ArticleDigestive diseases and sciences2018
Molecular Profiling Based on KRAS/BRAF Mutation, Methylation, and Microsatellite Statuses in Serrated Lesions.
Article in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed.
- Whole Tumor Heterogeneity Topography (WTHT)-A New Approach for Assessment of Intratumor Mutational Heterogeneity in Colorectal Adenomas.International journal of molecular sciences · 2026Article
- Do Colorectal Serrated and Non-Serrated Adenocarcinomas Differ in Somatic Mutations and Clinicopathologic Features?Medicina (Kaunas, Lithuania) · 2025Article
- Genome-wide association study of colorectal polyps identified highly overlapping polygenic architecture with colorectal cancer.Journal of human genetics · 2022Article
- Duodenal sessile serrated adenoma/polyp with characteristic endoscopic and pathologic features.Clinical journal of gastroenterology · 2021Article
- Molecular Features of the Serrated Pathway to Colorectal Cancer: Current Knowledge and Future Directions.Gut and liver · 2021Review
- The Frequency of DNA Mismatch Repair Deficiency Is Very Low in Surgically Resected Lung Carcinoma.Frontiers in oncology · 2021Article
- Serrated adenomas with a BRAF mutation in a young patient with familial adenomatous polyposis.International journal of colorectal disease · 2020Article
- Traditional serrated adenoma has two distinct genetic pathways for molecular tumorigenesis with potential neoplastic progression.Journal of gastroenterology · 2020Article
- Role ofInternational journal of molecular sciences · 2020Article
- DNA methylation changes that precede onset of dysplasia in advanced sessile serrated adenomas.Clinical epigenetics · 2019Article
- The role of CDX2, MUC5AC, and p53 in the evaluation of the progression of serrated lesions toward colorectal carcinoma.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe aim of your study is to characterize serrated lesions according to their molecular patterns, specifically BRAF/KRAS mutation, methylation, and microsatellite statuses. We evaluated the molecular patterns of 163 serrated lesions, including 37 microvesicular hyperplastic polyps, 73 sessile serrated adenomas/polyps (SSA/Ps), 31 traditional serrated adenomas, and 22 SSA/Ps with cytological dysplasia/adenocarcinoma.
methodsMutations in BRAF (V600E)/KRAS (exon 2) and microsatellite status [microsatellite stability (MSS) vs. MSI] were examined using a pyrosequencer and the PCR-based microsatellite method, respectively. DNA methylation status was classified as low (LME), intermediate (IME), or high methylation epigenotype (HME) according to a PCR-based two-step method. In addition, mucin and annexin A10 expression was examined. Finally, we performed a hierarchical clustering analysis of the BRAF/KRAS mutation, DNA methylation, and microsatellite statuses.
resultsThe molecular patterns observed in the serrated lesions could be divided into five subgroups: lesions characterized by (1) BRAF mutation, HME, and MSI; (2) BRAF mutation, HME, and MSS; (3) BRAF mutation, LME/IME, and MSS; (4) no BRAF/KRAS mutations, LME/IME, and MSS; and (5) KRAS mutation, LME/IME, and MSS. In addition, we demonstrated that these observed molecular patterns help identify the associations of the molecular patterns and markers (i.e., mucin and annexin A10) with the clinicopathological findings, including histological features and histological diagnosis.
conclusionsWe suggest that the identified molecular patterns play an important role in the pathway of serrated lesion development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.