High ANKZF1 expression is associated with poor overall survival and recurrence-free survival in colon cancer

To investigate the association and prognostic value of gene for survival in colorectal cancer, the mechanism of level alteration and correlated signaling pathways is involved. The Cancer Genome Atlas COREAD dataset was analyzed by bioinformatical investigation. High expression is associated with poo...

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Bibliographic Details
Published in:Future oncology (London, England) England), 2019-06, Vol.15 (18), p.2093-2106
Main Authors: Zhou, Xin, Shang, Yan-Na, Lu, Ran, Fan, Chuan-Wen, Mo, Xian-Ming
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Apoptosis
Biomarkers
Biomarkers, Tumor
Cancer therapies
Carrier Proteins - genetics
Cell cycle
Chemotherapy
Colonic Neoplasms - genetics
Colonic Neoplasms - mortality
Colonic Neoplasms - pathology
Colonic Neoplasms - therapy
Colorectal cancer
Computational Biology - methods
Female
Gene Expression
Genomics
High-Throughput Nucleotide Sequencing
Humans
Inflammatory bowel disease
Kaplan-Meier Estimate
Kinases
Male
Medical prognosis
Metastasis
Microsatellite Instability
Middle Aged
Mutation
Neoplasm Grading
Neoplasm Staging
Patients
Prognosis
Proteins
Quality control
Surveillance
Survival Analysis
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Summary:To investigate the association and prognostic value of gene for survival in colorectal cancer, the mechanism of level alteration and correlated signaling pathways is involved. The Cancer Genome Atlas COREAD dataset was analyzed by bioinformatical investigation. High expression is associated with poor overall survival (hazard ratio [HR]: 2.094; 95% CI: 1.188-3.689; p = 0.011) and recurrence-free survival (HR: 1.762; 95% CI: 1.021-3.042; p = 0.042) in colon cancer. Bioinformatical analysis showed was upregulated by amplification and exon expression. was associated with angiogenesis and cancer signaling pathways. High is an independent factor of poor survival (overall survival and recurrence-free survival) in colon cancer by taking part in angiogenesis and some cancer signaling pathways.
ISSN:1479-6694
1744-8301
1744-8301
DOI:10.2217/fon-2018-0920