Evidence map›Paper›PMID 26336987›Full record

ArticleOncotarget2015

Clonal origins and parallel evolution of regionally synchronous colorectal adenoma and carcinoma.

Tae-Min Kim, Chang Hyeok An, Je-Keun Rhee, Seung-Hyun Jung, Sung Hak Lee, In-Pyo Baek, Min Sung Kim, Sug Hyung Lee, Yeun-Jun Chung

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.Current issues in molecular biology · 2026
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  14. Mutation heterogeneity between primary gastric cancers and their matched lymph node metastases.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
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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

9 authors at 1 institution in 1 country.

Tae-Min KimDepartment of Medical Informatics, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Chang Hyeok AnDepartment of Surgery, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Je-Keun RheeDepartment of Medical Informatics, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Seung-Hyun JungDepartment of Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Sung Hak LeeDepartment of Hospital Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
In-Pyo BaekDepartment of Integrated Research Center for Genome Polymorphism, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Min Sung KimDepartment of Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Sug Hyung LeeDepartment of Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Yeun-Jun ChungDepartment of Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the colorectal adenoma-to-carcinoma sequence represents a classical cancer progression model, the evolution of the mutational landscape underlying this model is not fully understood. In this study, we analyzed eight synchronous pairs of colorectal high-grade adenomas and carcinomas, four microsatellite-unstable (MSU) and four-stable (MSS) pairs, using whole-exome sequencing. In the MSU adenoma-carcinoma pairs, we observed no subclonal mutations in adenomas that became fixed in paired carcinomas, suggesting a 'parallel' evolution of synchronous adenoma-to-carcinoma, rather than a 'stepwise' evolution. The abundance of indel (in MSU and MSS pairs) and microsatellite instability (in MSU pairs) was noted in the later adenoma- or carcinoma-specific mutations, indicating that the mutational processes and functional constraints operative in early and late colorectal carcinogenesis are different. All MSU cases exhibited clonal, truncating mutations in ACVR2A, TGFBR2, and DNA mismatch repair genes, but none were present in APC or KRAS. In three MSS pairs, both APC and KRAS mutations were identified as both early and clonal events, often accompanying clonal copy number changes. An MSS case uniquely exhibited clonal ERBB2 amplification, followed by APC and TP53 mutations as carcinoma-specific events. Along with the previously unrecognized clonal origins of synchronous colorectal adenoma-carcinoma pairs, our study revealed that the preferred sequence of mutational events during colorectal carcinogenesis can be context-dependent.

Indexed as

Microsatellite InstabilityAdenomaAgedAged, 80 and overCarcinomaColorectal NeoplasmsDisease ProgressionDNA MethylationDNA Mismatch RepairDNA Mutational AnalysisDNA RepairEvolution, MolecularExomeFemaleGene Expression ProfilingGenetic Variationcarcinogenesiscolorectal cancerevolutionexome sequencingmutations

Identifiers

PMID26336987
PMCPMC4695021
OpenAlexW2177433273

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.