Clinical and Molecular Features of Post-Colonoscopy Colorectal Cancers.


Journal

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775

Informations de publication

Date de publication:
12 2019
Historique:
received: 16 11 2018
revised: 15 02 2019
accepted: 25 02 2019
pubmed: 2 4 2019
medline: 16 3 2021
entrez: 2 4 2019
Statut: ppublish

Résumé

Post-colonoscopy colorectal cancers (PCCRCs) may arise from missed lesions or due to molecular features of tumors that allow them to grow rapidly. We aimed to compare clinical, pathology, and molecular features of PCCRCs (those detected within 6-60 months of colonoscopy) and detected CRCs (those detected within 6 months of a colonoscopy). Within a population-based cross-sectional study of incident CRC cases in Utah (from 1995 through 2009), we identified PCCRCs (those cancers that developed within 5 years of a colonoscopy) and matched the patients by age, sex, and hospital site to patients with detected CRC. Archived specimens were retrieved and tested for microsatellite instability (MSI), CpG island methylation, and mutations in KRAS and BRAF. There were 2659 cases of CRC diagnosed within the study window; 6% of these (n = 159) were defined as PCCRCs; 84 of these cases had tissue available and were matched to 84 subjects with detected CRC. Higher proportions of PCCRCs than detected CRCs formed in the proximal colon (64% vs 44%; P = .016) and were of an early stage (86% vs 69%; P = .040). MSI was observed in 32% of PCCRCs compared with 13% of detected CRCs (P = .005). The other molecular features were found in similar proportions of PCCRCs and detected CRCs. In a multivariable logistic regression, MSI (odds ratio, 4.20; 95% CI, 1.58-11.14) was associated with PCCRC. There was no difference in 5-year survival between patients with PCCRCs vs detected CRCs. In this population-based cross-sectional study of incident CRC cases in Utah, we found PCCRCs to be more likely to arise in the proximal colon and demonstrate MSI, so PCCRCs and detected CRC appear to have different features or processes of tumorigenesis. Additional studies are needed to determine if post-colonoscopy cancers arise through a specific genetic pathway.

Sections du résumé

BACKGROUND & AIMS
Post-colonoscopy colorectal cancers (PCCRCs) may arise from missed lesions or due to molecular features of tumors that allow them to grow rapidly. We aimed to compare clinical, pathology, and molecular features of PCCRCs (those detected within 6-60 months of colonoscopy) and detected CRCs (those detected within 6 months of a colonoscopy).
METHODS
Within a population-based cross-sectional study of incident CRC cases in Utah (from 1995 through 2009), we identified PCCRCs (those cancers that developed within 5 years of a colonoscopy) and matched the patients by age, sex, and hospital site to patients with detected CRC. Archived specimens were retrieved and tested for microsatellite instability (MSI), CpG island methylation, and mutations in KRAS and BRAF. There were 2659 cases of CRC diagnosed within the study window; 6% of these (n = 159) were defined as PCCRCs; 84 of these cases had tissue available and were matched to 84 subjects with detected CRC.
RESULTS
Higher proportions of PCCRCs than detected CRCs formed in the proximal colon (64% vs 44%; P = .016) and were of an early stage (86% vs 69%; P = .040). MSI was observed in 32% of PCCRCs compared with 13% of detected CRCs (P = .005). The other molecular features were found in similar proportions of PCCRCs and detected CRCs. In a multivariable logistic regression, MSI (odds ratio, 4.20; 95% CI, 1.58-11.14) was associated with PCCRC. There was no difference in 5-year survival between patients with PCCRCs vs detected CRCs.
CONCLUSION
In this population-based cross-sectional study of incident CRC cases in Utah, we found PCCRCs to be more likely to arise in the proximal colon and demonstrate MSI, so PCCRCs and detected CRC appear to have different features or processes of tumorigenesis. Additional studies are needed to determine if post-colonoscopy cancers arise through a specific genetic pathway.

Identifiants

pubmed: 30930275
pii: S1542-3565(19)30246-0
doi: 10.1016/j.cgh.2019.02.040
pii:
doi:

Substances chimiques

KRAS protein, human 0
BRAF protein, human EC 2.7.11.1
Proto-Oncogene Proteins B-raf EC 2.7.11.1
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2731-2739.e2

Subventions

Organisme : NCI NIH HHS
ID : P01 CA073992
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA040641
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261201000026C
Pays : United States

Informations de copyright

Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.

Auteurs

N Jewel Samadder (NJ)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Gastroenterology), University of Utah, Salt Lake City, Utah; Department of Medicine (Gastroenterology), Mayo Clinic, Phoenix, Arizona. Electronic address: Samadder.jewel@mayo.edu.

Deb Neklason (D)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Genetic Epidemiology), University of Utah, Salt Lake City, Utah.

Angela Snow (A)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Wade Samowitz (W)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Pathology, University of Utah, Salt Lake City, Utah.

Melissa H Cessna (MH)

Department of Pathology and Biorepository, Intermountain Healthcare, Salt Lake City, Utah.

Kerry Rowe (K)

Department of Medicine, Intermountain Healthcare, Salt Lake City, Utah.

Iqbal Sandhu (I)

Department of Bioinformatics, Intermountain Healthcare, Salt Lake City, Utah.

Kenneth Boucher (K)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Lisa Pappas (L)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Ken Robert Smith (KR)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Jathine Wong (J)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

Karen Curtin (K)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Genetic Epidemiology), University of Utah, Salt Lake City, Utah.

Dawn Provenzale (D)

Department of Medicine (Gastroenterology), Duke University, Durham, North Carolina; VA Cooperative Studies Program Epidemiology Center, Departments of Medicine (Gastroenterology) and Clinical Genomics, Mayo Clinic, Phoenix, Arizona.

Randall W Burt (RW)

Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah; Department of Medicine (Gastroenterology), University of Utah, Salt Lake City, Utah; Department of Oncological Sciences, University of Utah, Salt Lake City, Utah.

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Classifications MeSH