Evidence map›Paper›PMID 26898652›Full record

ArticleClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2016

Sessile Serrated Polyps are Precursors of Colon Carcinomas With Deficient DNA Mismatch Repair.

Seth Sweetser, Andrea Jones, Thomas C Smyrk, Frank A Sinicrope

Open access · hybridAbstract read
In one paragraph

Article in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  9. Role ofInternational journal of molecular sciences · 2020
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  10. Clinical significance ofWorld journal of gastrointestinal oncology · 2019
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  14. Clinicopathologic parameters associated with postoperative complications and risk factors for tumor recurrence and mortality after tumor resection of patients with colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
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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

4 authors at 2 institutions in 1 country.

Seth SweetserDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
Andrea JonesDivision of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota.
Thomas C SmyrkDivision of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota.
Frank A SinicropeDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota; Division of Medical Oncology, Mayo Clinic, Rochester, Minnesota. Electronic address: sinicrope.frank@mayo.edu.
Mayo Clinic · USWinnMed · US

Funding

Translational Research in Colon Cancer Prevention & TreatmentK05CA142885 · NCI · MAYO CLINIC ROCHESTER · PI SINICROPE, FRANK A. · 2009 to 2013
$808k
NCI NIH HHS K05 CA142885
6 · The paper itself

Abstract

We investigated whether sessile serrated adenomas/polyps (SSA/Ps) are direct precursors of colorectal carcinomas. We identified colon carcinomas that arose from SSA/Ps among 2646 colorectal cancers included in the surgical pathology database at the Mayo Clinic (2006-2012). Molecular features of the serrated neoplasia pathway were analyzed in these tumors by immunohistochemical analyses of mutant BRAF (V600E) and MLH1 proteins. Among the 33 identified SSA/P-associated colonic adenocarcinomas (median patient age, 75 y), 24 developed in women (73%), 31 were located in the proximal colon (94%), and 23 (69%) were TNM stage I or II. Thirty-one of the tumors (94%) expressed mutant BRAF; of these, 26 also had loss of MLH1 (79%), indicating deficient DNA mismatch repair of sporadic origin. Twenty-two of the tumors (67%) were interval cancers that were more common in women and did not differ significantly in TNM stage, BRAF mutation, or loss of MLH1. By histopathology, SSA/Ps that were associated with colon carcinomas contained frequent dysplasia (48%). Most cancers that arose from SSA/Ps were located on the right side of the colon and had mutant BRAF and loss of MLH1. These findings indicate that SSA/Ps are precursors of most sporadic colon carcinomas with deficient DNA mismatch repair.

Indexed as

DNA Mismatch RepairAgedAged, 80 and overCarcinomaCohort StudiesColonic NeoplasmsDNA Repair EnzymesFemaleHistocytochemistryHumansImmunohistochemistryMaleMicroscopyMiddle AgedMutL Protein Homolog 1PolypsBRAF protein, humanDNA Repair EnzymesMLH1 protein, humanMutL Protein Homolog 1Proto-Oncogene Proteins B-rafColon CancerGeneticsMMRProgression

Identifiers

PMID26898652
PMCPMC4912894
OpenAlexW2346278366

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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.