Journal article
Targeted mutational analysis of inflammatory bowel disease–associated colorectal cancers
Human pathology, Vol.89, pp.44-50
07/2019
DOI: 10.1016/j.humpath.2019.04.013
PMID: 31054900
Abstract
Inflammatory bowel disease–associated colorectal carcinomas (IBD-CRCs) develop in a background of chronic inflammation, and thus, the molecular landscape of these tumors likely differs from that of sporadic colorectal cancer. To add to emerging data on molecular alterations present in these tumors, we analyzed our institution's cohort of IBD-CRCs. CRCs resected from patients with IBD underwent molecular analysis via a 50-gene hot-spot solid tumor panel (OncoScreen ST2.0). In-house sporadic CRCs and The Cancer Genome Atlas project data were used for comparison. Fifty-five IBD-CRCs from 48 patients were successfully analyzed. Mutations in TP53 were most common and were present in 69% of IBD-CRCs; a similar percentage of TP53 mutations was detected in sporadic colorectal carcinomas (70%). APC and KRAS mutations were significantly less common in IBD-CRCs than in sporadic CRCs (15% versus 53%, P < .001 and 20% versus 38%, P = .02, respectively). Additionally, the potentially targetable IDH1 R132 mutation was present in 7% of IBD-CRCs but only 1% of sporadic CRCs and The Cancer Genome Atlas CRCs; alterations in other genes with potential targeted therapies were very rare. In conclusion, IBD-CRCs exhibit molecular differences when compared to sporadic CRCs, suggesting different pathways of carcinogenesis, although certain alterations are common to both types of tumors. IDH1 mutations are present in a subset of IBD-CRCs, which may expand therapeutic options in the future.
•TP53 mutations are common in inflammatory bowel disease–associated colon cancer.•APC and KRAS mutations are much less common in these tumors.•Potentially targetable IDH1 R132 mutations are present in a subset of these tumors.
Details
- Title: Subtitle
- Targeted mutational analysis of inflammatory bowel disease–associated colorectal cancers
- Creators
- Lindsay Alpert - University of ChicagoLindsay Yassan - University of ChicagoRachel Poon - University of ChicagoSabah Kadri - University of ChicagoNifang Niu - University of ChicagoSushant A. Patil - University of ChicagoIbro Mujacic - University of ChicagoDavid Montes - University of ChicagoFilippo Galbo - University of ChicagoMichelle N. Wurst - University of ChicagoChao Jie Zhen - University of ChicagoRussell D. Cohen - University of ChicagoDavid T. Rubin - University of ChicagoJoel R. Pekow - University of ChicagoChristopher R. Weber - University of ChicagoShu-Yuan Xiao - University of ChicagoJohn Hart - University of ChicagoJeremy Segal - University of ChicagoNamrata Setia - University of Chicago
- Resource Type
- Journal article
- Publication Details
- Human pathology, Vol.89, pp.44-50
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.humpath.2019.04.013
- PMID
- 31054900
- ISSN
- 0046-8177
- eISSN
- 1532-8392
- Number of pages
- 7
- Language
- English
- Date published
- 07/2019
- Academic Unit
- Stead Family Department of Pediatrics; Medical Genetics and Genomics
- Record Identifier
- 9984701542802771
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