Evidence map›Paper›PMID 33753878›Full record

ArticleExperimental & molecular medicine2021

High prevalence of TP53 loss and whole-genome doubling in early-onset colorectal cancer.

Jeong Eun Kim, Jaeyong Choi, Chang-Ohk Sung, Yong Sang Hong, Sun Young Kim, Hyunjung Lee, Tae Won Kim, Jong-Il Kim

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  10. Current issues in molecular biology · 2025
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  13. Geographic and age-related variations in mutational processes in colorectal cancer.medRxiv : the preprint server for health sciences · 2025
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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

8 authors at 2 institutions in 3 countries.

Jeong Eun Kim *Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Jaeyong Choi *Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Chang-Ohk SungDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Yong Sang HongDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Sun Young KimDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Hyunjung LeeDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.ORCID http://orcid.org/0000-0001-7243-3348
Tae Won KimDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. twkimmd@amc.seoul.kr.ORCID http://orcid.org/0000-0001-9522-1997
Jong-Il KimDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea. jongil@snu.ac.kr.ORCID http://orcid.org/0000-0002-7240-3744
Ulsan College · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global incidence of early-onset colorectal cancer (EO-CRC) is rapidly rising. However, the reason for this rise in incidence as well as the genomic characteristics of EO-CRC remain largely unknown. We performed whole-exome sequencing in 47 cases of EO-CRC and targeted deep sequencing in 833 cases of CRC. Mutational profiles of EO-CRC were compared with previously published large-scale studies. EO-CRC and The Cancer Genome Atlas (TCGA) data were further investigated according to copy number profiles and mutation timing. We classified colorectal cancer into three subgroups: the hypermutated group consisted of mutations in POLE and mismatch repair genes; the whole-genome doubling group had early functional loss of TP53 that led to whole-genome doubling and focal oncogene amplification; the genome-stable group had mutations in APC and KRAS, similar to conventional colon cancer. Among non-hypermutated samples, whole-genome doubling was more prevalent in early-onset than in late-onset disease (54% vs 38%, Fisher's exact P = 0.04). More than half of non-hypermutated EO-CRC cases involved early TP53 mutation and whole-genome doubling, which led to notable differences in mutation frequencies between age groups. Alternative carcinogenesis involving genomic instability via loss of TP53 may be related to the rise in EO-CRC.

Indexed as

Genome, HumanLoss of Function MutationMicrosatellite InstabilityAdultAge of OnsetColorectal NeoplasmsExome SequencingFemaleHumansMaleTumor Suppressor Protein p53Young AdultTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33753878
PMCPMC8080557
OpenAlexW3138934519

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.