ArticlePloS one2012
A comprehensive characterization of genome-wide copy number aberrations in colorectal cancer reveals novel oncogenes and patterns of alterations.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- Focus on 16p13.3 Locus in Colon Cancer.PloS one · 2015Trial
- Somatic copy number alterations associated with Japanese or endometriosis in ovarian clear cell adenocarcinoma.PloS one · 2015Trial
- Genomic landscape of metastatic colorectal cancer.Nature communications · 2014Trial
- Integrated analysis of copy number variation and genome-wide expression profiling in colorectal cancer tissues.PloS one · 2014Trial
- Tackling exosome and nuclear receptor interaction: an emerging paradigm in the treatment of chronic diseases.Military Medical Research · 2024Review
- The genomic landscape of 2,023 colorectal cancers.Nature · 2024Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- Genome-wide analysis of colorectal cancer based on gene-based somatic copy number alterations during neoplastic progression within the same tumor.Cancer medicine · 2023Article
- Copy Number Variations as Determinants of Colorectal Tumor Progression in Liquid Biopsies.International journal of molecular sciences · 2023Review
- Identification of a Class of WNK Isoform-Specific Inhibitors Through High-Throughput Screening.Drug design, development and therapy · 2023Article
- Synthesis and Structural Characterization of Novel Trihalo-sulfone Inhibitors of WNK1.ACS medicinal chemistry letters · 2022Article
- Article
- Copy Number Alterations as Novel Biomarkers and Therapeutic Targets in Colorectal Cancer.Cancers · 2022Review
- Article
- TYMS-TM4SF4 axis promotes the progression of colorectal cancer by EMT and upregulating stem cell marker.American journal of cancer research · 2022Article
- Article
- Copy Number Variants Captured by the Array Comparative Genomic Hybridization in a Cohort of Patients Affected with Hereditary Colorectal Cancer in Sri Lanka: The First CNV Analysis Study of the Hereditary Colorectal Cancer in the Sri Lankan Population.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- A genome-wide study of the relationship between chromosomal abnormalities and gene expression in colorectal tumors.Genes, chromosomes & cancer · 2021Article
- Signatures of Discriminative Copy Number Aberrations in 31 Cancer Subtypes.Frontiers in genetics · 2021Article
- Genomic amplification of chromosome 20q13.33 is the early biomarker for the development of sporadic colorectal carcinoma.BMC medical genomics · 2020Article
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To develop a comprehensive overview of copy number aberrations (CNAs) in stage-II/III colorectal cancer (CRC), we characterized 302 tumors from the PETACC-3 clinical trial. Microsatellite-stable (MSS) samples (n = 269) had 66 minimal common CNA regions, with frequent gains on 20 q (72.5%), 7 (41.8%), 8 q (33.1%) and 13 q (51.0%) and losses on 18 (58.6%), 4 q (26%) and 21 q (21.6%). MSS tumors have significantly more CNAs than microsatellite-instable (MSI) tumors: within the MSI tumors a novel deletion of the tumor suppressor WWOX at 16 q23.1 was identified (p<0.01). Focal aberrations identified by the GISTIC method confirmed amplifications of oncogenes including EGFR, ERBB2, CCND1, MET, and MYC, and deletions of tumor suppressors including TP53, APC, and SMAD4, and gene expression was highly concordant with copy number aberration for these genes. Novel amplicons included putative oncogenes such as WNK1 and HNF4A, which also showed high concordance between copy number and expression. Survival analysis associated a specific patient segment featured by chromosome 20 q gains to an improved overall survival, which might be due to higher expression of genes such as EEF1B2 and PTK6. The CNA clustering also grouped tumors characterized by a poor prognosis BRAF-mutant-like signature derived from mRNA data from this cohort. We further revealed non-random correlation between CNAs among unlinked loci, including positive correlation between 20 q gain and 8 q gain, and 20 q gain and chromosome 18 loss, consistent with co-selection of these CNAs. These results reinforce the non-random nature of somatic CNAs in stage-II/III CRC and highlight loci and genes that may play an important role in driving the development and outcome of this disease.
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