Background/aim: Bladder urothelial carcinoma (BUC) poses a significant health challenge, ranking as the fourth most common cancer among men in the United States, with a mortality rate of approximately 20%. Genetic abnormalities such as mutations in the telomerase reverse transcriptase (TERT) gene and loss of heterozygosity (LOH) on chromosome 9 are commonly observed in BUC; however, many genes involved remain unidentified. This study aimed to explore the role of HOOK3 in BUC and its impact on survival.
Materials And Methods: Using data from The Cancer Genome Atlas (TCGA) and cBioPortal, we performed differential gene expression and survival analyses to compare the patients with and without HOOK3 amplification.
Results: Our findings revealed that 2.2% of genes were up-regulated and 5.3% down-regulated in the HOOK3-amplified group. These changes suggest that HOOK3 amplification is linked to distinct gene expression patterns, with a higher proportion of down-regulated genes. Pathway enrichment related to chromatin remodeling, ion transport, and mitochondrial function suggests that HOOK3 may promote genomic stability and transcriptional regulation, contributing to tumor suppression. The involvement of mitochondrial and ribosomal pathways in protein synthesis and chromosome segregation may also protect against chromosomal abnormalities and uncontrolled cell growth. HOOK3 amplification appears to correlate with improved patient survival.
Conclusion: These results suggest a potential protective role of HOOK3 amplification in BUC. Further research is needed to explore the underlying mechanisms and their therapeutic potential for reducing BUC-related mortality.
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http://dx.doi.org/10.21873/anticanres.17343 | DOI Listing |
Anticancer Res
December 2024
Department of Medicine, Division of Hematology & Oncology, University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A.;
Acta Neuropathol Commun
July 2024
Department of Pathology, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-Gu, Seoul, Republic of Korea.
Orphanet J Rare Dis
June 2024
Cancer Discovery Hub, National Cancer Centre Singapore, Singapore, Singapore.
PLoS One
October 2020
Department of Hematopathology, Section of Clinical Cytogenetics, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Somatic copy number alterations (CNA) are common in endometrial serous carcinoma (ESC). We used the Tumor Cancer Genome Atlas Pan Cancer dataset (TCGA Pan Can) to explore the impact of somatic CNA and gene expression levels (mRNA) of cancer-related genes in ESC. Results were correlated with clinico-pathologic parameters such as age of onset, disease stage, progression-free survival (PFS) and overall survival (OS) (n = 108).
View Article and Find Full Text PDFJ Clin Invest
June 2013
Division of Medical Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Small intestine neuroendocrine tumors (SI-NETs) are the most common malignancy of the small bowel. Several clinical trials target PI3K/Akt/mTOR signaling; however, it is unknown whether these or other genes are genetically altered in these tumors. To address the underlying genetics, we analyzed 48 SI-NETs by massively parallel exome sequencing.
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