ArticleJournal of gastroenterology2015
Genome-wide linkage analysis and tumoral characterization reveal heterogeneity in familial colorectal cancer type X.
Article in Journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 45 citations in OpenAlex.
- New insights on familial colorectal cancer type X syndrome.Scientific reports · 2022Article
- Comprehensive analysis of somatic mutator-derived and immune infiltrates related lncRNA signatures of genome instability reveals potential prognostic biomarkers involved in non-small cell lung cancer.Frontiers in genetics · 2022Article
- Phenotypic and genotypic heterogeneity of Lynch syndrome: a complex diagnostic challenge.Familial cancer · 2018Review
- Hereditary Nonpolyposis Colorectal Cancer and Cancer Syndromes: Recent Basic and Clinical Discoveries.Journal of oncology · 2018Review
- Germline INDELs and CNVs in a cohort of colorectal cancer patients: their characteristics, associations with relapse-free survival time, and potential time-varying effects on the risk of relapse.Cancer medicine · 2017Article
- Differential expression of CK20, β-catenin, and MUC2/5AC/6 in Lynch syndrome and familial colorectal cancer type X.BMC clinical pathology · 2017Article
- Molecular approach to genetic and epigenetic pathogenesis of early-onset colorectal cancer.World journal of gastrointestinal oncology · 2016Review
- Classifying early-onset colorectal cancer according to tumor location: new potential subcategories to explore.American journal of cancer research · 2015Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFamilial colorectal cancer type X (FCCTX) fulfils clinical criteria defining Lynch syndrome (LS), but is not related to germline mutations in DNA mismatch-repair genes. Its aetiology remains unexplained and there is little evidence of involvement of the common colorectal carcinogenetic pathways. We aimed to identify susceptibility loci and gain insights into carcinogenic pathways involved FCCTX tumour development.
methodsWe performed a linkage analysis in 22 FCCTX families. We also constructed a tissue microarray in order to define an immunohistochemical (IHC) profile for FCCTX tumours (N = 27) by comparing them to three other types of colorectal tumors: LS (N = 18), stable early-onset (N = 31) and other sporadic disease (N = 80). Additionally, we screened for BRAF/KRAS mutations and determined CpG island methylator phenotype (CIMP) status for all FCCTX tumours.
resultsWe found suggestive evidence of linkage at four chromosomal regions; 2p24.3, 4q13.1, 4q31.21 and 12q21.2-q21.31. We screened genes in 12q21 and ruled out the implication of RASSF9 and NTS, good candidates due to their potential involvement in carcinogenesis and colorectal epithelium development. Based on IHC profiles FCCTX tumours did not form a single, exclusive cluster. They were clearly different from LS, but very similar to stable early onset tumours. The CIMP and chromosomal instability pathways were implicated in one-third and one-quarter of FCCTX cases, respectively. The remaining cases did not have alterations in any known carcinogenic pathways.
conclusionsOur results highlight the heterogeneity of FCCTX tumours and call into question the utility of using only clinical criteria to identify FCCTX cases.
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