ArticlePloS one2010
Distinct genetic alterations in colorectal cancer.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- X-ray repair cross-complementing group 1 Arg399Gln gene polymorphism and susceptibility to colorectal cancer:a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- Genomic alterations in rectal tumors and response to neoadjuvant chemoradiotherapy: an exploratory study.Radiation oncology (London, England) · 2011Trial
- Functional role of small extrachromosomal circular DNA in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Multi-omic characterization of consensus molecular subtype 1 (CMS1) colorectal cancer with dampened immune response improves precision medicine.Molecular oncology · 2025Article
- Data-Driven Identification of Early Cancer-Associated Genes via Penalized Trans-Dimensional Hidden Markov Models.Biomolecules · 2025Article
- A Hyaluronan and Proteoglycan Link Protein 1 Matrikine: Role of Matrix Metalloproteinase 2 in Multiple Myeloma NF-κB Activation and Drug Resistance.Molecular cancer research : MCR · 2022Article
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- Genomic and transcriptomic analyses reveal a tandem amplification unit of 11 genes and mutations in mismatch repair genes in methotrexate-resistant HT-29 cells.Experimental & molecular medicine · 2021Article
- Transcriptional dysregulation by aberrant enhancer activation and rewiring in cancer.Cancer science · 2021Review
- Loss of Hyaluronan and Proteoglycan Link Protein-1 Induces Tumorigenesis in Colorectal Cancer.Frontiers in oncology · 2021Article
- Structure of the EphB6 receptor ectodomain.PloS one · 2021Article
- Noncoding RNAs in inflammation and colorectal cancer.RNA biology · 2020Article
- Genomic amplification of chromosome 20q13.33 is the early biomarker for the development of sporadic colorectal carcinoma.BMC medical genomics · 2020Article
- Decreased copy-neutral loss of heterozygosity in African American colorectal cancers.Genes, chromosomes & cancer · 2020Article
- Twist1 induces chromosomal instability (CIN) in colorectal cancer cells.Human molecular genetics · 2020Article
- Restoration of KMT2C/MLL3 in human colorectal cancer cells reinforces genome-wide H3K4me1 profiles and influences cell growth and gene expression.Clinical epigenetics · 2020Article
- A review on role of ATM gene in hereditary transfer of colorectal cancer.Acta bio-medica : Atenei Parmensis · 2019Review
- Clinical significance of ADAM29 promoting the invasion and growth of gastric cancer cellsOncology letters · 2018Article
- Genetic and epigenetic alterations of colorectal cancer.Intestinal research · 2018Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundColon cancer (CRC) development often includes chromosomal instability (CIN) leading to amplifications and deletions of large DNA segments. Epidemiological, clinical, and cytogenetic studies showed that there are considerable differences between CRC tumors from African Americans (AAs) and Caucasian patients. In this study, we determined genomic copy number aberrations in sporadic CRC tumors from AAs, in order to investigate possible explanations for the observed disparities. METHODOLOGY/PRINCIPAL
findingsWe applied genome-wide array comparative genome hybridization (aCGH) using a 105k chip to identify copy number aberrations in samples from 15 AAs. In addition, we did a population comparative analysis with aCGH data in Caucasians as well as with a widely publicized list of colon cancer genes (CAN genes). There was an average of 20 aberrations per patient with more amplifications than deletions. Analysis of DNA copy number of frequently altered chromosomes revealed that deletions occurred primarily in chromosomes 4, 8 and 18. Chromosomal duplications occurred in more than 50% of cases on chromosomes 7, 8, 13, 20 and X. The CIN profile showed some differences when compared to Caucasian alterations. CONCLUSIONS/SIGNIFICANCE: Chromosome X amplification in male patients and chromosomes 4, 8 and 18 deletions were prominent aberrations in AAs. Some CAN genes were altered at high frequencies in AAs with EXOC4, EPHB6, GNAS, MLL3 and TBX22 as the most frequently deleted genes and HAPLN1, ADAM29, SMAD2 and SMAD4 as the most frequently amplified genes. The observed CIN may play a distinctive role in CRC in AAs.
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