Evidence map›Paper›PMID 28524162›Full record

ArticleBritish journal of cancer2017

Targeted sequencing-based analyses of candidate gene variants in ulcerative colitis-associated colorectal neoplasia.

Sanjiban Chakrabarty, Vinay Koshy Varghese, Pranoy Sahu, Pradyumna Jayaram, Bhadravathi M Shivakumar, Cannanore Ganesh Pai, Kapaettu Satyamoorthy

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Sanjiban ChakrabartyDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Vinay Koshy VargheseDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Pranoy SahuDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Pradyumna JayaramDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Bhadravathi M ShivakumarDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Cannanore Ganesh PaiDepartment of Gastroenterology and Hepatology, Kasturba Medical College, Manipal University, Manipal, Karnataka 576104, India.
Kapaettu SatyamoorthyDepartment of Cell and Molecular Biology, School of Life Sciences, Manipal University, Manipal, Karnataka 576104, India.
Manipal Academy of Higher Education · INKasturba Medical College, Manipal · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong-standing ulcerative colitis (UC) leading to colorectal cancer (CRC) is one of the most serious and life-threatening consequences acknowledged globally. Ulcerative colitis-associated colorectal carcinogenesis showed distinct molecular alterations when compared with sporadic colorectal carcinoma.

methodsTargeted sequencing of 409 genes in tissue samples of 18 long-standing UC subjects at high risk of colorectal carcinoma (UCHR) was performed to identify somatic driver mutations, which may be involved in the molecular changes during the transformation of non-dysplastic mucosa to high-grade dysplasia. Findings from the study are also compared with previously published genome wide and exome sequencing data in inflammatory bowel disease-associated and sporadic colorectal carcinoma.

resultsNext-generation sequencing analysis identified 1107 mutations in 275 genes in UCHR subjects. In addition to TP53 (17%) and KRAS (22%) mutations, recurrent mutations in APC (33%), ACVR2A (61%), ARID1A (44%), RAF1 (39%) and MTOR (61%) were observed in UCHR subjects. In addition, APC, FGFR3, FGFR2 and PIK3CA driver mutations were identified in UCHR subjects. Recurrent mutations in ARID1A (44%), SMARCA4 (17%), MLL2 (44%), MLL3 (67%), SETD2 (17%) and TET2 (50%) genes involved in histone modification and chromatin remodelling were identified in UCHR subjects.

conclusionsOur study identifies new oncogenic driver mutations which may be involved in the transition of non-dysplastic cells to dysplastic phenotype in the subjects with long-standing UC with high risk of progression into colorectal neoplasia.

Indexed as

Activin Receptors, Type IIAdenomatous Polyposis Coli ProteinClass I Phosphatidylinositol 3-KinasesColitis, UlcerativeColorectal NeoplasmsDioxygenasesDNA-Binding ProteinsDNA HelicasesHistone-Lysine N-MethyltransferaseHumansMutationMutation, MissenseNeoplasm ProteinsNuclear ProteinsPhosphatidylinositol 3-KinasesPolymerase Chain ReactionActivin Receptors, Type IIactivin receptor type II-AAdenomatous Polyposis Coli ProteinAPC protein, humanARID1A protein, humanClass I Phosphatidylinositol 3-KinasesDioxygenasesDNA-Binding ProteinsDNA HelicasesFGFR2 protein, humanFGFR3 protein, humanHistone-Lysine N-MethyltransferaseKMT2C protein, humanKMT2D protein, humanKRAS protein, humanMTOR protein, humanNeoplasm ProteinsNuclear ProteinsPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)Receptor, Fibroblast Growth Factor, Type 2Receptor, Fibroblast Growth Factor, Type 3SETD2 protein, humanSMARCA4 protein, humanTET2 protein, humanTOR Serine-Threonine KinasesTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID28524162
PMCPMC5520210
OpenAlexW2615464843

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.