Expression data for 52 microsatellite stable (MSS) primary tumors from patients with proximal colon cancer.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE63624 | GEO | 2016/03/02
SECONDARY ACCESSION(S): PRJNA268492
REPOSITORIES: GEO
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Project description:Samples were taken from surgically resected tumor specimens from patients with proximal colon cancer. The expression profiles were determined using the Affymetrix GeneChip Human Exon 1.0 ST Array version 2. APC gene mutation status was determined using Sanger sequencing. A classifier for APC mutation status was trained using these expression data. 52 microsatellite stable (MSS) proximal colon cancers samples were analyzed. 17 samples were APC wild-type and 35 had APC protein-truncating mutations.
2016-03-02 | E-GEOD-63624 | biostudies-arrayexpress
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Project description:Samples were taken from colorectal cancers in surgically resected specimens in 84 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes between MSI and MSS cancers and, furthermore, to determine the distinct characteristics of proximal and distal MSI cancers. Keywords: repeat
2006-10-17 | GSE4554 | GEO
Project description:Although fine needle aspiration (FNA) cytology is helpful in determining whether thyroid nodules are benign or malignant, this distinction remains challenging in follicular neoplasms. Identification of genomic alterations in cytological specimens that distinguish between benign and malignant follicular tumors would have great clinical value. This study identified chromosomal imbalances in a set of 126 thyroid frozen follicular lesions characterized by histopathology, using aCGH, FISH, and DNA ploidy determination. An evaluation algorithm was developed based on a panel of three FISH experiments to better distinguish between follicular adenomas and carcinomas of the thyroid. This algorithm detects structural abnormalities that were observed in about half of the follicular thyroid carcinomas. These molecular markers may be therefore useful as an adjunct for making a differential diagnosis of follicular adenoma versus follicular carcinoma using cytological material obtained by FNA. Further information on the values in the comment columns: [FISH_1p_Loss : Status for abnormality found in terms of copy number variation for chr1p by FISH], [FISH_22_Loss : Status for abnormality found in terms of copy number variation for chr22 by FISH], [FISH_X_Gain : Status for abnormality found in terms of copy number variation for chrX by FISH], [FISH_Global : Status for abnormality found in terms of copy number variation for at least one of these (chr1p, chr22, chrX) by FISH], [DNA_Index : Measured by flow cytometry], [KRAS_Mutation : Mutation status for KRAS, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [HRAS_Mutation : Mutation status for HRAS, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [NRAS_Mutation : Mutation status for NRAS, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [BRAF_Mutation : Mutation status for BRAF, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [CTNNB1_Mutation : Mutation status for CTNNB1, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [PIK3CA_Mutation : Mutation status for PIK3CA, obtained from Sanger sequencing. wt for wild-type, mut for mutant], [PAX8-PPARg_Fusion : Status for the PAX8-PPARG gene fusion, obtained from qRT-PCR. pos for presence of fusion, neg for absence], [RET-PTC_Fusion : Status for the RET-PTC gene fusion, obtained from qRT-PCR. pos for presence of fusion, neg for absence], [Mutation_Status : Global mutation status, combining results from HRAS, NRAS mutation status, and PAX8-PPARG fusion status], [Tumor_Size_cm : Tumor size in centimeters], [pT : Classes defined according to the size of the tumors (for more information, check AJCC classification)], [pN : Classes defined according to the number of nodes involved or not (for more information, check AJCC classification)], [pM : Classes defined according to the presence or absence of distant metastases (for more information, check AJCC classification)], [Carcinoma_Histo_Type : Histological type for carcinoma. MIF for minimally invasive, WIF for widely invasive], [Adenoma_Histo_Type : Histological type for adenoma. MIC for microvesicular, MAC for macrovesicular, BOTH for both], [Follow-up_month : Patient follow-up in months], [Alive_status : Patient alive status. yes for alive patient, no for deceased patient], [Metastasis_status : Presence of metastasis during the follow-up. yes for positive, no for negative, possible when uncertainty remains].
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Project description:Abstract: Altered expression of microRNAs (miRNAs) is associated with development and progression of various human cancers by regulating the translation of oncogenes and tumor suppressor genes. In colorectal cancer (CRC), these regulators complement the Vogelstein multi-step model of pathogenesis and have the potential of becoming a novel class of tumor biomarkers and therapeutic targets. Using QRT-PCR, we measured the expression of 621 mature miRNAs in 40 CRCs and their paired normal tissues and identified 23 significantly deregulated miRNAs. We subsequently evaluated their association with clinical characteristics of the samples and presence of alterations in the molecular markers of CRC progression. Expression levels of miR-31 were correlated with CA19-9 and miR-18a, miR-21 and miR-31 were associated with mutations in APC gene. To investigate the downstream regulation of the differentially expressed miRNAs identified we integrated putative mRNA target predictions with the results of a meta-analysis of seven public gene expression datasets of normal and tumor samples of CRC patients. Many of the CRC deregulated miRNAs computationally map to targets involved in pathways related to progression. Here one promising candidate pair (miR-1 and MET) was studied and functionally validated. We show that miR-1 can have a tumor suppressor function in CRC by directly down-regulating MET oncogene both at RNA and protein level and that re-expression of miR-1 leads to MET driven reduction of cell proliferation and motility, identifying the miR-1 down-modulation as one of the events that could enhance CRC progression. Note: Each sample has the following information: Type - tissue type (T : Tumor or N: Normal), Patient - patient identifier, Stage - tumor stage (I - IV), Status - disease status at last check-up (ED: evident disease, NED: non-evident disease), CEA - carcinoembryonic antigen (continuous), CA199 - carbohydrate antigen 19-9 (continuous), APC - mutation status of APC gene (0: wild-type, 1: mutated), KRAS - mutation status of KRAS gene (0: wild-type, 1: mutated), chr18qLOH - LOH status of 18q (0: no LOH, 1: LOH), TP53 - mutation status of TP53 gene (0: wild-type, 1: mutated). Tumor and normal counter-parts of 40 colorectal cancer patients (10 of each Stage I to IV) where profiled using TaqMan(r) Array Human MicroRNA A+B Cards v2.0
2012-02-22 | E-GEOD-28364 | biostudies-arrayexpress
Project description:Immunotherapy based on immune checkpoint inhibitors (ICIs) has provided revolutionary results in treating various cancers. However, its efficacy in colorectal cancer (CRC), especially in microsatellite stability-CRC, is limited. This study aimed to observe the efficacy of personalized neoantigen vaccine in treating MSS-CRC patients with recurrence or metastasis after surgery and chemotherapy. Candidate neoantigens were analyzed from whole-exome and RNA sequencing of tumor tissues. The safety and immune response were assessed through adverse events and ELISpot. The clinical response was evaluated by progression-free survival (PFS), imaging examination, clinical tumor marker detection, circulating tumor DNA (ctDNA) sequencing. Changes in health-related quality of life were measured by the FACT-C scale. A total of six MSS-CRC patients with recurrence or metastasis after surgery and chemotherapy were administered with personalized neoantigen vaccines. Neoantigen-specific immune response was observed in 66.67% of the vaccinated patients. Four patients remained progression-free up to the completion of clinical trial. They also had a significantly longer progression-free survival time than the other two patients without neoantigen-specific immune response (19 vs. 11 months). Changes in health-related quality of life improved for almost all patients after the vaccine treatment. Our results shown that personalized neoantigen vaccine therapy is likely to be a safe, feasible and effective strategy for MSS-CRC patients with postoperative recurrence or metastasis.
| S-EPMC10264512 | biostudies-literature
Project description:Samples were taken from colorectal cancers in surgically resected specimens in 84 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes between MSI and MSS cancers and, furthermore, to determine the distinct characteristics of proximal and distal MSI cancers. Experiment Overall Design: Eighty-four colorectal cancer patients who had undergone surgical resection of colorectal cancer were studied. To identify molecular signatures of MSI cancers, gene expression profiles were compared between MSI and MSS cancers. Next, we examined the difference in gene expression profiles between proximal and distal MSI cancers.
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Project description:Abstract: Altered expression of microRNAs (miRNAs) is associated with development and progression of various human cancers by regulating the translation of oncogenes and tumor suppressor genes. In colorectal cancer (CRC), these regulators complement the Vogelstein multi-step model of pathogenesis and have the potential of becoming a novel class of tumor biomarkers and therapeutic targets. Using QRT-PCR, we measured the expression of 621 mature miRNAs in 40 CRCs and their paired normal tissues and identified 23 significantly deregulated miRNAs. We subsequently evaluated their association with clinical characteristics of the samples and presence of alterations in the molecular markers of CRC progression. Expression levels of miR-31 were correlated with CA19-9 and miR-18a, miR-21 and miR-31 were associated with mutations in APC gene. To investigate the downstream regulation of the differentially expressed miRNAs identified we integrated putative mRNA target predictions with the results of a meta-analysis of seven public gene expression datasets of normal and tumor samples of CRC patients. Many of the CRC deregulated miRNAs computationally map to targets involved in pathways related to progression. Here one promising candidate pair (miR-1 and MET) was studied and functionally validated. We show that miR-1 can have a tumor suppressor function in CRC by directly down-regulating MET oncogene both at RNA and protein level and that re-expression of miR-1 leads to MET driven reduction of cell proliferation and motility, identifying the miR-1 down-modulation as one of the events that could enhance CRC progression. Note: Each sample has the following information: Type - tissue type (T : Tumor or N: Normal), Patient - patient identifier, Stage - tumor stage (I - IV), Status - disease status at last check-up (ED: evident disease, NED: non-evident disease), CEA - carcinoembryonic antigen (continuous), CA199 - carbohydrate antigen 19-9 (continuous), APC - mutation status of APC gene (0: wild-type, 1: mutated), KRAS - mutation status of KRAS gene (0: wild-type, 1: mutated), chr18qLOH - LOH status of 18q (0: no LOH, 1: LOH), TP53 - mutation status of TP53 gene (0: wild-type, 1: mutated).
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