ArticleBMC medical genomics2020
Genomic amplification of chromosome 20q13.33 is the early biomarker for the development of sporadic colorectal carcinoma.
Article in BMC medical genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 15 citations in OpenAlex.
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- The possibility of prognostic and functional values of the 8q24 and 20q13 chromosomal bands in colorectal cancer.Molecular biology research communications · 2026Article
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- Integrated analyses of multi-omic data derived from paired primary lung cancer and brain metastasis reveal the metabolic vulnerability as a novel therapeutic target.Genome medicine · 2024Article
- Use of Enzymatically Converted Cell-Free DNA (cfDNA) Data for Copy Number Variation-Linked Fragmentation Analysis Allows for Early Colorectal Cancer Detection.International journal of molecular sciences · 2024Article
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Somatic Mutational Landscape in Mexican Patients:International journal of molecular sciences · 2022Article
- Clinical Impact of X-Ray Repair Cross-Complementary 1 (Journal of inflammation research · 2021Article
- Identification of Germline Mutations in Genes Involved in Classic FAP in Patients from Northern Brazil.Cancer diagnosis & prognosisArticle
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Authors and funding
4 authors at 3 institutions in 4 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal carcinoma (CRC) is the third most common cancer in the world and also the third leading cause of cancer-related mortality in Taiwan. CRC tumorigenesis is a multistep process, starting from mutations causing loss of function of tumor suppressor genes, canonically demonstrated in adenomatous polyposis coli pathogenesis. Although many genes or chromosomal alterations have been shown to be involved in this process, there are still unrecognized molecular events within CRC tumorigenesis. Elucidating these mechanisms may help improve the management and treatment.
methodsIn this study, we aimed to identify copy number alteration of the smallest chromosomal regions that is significantly associated with sporadic CRC tumorigenesis using high-resolution array-based Comparative Genomic Hybridization (aCGH) and quantitative Polymerase chain reaction (qPCR). In addition, microsatellite instability assay and sequencing-based mutation assay were performed to illustrate the initiation event of CRC tumorigenesis.
resultsA total of 571 CRC patients were recruited and 377 paired CRC tissues from sporadic CRC cases were used to define the smallest regions with chromosome copy number changes. In addition, 198 colorectal polyps from 160 patients were also used to study the role of 20q13.33 gain in CRC tumorigenesis. We found that gain in 20q13.33 is the main chromosomal abnormalities in this patient population and counts 50.9 and 62.8% in CRC and colon polyps, respectively. Furthermore, APC and KRAS gene mutations were profiled simultaneously and co-analyzed with microsatellite instability and 20q13.33 gain in CRC patients. Our study showed that the frequency of 20q13.33 copy number gain was highest among all reported CRC mutations.
conclusionAs APC or KRAS mutations are currently identified as the most important targets for CRC therapy, this study proposes that 20q13.33 copy number gain and the associated chromosomal genes function as promising biomarkers for both early stage detection and targeted therapy of sporadic CRCs in the future.
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