Gene expression changes in patient-matched gastric normal mucosa, adenomas, and carcinomas
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE24375 | GEO | 2010/09/28
SECONDARY ACCESSION(S): PRJNA132855
REPOSITORIES: GEO
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Project description:sequential changes in gene expression profiles in the gastric adenoma-carcinoma sequence by analyzing eight patient-matched gastric normal mucosa, adenomas and carcinomas. We examined gene expression changes during the gastric adenoma-carcinoma sequence in 26 snap-frozen samples (normal mucosa, adenoma, and carcinoma samples from eight patients and two additional carcinomas) by oligonucleotide microarray
2010-09-27 | E-GEOD-24375 | biostudies-arrayexpress
Project description:Background: Duodenal adenoma/adenocarcinomas are rare, and the global gene expression changes associated with the initial stages of carcinogenesis of these neoplasms have not been elucidated. Results: To comprehensively analyze genetic markers and pathways specific to early-stage duodenal adenoma/adenocarcinomas, transcriptional profiles of 4 fresh-frozen non-ampullary duodenal adenoma/adenocarcinomas and surrounding duodenal normal mucosa were compared. Key features of gene expression analysis demonstrated a strong correlation between these tumors and colorectal adenomas, as well as the Wnt/β-catenin pathway. These results shed new light on the transcriptional changes that occur during the early stages of duodenal tumorigenesis. All samples were obtained prior to treatment in order to minimize effects of cauterization, and immediately fresh-frozen.
2018-08-06 | GSE102208 | GEO
Project description:Traditional serrated adenoma (TSA) remains the least understood of all the colorectal adenomas although these lesions have been associated with a significant cancer risk- twice that of the conventional adenoma (CAD) and of the sessile serrated adenoma (SSA/P). This study was performed to investigate the proteomic profiles of the different colorectal adenomas to better assess the pathogenesis of TSA. We performed a global quantitative expression profile of 44 colorectal adenomas (12 TSA, 15 CAD, 17 SSA/Ps) and 17 normal colonic mucosa, conserved as formalin-fixed paraffin-embedded samples, by the label-free quantification (LFQ) method. Unsupervised consensus hierarchical clustering applied to the whole proteomic profile of the 44 colorectal adenomas identified four subtypes. The C1 and C2 were well-individualized clusters composed of most of the CAD (14/15) and most of the SSA (13/17) respectively. This is consistent with the fact that CAD and SSA/Ps are homogeneous but distinct colorectal adenoma entities. In contrast, TSA were subdivided into C3 and C4 clusters that also contained CAD and SSA/Ps, consistent with the more heterogeneous entity of TSA at the morphological and molecular levels. The comparison of the proteome expression profile between the adenoma subtypes and normal colonic mucosa further confirmed the heterogeneous nature of TSA that merged either on CAD or SSA, while CAD and TSA formed homogeneous and distinct entities. Furthermore, we identified LEFTY1 a new potential marker for TSA that may be relevant for the TSA pathogenesis. LEFTY1 is an inhibitor of the Nodal/TGFb pathway that we found to be one of the most overexpressed proteins specifically in the TSA and confirmed by immunohistochemistry. Taken together, our study confirms that CAD and SSA form homogenous but distinct colorectal adenoma entities while TSA are an heterogeneous entity and may arise from either SSA or from normal mucosa that will evolve along the conventional adenoma pathway.
2020-01-21 | PXD014511 | Pride
Project description:Human samples of various thyroid carcinomas, adenomas, and normals, each from a different patient, had mRNA assays performed using Affymetrix HG_U133A arrays, with 22283 probe-sets. The 99 samples consisted of 4 normals, 10 follicular adenomas, 13 follicular carcinomas, 7 oncocytic adenomas, 8 oncocytic carcinomas, 51 papillary carcinomas (each typed as having classical, follicular or tall cell morphology), 4 anaplastic carcinomas, and 2 medullary carcinomas. Interesting additional information on common mutations are provided including RAS mutation, BRAF mutation, RET/PTC rearrangements, and PAX8/PPARG translocations. Details of those assays are provided in our linked publications, as well as additional details on the specific mutations in a few special cases. No survival data is provided. Information for 93 of the 99 samples was previously made available on the web. The anaplastic and medullary carcinoma data were not previously shared. A supplementary Excel spreadsheet holding the same processed data as the series matrix file is provided and is more compact. The raw (.CEL) files are also provided.
2011-02-09 | GSE27155 | GEO
Project description:Human samples of various thyroid carcinomas, adenomas, and normals, each from a different patient, had mRNA assays performed using Affymetrix HG_U133A arrays, with 22283 probe-sets. The 99 samples consisted of 4 normals, 10 follicular adenomas, 13 follicular carcinomas, 7 oncocytic adenomas, 8 oncocytic carcinomas, 51 papillary carcinomas (each typed as having classical, follicular or tall cell morphology), 4 anaplastic carcinomas, and 2 medullary carcinomas. Interesting additional information on common mutations are provided including RAS mutation, BRAF mutation, RET/PTC rearrangements, and PAX8/PPARG translocations. Details of those assays are provided in our linked publications, as well as additional details on the specific mutations in a few special cases. No survival data is provided. Information for 93 of the 99 samples was previously made available on the web. The anaplastic and medullary carcinoma data were not previously shared. A supplementary Excel spreadsheet holding the same processed data as the series matrix file is provided and is more compact. The raw (.CEL) files are also provided. Human samples of various thyroid carcinomas, adenomas, and normals. The 99 samples consisted of 4 normals, 10 follicular adenomas, 13 follicular carcinomas, 7 oncocytic adenomas, 8 oncocytic carcinomas, 51 papillary carcinomas (each typed as having classical, follicular or tall cell morphology), 4 anaplastic carcinomas, and 2 medullary carcinomas. Additional information on common mutations are provided including RAS mutation, BRAF mutation, RET/PTC rearrangements, and PAX8/PPARG translocations.
2011-02-09 | E-GEOD-27155 | biostudies-arrayexpress
Project description:SNP array data from 127 hepatocellular adenomas and carcinomas were used to detect recurrent copy number alterations.
2013-12-18 | GSE43092 | GEO
Project description:Total mesorectal excision (TME) is the standard treatment for rectal cancer, while transanal endoscopic microsurgery (TEM) is a recently introduced surgical approach for the treatment of rectal adenomas. Incorrect preoperative staging before TEM is a problem. To identify genetic changes that might correlate with tumour stage and could lead to optimized treatment selection we performed a genome-wide chromosomal instability search in a homogeneous, clinical cohort of rectal tumours. 78 rectal tumours during different clinical stages were analysed with 10K single nucleotide polymorphism (SNP) arrays. Logistic regression was performed to build a quantitative model of specific chromosomal aberrations. Overall, most cases (95%) had one or more chromosomal aberrations. We observed a clear correlation between the total number of aberrations and the different tumour stages. Specifically, the chromosomal events: gain of 8q22–24, 13q and 20q, and loss of 17p and 18q12–22, were far more abundant in carcinoma than in adenoma. In adenoma fractions from cases with a carcinoma (infiltrating at least in the submucosa), twice the amount of such ‘malignant aberrations’ was observed, compared to pure adenomas. Furthermore, combined aberrations such as gain of 13q and loss of 18q were only found in adenomatous fractions of carcinomas and not in benign lesions. Based on these five genomic events associated with carcinoma, a clear distinction between adenoma and carcinoma tissue could be made. These data should be validated further in order that they may be used in preoperative staging of rectal tumours. Keywords: SNP array copy number and LOH study
2007-05-30 | GSE7946 | GEO
Project description:Total mesorectal excision (TME) is the standard treatment for rectal cancer, while transanal endoscopic microsurgery (TEM) is a recently introduced surgical approach for the treatment of rectal adenomas. Incorrect preoperative staging before TEM is a problem. To identify genetic changes that might correlate with tumour stage and could lead to optimized treatment selection we performed a genome-wide chromosomal instability search in a homogeneous, clinical cohort of rectal tumours. 78 rectal tumours during different clinical stages were analysed with 10K single nucleotide polymorphism (SNP) arrays. Logistic regression was performed to build a quantitative model of specific chromosomal aberrations. Overall, most cases (95%) had one or more chromosomal aberrations. We observed a clear correlation between the total number of aberrations and the different tumour stages. Specifically, the chromosomal events: gain of 8q22â24, 13q and 20q, and loss of 17p and 18q12â22, were far more abundant in carcinoma than in adenoma. In adenoma fractions from cases with a carcinoma (infiltrating at least in the submucosa), twice the amount of such âmalignant aberrationsâ was observed, compared to pure adenomas. Furthermore, combined aberrations such as gain of 13q and loss of 18q were only found in adenomatous fractions of carcinomas and not in benign lesions. Based on these five genomic events associated with carcinoma, a clear distinction between adenoma and carcinoma tissue could be made. These data should be validated further in order that they may be used in preoperative staging of rectal tumours. Experiment Overall Design: 78 tumor samples and 19 reference normal samples
2008-06-17 | E-GEOD-7946 | biostudies-arrayexpress
Project description:AIM: To analyze the expression profiles of premalignant and/or preclinical lesions of gastric cancers. METHODS: We analyzed the expression profiles of normal gastric pit, tubular adenoma and carcinoma in situ using microdissected cells from routine gastric biopsies. For the DNA microarray analysis of formalin-fixed samples, we developed a simple and reproducible RNA extraction and linear amplification procedure applying two polymerase-binding sites. The amplification procedure took only 8 h and yielded comparable DNA microarray data between formalin-fixed tissues and unfixed controls. RESULTS: In comparison with normal pit, adenoma/carcinoma showed 504 up-regulated and 29 down-regulated genes at the expected false significance rate 0.15%. The differential expression between adenoma and carcinoma in situ was subtle: 50 and 22 genes were up-, and down-regulated in carcinomas at the expected false significance rate of 0.61%, respectively. Differentially expressed genes were grouped according to patterns of the sequential changes for the 'tendency analysis' in the gastric mucosa-adenoma-carcinoma sequence. CONCLUSION: Groups of genes are shown to reflect the sequential expression changes in the early carcinogenic steps of stomach cancer. It is suggested that molecular carcinogenic pathways could be analyzed using routinely processed biopsies. Keywords: other
2004-04-06 | GSE1279 | GEO
Project description:We showed that a large number of genes were deregulated in colorectal adenomas in comparison with colorectal normal mucosae. 37 colorectal adenoma and 9 colorectal normal mucosa samples were analyzed. We generated a comparison between adenomas and normal mucosae.
2013-08-27 | E-GEOD-50114 | biostudies-arrayexpress