Evidence map›Paper›PMID 26216840›Full record

ReviewGastroenterology2015

Genetics and Genetic Biomarkers in Sporadic Colorectal Cancer.

John M Carethers, Barbara H Jung

Abstract readReview
In one paragraph

Review in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
283citing papers in PubMed, 3 pooled it
26.8field-weighted citation impact, top 1% 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

283 citing papers in PubMed, 3 syntheses or guidelines pooled it, 483 citations in OpenAlex.

  1. Pooled it
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  13. Distance-based evaluation of tumor budding in colorectal cancer.Virchows Archiv : an international journal of pathology · 2026
    Article
  14. A different perspective on the cancer stem cell theory.Medical oncology (Northwood, London, England) · 2026
    Review
  15. Article
  16. Article
  17. Review
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  20. Article

223 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

John M CarethersDivision of Gastroenterology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan. Electronic address: jcarethe@umich.edu.
Barbara H JungDivision of Gastroenterology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois.
University of Illinois Chicago · USUniversity of Michigan–Ann Arbor · US

Funding

MICROSATELLITE INSTABILITY &DNA MISMATCH REPAIR SYSTEMR01DK067287 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2005 to 2015
$3.2M
Mechanism of colon cancer metastasis: combined role of activin and TGF-beta signalingR01CA141057 · NCI · UNIVERSITY OF WASHINGTON · PI JUNG, BARBARA H · 2010 to 2021
$3.0M
Inflammatory Differentiation of Colorectal Cancer Among African AmericansU01CA162147 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2012 to 2016
$1.4M
NCI NIH HHS R01 CA141057NCI NIH HHS U01 CA162147NCI NIH HHS UO1 CA162147NIDDK NIH HHS R01 DK067287NIDDK NIH HHS R01 DK06728709
6 · The paper itself

Abstract

Sporadic colorectal cancer (CRC) is a somatic genetic disease in which pathogenesis is influenced by the local colonic environment and the patient's genetic background. Consolidating the knowledge of genetic and epigenetic events that occur with initiation, progression, and metastasis of sporadic CRC has identified some biomarkers that might be utilized to predict behavior and prognosis beyond staging, and inform treatment approaches. Modern next-generation sequencing of sporadic CRCs has confirmed prior identified genetic alterations and has classified new alterations. Each patient's CRC is genetically unique, propelled by 2-8 driver gene alterations that have accumulated within the CRC since initiation. Commonly observed alterations across sporadic CRCs have allowed classification into a (1) hypermutated group that includes defective DNA mismatch repair with microsatellite instability and POLE mutations in ∼15%, containing multiple frameshifted genes and BRAF(V600E); (2) nonhypermutated group with multiple somatic copy number alterations and aneuploidy in ∼85%, containing oncogenic activation of KRAS and PIK3CA and mutation and loss of heterozygosity of tumor suppressor genes, such as APC and TP53; (3) CpG island methylator phenotype CRCs in ∼20% that overlap greatly with microsatellite instability CRCs and some nonhypermutated CRCs; and (4) elevated microsatellite alterations at selected tetranucleotide repeats in ∼60% that associates with metastatic behavior in both hypermutated and nonhypermutated groups. Components from these classifications are now used as diagnostic, prognostic, and treatment biomarkers. Additional common biomarkers may come from genome-wide association studies and microRNAs among other sources, as well as from the unique alteration profile of an individual CRC to apply a precision medicine approach to care.

Indexed as

Gene Expression Regulation, NeoplasticGenetic MarkersColorectal NeoplasmsCpG IslandsDNA MethylationGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMicroRNAsMicrosatellite InstabilityMutationPrognosisGenetic MarkersMicroRNAsChromosomal InstabilityCIMPGenomic InstabilityMicrosatellite Instability

Identifiers

PMID26216840
PMCPMC4589489
OpenAlexW2117922162

What OpenQuestion holds

Textmetadata
LicenceTDM
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.