ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
CpG island methylator phenotype-positive tumors in the absence of MLH1 methylation constitute a distinct subset of duodenal adenocarcinomas and are associated with poor prognosis.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Evaluation of Systemic Treatments of Small Intestinal Adenocarcinomas: A Systematic Review and Meta-analysis.JAMA network open · 2023Pooled it
- Clinical practice guidelines for duodenal cancer 2021.Journal of gastroenterology · 2022Guideline
- Trial
- Methylation-sensitive high-resolution melting technology is a simple and sensitive method to detect germline epimutation of the MLH1 gene promoter.Clinical epigenetics · 2025Article
- Duodenal Adenocarcinoma with a Gastric Phenotype Demonstrating a Rapidly Progressive Course.Internal medicine (Tokyo, Japan) · 2025Article
- Epigenetic reprogramming in gastrointestinal cancer: biology and translational perspectives.MedComm · 2024Review
- Mixed adenoneuroendocrine carcinoma of the non-ampullary duodenum with mismatch repair deficiency: a rare case report.Medical molecular morphology · 2022Article
- Deciphering the etiology and role in oncogenic transformation of the CpG island methylator phenotype: a pan-cancer analysis.Briefings in bioinformatics · 2022Article
- Small Bowel Epithelial Precursor Lesions: A Focus on Molecular Alterations.International journal of molecular sciences · 2021Review
- Screening and Prognostic Value of Methylated Septin9 and its Association With Clinicopathological and Molecular Characteristics in Colorectal Cancer.Frontiers in molecular biosciences · 2021Article
- Integrated genetic and epigenetic analysis of cancer-related genes in non-ampullary duodenal adenomas and intramucosal adenocarcinomas.The Journal of pathology · 2020Article
- Beyond bevacizumab: a review of targeted agents in metastatic small bowel adenocarcinoma.Medical oncology (Northwood, London, England) · 2020Review
- Article
- Molecular alterations and PD-L1 expression in non-ampullary duodenal adenocarcinoma: Associations among clinicopathological, immunophenotypic and molecular features.Scientific reports · 2019Article
- Article
- Clinical significance of cancer specific methylation of the CDO1 gene in small bowel cancer.PloS one · 2019Article
- Genetic Alterations of Periampullary and Pancreatic Ductal Adenocarcinoma: An Overview.Current genomics · 2018Review
- Pathologic Response to Preoperative Therapy as a Novel Prognosticator for Ampullary and Duodenal Adenocarcinoma.Annals of surgical oncology · 2017Article
- CpG island methylator phenotype in adenocarcinomas from the digestive tract: Methods, conclusions, and controversies.World journal of gastrointestinal oncology · 2017Article
- Tumors with unmethylated MLH1 and the CpG island methylator phenotype are associated with a poor prognosis in stage II colorectal cancer patients.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
purposeLittle information is available on genetic and epigenetic changes in duodenal adenocarcinomas. The purpose was to identify possible subsets of duodenal adenocarcinomas based on microsatellite instability (MSI), DNA methylation, mutations in the KRAS and BRAF genes, clinicopathologic features, and prognosis. EXPERIMENTAL
designDemographics, tumor characteristics, and survival were available for 99 duodenal adenocarcinoma patients. Testing for KRAS and BRAF mutations, MSI, MLH1 methylation, and CpG island methylator phenotype (CIMP) status was conducted. A Cox proportional hazard model was built to predict survival.
resultsCIMP(+) was detected in 27 of 99 (27.3%) duodenal adenocarcinomas and was associated with MSI (P = 0.011) and MLH1 methylation (P < 0.001), but not with KRAS mutations (P = 0.114), as compared with CIMP(-) tumors. No BRAF V600E mutation was detected. Among the CIMP(+) tumors, 15 (55.6%) were CIMP(+)/MLH1-unmethylated (MLH1-U). Kaplan-Meier analysis showed that tumors classified by CIMP, CIMP/MLH1 methylation status, or CIMP/MSI status could predict overall survival (OS; P = 0.047, 0.002, and 0.002, respectively), whereas CIMP/MLH1 methylation status could also predict time-to-recurrence (TTR; P = 0.016). In multivariate analysis, CIMP/MLH1 methylation status showed a significant prognostic value in both OS (P < 0.001) and TTR (P = 0.023). Patients with CIMP(+)/MLH1-U tumors had the worst OS and TTR.
conclusionsOur results showed existence of CIMP in duodenal adenocarcinomas. The combination of CIMP(+)/MLH1-U seems to be independently associated with poor prognosis in patients with duodenal adenocarcinomas. This study also suggests that BRAF mutations are not involved in duodenal tumorigenesis, MSI, or CIMP development.
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