The Identification of Alternative Polyadenylation in Stomach Adenocarcinomas Using the Genotype-Tissue Expression Project and the Cancer Genome Atlas– Stomach Adenocarcinoma Profiles

ST7 (Suppression of Tumorigenicity 7) was reported as a protein playing a role in maintaining cellular structure. This study aims to investigate the ST7 alteration profiles and frequency of alteration in different cancers using data from The Cancer Genome Atlas (TCGA). The correlation between alterations of ST7 and angiogenesis-related genes, SERPINE1, MMP13, and VEGFA, was determined and the relation between ST7 and genes involved in suppression of ST7 transcription, PRMT5 and SMARCA4, were also analyzed. Data of 6 cancer groups from The Cancer Genome Atlas (TCGA) including ovarian serous cystadenocarcinoma (OSC), liver hepatocellular carcinoma (LHC), bladder urothelial adenocarcinoma (BUA), stomach adenocarcinoma (SC), prostate adenocarcinoma (PRAD) and glioblastoma multiforme (GBM) were downloaded for this study. The results indicated that 3 alteration patterns including amplification, missense mutation, and deletion were observed in 6 cancer studies. Gene pair between ST7 and SERPINE1 indicated the co-occurrent alteration in BUC, OSC and SC (p < 0.05). However, no association between alterations of these 2 genes and survival events in our study was observed. Shorter overall survival rate and disease-free survival were found in BUC patients with ST7, PRMT5, and SMARCA4 alterations. These findings suggest that using TCGA data can target the potential genes involved in carcinogenesis. Combining ST7 with PRMT5 and SMARCA4 could be used as indicators for analyzing the patient survival in BUC patients and may serve as the potential therapeutic target for cancer in the future.

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Identification of key miRNAs and genes associated with stomach adenocarcinoma from The Cancer Genome Atlas database

FEBS Open Bio ◽

10.1002/2211-5463.12365 ◽

2018 ◽

Vol 8 (2) ◽

pp. 279-294 ◽

Cited By ~ 8

Author(s):

Jixi Liu ◽

Fang Liu ◽

Yanfen Shi ◽

Huangying Tan ◽

Lei Zhou

Keyword(s):

Cancer Genome ◽

The Cancer Genome Atlas ◽

Cancer Genome Atlas ◽

Stomach Adenocarcinoma ◽

Genome Atlas

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Increased Expression of T-Box Transcription Factor Protein 21 (TBX21) in Skin Cutaneous Melanoma Predicts Better Prognosis: A Study Based on The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) Databases

Medical Science Monitor ◽

10.12659/msm.923087 ◽

2020 ◽

Vol 26 ◽

Author(s):

Xingying Zhang ◽

Xin Wen ◽

Ning Feng ◽

Aoxing Chen ◽

Senbang Yao ◽

...

Keyword(s):

Transcription Factor ◽

Cutaneous Melanoma ◽

Tissue Expression ◽

Cancer Genome ◽

The Cancer Genome Atlas ◽

T Box ◽

Cancer Genome Atlas ◽

Genome Atlas

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Special Report: The Cancer Genome Atlas Begins with 3-Year, $100 Million Pilot

PsycEXTRA Dataset ◽

10.1037/e481292006-009 ◽

2005 ◽

Author(s):

Keyword(s):

Cancer Genome ◽

The Cancer Genome Atlas ◽

Special Report ◽

Cancer Genome Atlas ◽

Genome Atlas

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Differences in endometrial cancer molecular portraits based on ethnicity in The Cancer Genome Atlas

10.26226/morressier.59ba7298d462b80296ca20c6 ◽

2017 ◽

Author(s):

David Guttery

Keyword(s):

Endometrial Cancer ◽

Cancer Genome ◽

The Cancer Genome Atlas ◽

Cancer Genome Atlas ◽

Genome Atlas

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Exceptional Chemotherapy Response in Metastatic Colorectal Cancer Associated With Hyper-Indel–Hypermutated Cancer Genome and Comutation of POLD1 and MLH1

JCO Precision Oncology ◽

10.1200/po.16.00015 ◽

2017 ◽

pp. 1-12

Author(s):

Manish R. Sharma ◽

James T. Auman ◽

Nirali M. Patel ◽

Juneko E. Grilley-Olson ◽

Xiaobei Zhao ◽

...

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Somatic Mutation ◽

Mutation Rate ◽

Germ Line ◽

Cancer Genome ◽

The Cancer Genome Atlas ◽

Response To Chemotherapy ◽

Cancer Genome Atlas ◽

Genome Atlas

Purpose A 73-year-old woman with metastatic colon cancer experienced a complete response to chemotherapy with dose-intensified irinotecan that has been durable for 5 years. We sequenced her tumor and germ line DNA and looked for similar patterns in publicly available genomic data from patients with colorectal cancer. Patients and Methods Tumor DNA was obtained from a biopsy before therapy, and germ line DNA was obtained from blood. Tumor and germline DNA were sequenced using a commercial panel with approximately 250 genes. Whole-genome amplification and exome sequencing were performed for POLE and POLD1. A POLD1 mutation was confirmed by Sanger sequencing. The somatic mutation and clinical annotation data files from the colon (n = 461) and rectal (n = 171) adenocarcinoma data sets were downloaded from The Cancer Genome Atlas data portal and analyzed for patterns of mutations and clinical outcomes in patients with POLE- and/or POLD1-mutated tumors. Results The pattern of alterations included APC biallelic inactivation and microsatellite instability high (MSI-H) phenotype, with somatic inactivation of MLH1 and hypermutation (estimated mutation rate > 200 per megabase). The extremely high mutation rate led us to investigate additional mechanisms for hypermutation, including loss of function of POLE. POLE was unaltered, but a related gene not typically associated with somatic mutation in colon cancer, POLD1, had a somatic mutation c.2171G>A [p.Gly724Glu]. Additionally, we noted that the high mutation rate was largely composed of dinucleotide deletions. A similar pattern of hypermutation (dinucleotide deletions, POLD1 mutations, MSI-H) was found in tumors from The Cancer Genome Atlas. Conclusion POLD1 mutation with associated MSI-H and hyper-indel–hypermutated cancer genome characterizes a previously unrecognized variant of colon cancer that was found in this patient with an exceptional response to chemotherapy.

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