Evidence map›Paper›PMID 36718360›Full record

ArticleiScience2023

Distinct but interchangeable subpopulations of colorectal cancer cells with different growth fates and drug sensitivity.

Roberto Coppo, Jumpei Kondo, Keita Iida, Mariko Okada, Kunishige Onuma, Yoshihisa Tanaka, Mayumi Kamada, Masayuki Ohue, Kenji Kawada, Kazutaka Obama and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Frontiers in genetics · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Spheroids and organoids derived from colorectal cancer as tools forExploration of targeted anti-tumor therapy · 2024
    Review
  13. Emerging roles of 3D-culture systems in tackling tumor drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2023
    Review
  14. Article
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

11 authors at 3 institutions in 1 country.

Roberto CoppoDepartment 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.
Keita IidaInstitute for Protein Research, Osaka University, Suita, Osaka, Japan.
Mariko OkadaInstitute for Protein Research, Osaka University, Suita, Osaka, Japan.
Kunishige OnumaDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshihisa TanakaGraduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Mayumi KamadaDepartment of Biomedical Data Intelligence, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masayuki OhueDepartment of Gastroenterological Surgery, Osaka International Cancer Institute, Osaka, Japan.
Kenji KawadaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kazutaka ObamaDepartment of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masahiro InoueDepartment of Clinical Bio-resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JPProtein Research Foundation · JPOsaka International Cancer Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dynamic changes in cell properties lead to intratumor heterogeneity; however, the mechanisms of nongenetic cellular plasticity remain elusive. When the fate of each cell from colorectal cancer organoids was tracked through a clonogenic growth assay, the cells showed a wide range of growth ability even within the clonal organoids, consisting of distinct subpopulations; the cells generating large spheroids and the cells generating small spheroids. The cells from the small spheroids generated only small spheroids (S-pattern), while the cells from the large spheroids generated both small and large spheroids (D-pattern), both of which were tumorigenic. Transition from the S-pattern to the D-pattern occurred by various extrinsic triggers, in which Notch signaling and Musashi-1 played a key role. The S-pattern spheroids were resistant to chemotherapy and transited to the D-pattern upon drug treatment through Notch signaling. As the transition is linked to the drug resistance, it can be a therapeutic target.

Indexed as

CancerCell biologyTherapy

Identifiers

PMID36718360
PMCPMC9883198
OpenAlexW4315864193

What OpenQuestion holds

Textmetadata
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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.