Evidence map›Paper›PMID 42491749›Full record

ArticleiScience2026

IGF2BP3 is essential for the growth heterogeneity of colorectal adenoma cells by regulating MYC.

Tomohiko Sunami, Roberto Coppo, Kunishige Onuma, Jumpei Kondo, Hiroyuki Uematsu, Daisuke Hoshi, Yoshihiro Yamamoto, Osamu Kikuchi, Shinya Ohashi, Yasuhide Takeuchi and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Tomohiko SunamiDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Roberto CoppoDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kunishige OnumaDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Jumpei KondoDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiroyuki UematsuDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Daisuke HoshiDivision of Molecular Carcinogenesis, Chiba Cancer Center Research Institute, 666-2 Nitona-cho, Chuo-ku, Chiba-shi, Chiba 260-8717, Japan.
Yoshihiro YamamotoDepartment of Medical Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Osamu KikuchiDepartment of Medical Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Shinya OhashiDepartment of Medical Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Yasuhide TakeuchiDepartment of Diagnostic Pathology, Kyoto University Hospital, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Kazuto KugouDepartment of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 290-0818, Japan.
Yoshinori HasegawaDepartment of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 290-0818, Japan.
Yoshiro ItataniDepartment of Surgery, Graduate Schoolof Medicine, Kyoto University, Kyoto, Japan.
Kazutaka ObamaDepartment of Surgery, Graduate Schoolof Medicine, Kyoto University, Kyoto, Japan.
Yoshitaka HippoDepartment of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 290-0818, Japan.
Manabu MutoDepartment of Medical Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Atsushi YamadaDepartment of Medical Oncology, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Masahiro InoueDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal adenoma is a major precancerous lesion of colorectal cancer (CRC). The adenoma-carcinoma sequence is a multistep progression to CRC caused by the accumulation of genetic mutations. However, the non-genetic mechanisms underlying this process remain largely unknown. In this study, organoids were established from colorectal adenomas patients. Some organoids showed heterogeneity in the proliferative potential of single cells, which is regulated by non-genetic mechanisms. IGF2BP3 was identified as a differentially expressed gene associated with different growth patterns. IGF2BP3 modulated MYC expression levels in positive and negative directions, enabling high proliferative capacity and preventing MYC-induced cell death. IGF2BP3 affected tumorigenicity of mouse adenomas

Indexed as

adenoma-carcinoma sequenceHeterogeneityIGF2BP3MYC

Identifiers

PMID42491749
PMCPMC13378308

What OpenQuestion holds

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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.