyperplastic polyps lack malignant potential. The purpose of this study was to identify differences in gene expression between normal colonic mucosa, hyperplastic and adenomatous polyps from disease-free individuals. By comparing polyps believed to have malignant potential (adenomatous polyps) with hyperplastic polyps it is hoped that new insights into colorectal carcinogenesis can be achieved. 24 colonic samples comprising 8 normal colonic mucosa, 8 hyperplastic polyps and 8 adenomatous polyps.
2012-08-25 | E-GEOD-40362 | biostudies-arrayexpress
Project description:Colorectal cancer (CRC) is the third most common cancer worldwide. Colorectal polyps are recognised pre-cursors of CRC, however hyperplastic polyps lack malignant potential. The purpose of this study was to identify differences in gene expression between normal colonic mucosa, hyperplastic and adenomatous polyps from disease-free individuals. By comparing polyps believed to have malignant potential (adenomatous polyps) with hyperplastic polyps it is hoped that new insights into colorectal carcinogenesis can be achieved.
2012-08-25 | GSE40362 | GEO
Project description:Colorectal cancer often arises from adenomatous polyps. Polyps can grow and progress to cancer, but may also remain static in size, regress, or resolve. Prediciting which progress to cancer and which remain benign is difficult. We developed a long-lived murine model of colorectal cancer with tumors that can be followed by colonoscopy. Our aim was to assess whether these tumors have similar growth patterns and histologic fates to human colorectal polyps to identify features to aid in risk stratification of colonic tumors. Long-lived Apc^Min/+ mice were treated with 4% dextran sodium sulfate to promote colonic tumorigenesis. Tumor growth patterns were characterized by serial colonoscopy, and pathology was determined. Serial biopsies of tumors were obtained for immunohistochemistry and gene expression profiling by microarray analysis with Affymetrix Whole Genome array. Tumors (n=424) grew, remained static, regressed, or resolved over time with different relative frequencies. Newly developed tumors demonstrated dynamic growth patterns with higher rates of growth and resolution, while more established tumors tended to remain static in size. Colonic tumors were hyperplastic lesions (3%), adenomas (73%), intramucosal carcinomas (20%), or adenocarcinomas (3%). Differentially expressed genes between adenomas and intramucosal carcinomas were identified. We did not identify differentially expressed genes between early and late biopsies from the same tumor. This novel murine model of intestinal tumorigenesis develops colonic tumors that can be monitored by serial colonoscopy, mirror growth patterns seen in human colorectal polyps, and progress to colorectal cancer. Further characterization of cellular and molecular features are needed to determine which features can be used to risk-stratify polyps for progress to colorectal cancer and potentially guide prevention strategies.
2014-05-03 | GSE46626 | GEO
Project description:We performed proteomic profiling on serum samples from paired pre- and post-operative CRC patients, colorectal polyps patients and healthy controls using an approach combining magnetic bead-based weak cation exchange and matrix-assisted laser desorption ionization-time of flight mass spectrometry. We next performed liquid chromatography-electrospray ionization-tandem mass spectrometry to identify the proteins and selected potential biomarker based on bioinformatics analysis of the TCGA and GEO dataset. 5 peptides showing the most significant changes in abundance across paired pre- and post-operation CRC patients, colorectal polyps patients and healthy controls were identified as peptide regions of FGA, MUC5AC and SETD7. Bioinformatics analysis suggested that the up-regulation of SETD7 in CRC is relatively specific. Validation studies showed that SETD7 expression increased from healthy controls to those with colorectal polyps and finally CRC patients, and decreased following surgery.
2019-04-17 | PXD011352 |
Project description:Colorectal cancer often arises from adenomatous polyps. Polyps can grow and progress to cancer, but may also remain static in size, regress, or resolve. Prediciting which progress to cancer and which remain benign is difficult. We developed a long-lived murine model of colorectal cancer with tumors that can be followed by colonoscopy. Our aim was to assess whether these tumors have similar growth patterns and histologic fates to human colorectal polyps to identify features to aid in risk stratification of colonic tumors. Long-lived Apcin/+ mice were treated with 4% dextran sodium sulfate to promote colonic tumorigenesis. Tumor growth patterns were characterized by serial colonoscopy, and pathology was determined. Serial biopsies of tumors were obtained for immunohistochemistry and gene expression profiling by microarray analysis with Affymetrix Whole Genome array. Tumors (n=424) grew, remained static, regressed, or resolved over time with different relative frequencies. Newly developed tumors demonstrated dynamic growth patterns with higher rates of growth and resolution, while more established tumors tended to remain static in size. Colonic tumors were hyperplastic lesions (3%), adenomas (73%), intramucosal carcinomas (20%), or adenocarcinomas (3%). Differentially expressed genes between adenomas and intramucosal carcinomas were identified. We did not identify differentially expressed genes between early and late biopsies from the same tumor. This novel murine model of intestinal tumorigenesis develops colonic tumors that can be monitored by serial colonoscopy, mirror growth patterns seen in human colorectal polyps, and progress to colorectal cancer. Further characterization of cellular and molecular features are needed to determine which features can be used to risk-stratify polyps for progress to colorectal cancer and potentially guide prevention strategies. F1 (SWR x C57BL/6) Apcin/+ mice who had been given two treatments of 4% dextran sodium sulfate in drinking water at weaning underwent colonoscopy around 80 days of age. Those with distal colonic tumors amenable to biopsy had two biopsies taken at that time. Tumors were monitored by colonoscopy every 14 days. Every 28 days, two additional biopsies were taken of each tumor. This protocol was repeated until mice were moribund. Six tumors were removed after sacrifice. The earliest and latest biopsies of each tumor were selected for RNA extraction and Affymetrix hybridization.
2014-05-03 | E-GEOD-46626 | biostudies-arrayexpress
Project description:By analyzing the scRNA-seq data from ten human colorectal specimens, which represent the four kinds of colorectal tissues (normal colorectal mucosa, inflammatory polyps, Adenomatous polyps and colorectal cancer), in combination with validation by immunofluorescence staining using expanded clinical samples, and together with verification using large scale TCGA and Kaplan–Meier data, we reveal a dynamic molecular landscape and the importance of ligand-receptor genes and transcription factors driving the colorectal carcinogenesis.
2025-02-01 | GSE261388 | GEO
Project description:Whole transcriptome expression levels of healthy colonic, colorectal adenoma and colorectal cancer biopsy samples were analyzed by HTA 2.0 microarrays
2019-09-13 | GSE100179 | GEO
Project description:Adenomatous polyps in the colorectal tract are benign tumors with the potential to develop cancer. In this study we perform a large scale proteomic study of comparing the proteomes of colorectal enterocytes (N) and the cells of the adenoma (A) and cancer (C). Using formalin fixed and paraffin embedded clinical material, we identified on average 10,000 proteins per sample of the microdissected cells and established a quantitative protein repository of the disease. Statistical analysis revealed 2300, 1780, and 2161 significant alterations between N and A, C and A, and C and N, respectively. In this work we did not aim identification of novel biomarkers but focus on depiction of the proteome alterations underlying the disease. The extent of the assessed changes reflects a varied cell size, the composition of different subcellular components, and basic biological processes including the energy metabolism, plasma membrane transport, DNA replication and transcription.
2015-08-10 | PXD002137 | Pride
Project description:<p>Background: The gut microbiota is a key hallmark of tumor and plays a central role in colorectal cancer (CRC). However, the contribution of gut fungi, an important community of gut microbes, remains substantially understudied in CRC.</p><p>Objective: To characterize the gut fungal landscape in CRC and elucidate its associations with bacterial communities, metabolites, and trace elements.</p><p>Methods: We conducted metagenomic sequencing on fecal samples from three cohorts: healthy controls (n = 401), colorectal polyp patients (n = 162), and CRC patients (n = 253). The fungal genomic data from NCBI database (PRJNA833221) was served as the reference for annotating gut fungi. Metabolites and trace elements were quantified via liquid chromatography and inductively Coupled Plasma Mass Spectrometry (ICP-MS), respectively. Fungal diversity and compositional differences were analyzed across groups. A random forest model was trained to discriminate healthy controls from intestinal disease groups (polyps and CRC) based on microbial biomarkers, with an ablation study optimizing co-marker selection. Structural equation modeling (SEM) was employed to dissect interactions among fungi, bacteria, metabolites, and trace elements.</p><p>Results: CRC patients exhibited increased fungal diversity at the genus level. Seven fungal genera displayed differential abundance across three groups: Rhizopus was specifically enriched in CRC, whereas Sporisorium, Cladosporium, Aureobasidium, Zygoascus, and Meyerozyma were enriched in polyps. Ablation study identified an optimal 31-microbial-marker panel (28 bacterial and 3 fungal species) that effectively distinguished intestinal disease groups (AUC = 0.89). SEM analysis identified three fungal markers—Penicillium citrinum, Penicillium sp. PG10607D, and Rhizopus stolonifera—that influence bacterial-metabolite-trace element networks through distinct correlations.</p><p>Conclusion: This study plots the first gut fungal atlas for CRC and reveals complex cross-kingdom interactions involving fungi, bacteria, metabolites, and trace elements, providing new insights into CRC research.</p>
2025-07-26 | MTBLS12776 | MetaboLights