ArticleCancer genomics & proteomics
Colitic Cancer Develops Through Mutational Alteration Distinct from that in Sporadic Colorectal Cancer: A Comparative Analysis of Mutational Rates at Each Step.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Gene panel testing detects important genetic alterations in ulcerative colitis-associated colorectal neoplasia.Oncology letters · 2022Article
- Genetic Profiling of Colorectal Carcinomas of Patients with Primary Sclerosing Cholangitis and Inflammatory Bowel Disease.Inflammatory bowel diseases · 2022Article
- 2b or Not 2b: How Opposing FGF Receptor Splice Variants Are Blocking Progress in Precision Oncology.Journal of oncology · 2021Review
- Article
- Hypermethylation of Corticotropin Releasing Hormone Receptor-2 Gene in Ulcerative Colitis Associated Colorectal Cancer.In vivo (Athens, Greece)Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPatients with ulcerative colitis (UC) are at risk of UC-associated colorectal cancer (CRC); however, little is known about genetic alterations occurring during UC carcinogenesis. We examined mutational changes in patients with colitic cancer and the features that differed between the carcinogenesis of UC and sporadic CRC. MATERIAL AND
methodsSpecimens were obtained from the non-neoplastic mucosa and cancer cells of 12 patients with colitic cancer. The mutational rate of oncogenes in colitic cancer was analyzed and compared to that of oncogenes in sporadic CRC.
resultsWe observed a lower mutation rate in adenomatous polyposis coli (APC) (16.7%(2/12) vs. 75.9%(161/212), respectively, p=0.0001) and KRAS (16.7%(2/12) vs. 42% (89/212), respectively, p=0.04) in colitic cancer than in sporadic CRC. With respect to cadherin 1 (CDH1) and fibroblast growth factor receptor 2 (FGFR2), the mutational rates for non-neoplastic colorectal mucosa were similar to those in sporadic CRC.
conclusionWe demonstrated that mutational rates for APC and KRAS differ between colitic cancer and sporadic CRC. Furthermore, we revealed that CDH1 and FGFR2 become mutated at an earlier stage in colitic carcinogenesis than in sporadic CRC.
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