Evidence map›Paper›PMID 37357016›Full record

ReviewCancer science2023

Genetic and nongenetic mechanisms for colorectal cancer evolution.

Sau Yee Kok, Mizuho Nakayama, Atsuya Morita, Hiroko Oshima, Masanobu Oshima

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Precision Oncology Framework Using Circulating Tumor Cells.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
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

5 authors at 1 institution in 1 country.

Sau Yee KokDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Mizuho NakayamaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Atsuya MoritaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Hiroko OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Masanobu OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-3304-0004
Kanazawa University · JP

Funding

Japan Agency for Medical Research and Development 22ck0106541h0003Japan Agency for Medical Research and Development 22gm4010012h0002Japan Society for the Promotion of Science 22H00454Japan Society for the Promotion of Science 22H02899Japan Society for the Promotion of Science 22KF0154Japan Society for the Promotion of Science 23K06631
6 · The paper itself

Abstract

The stepwise accumulation of key driver mutations is responsible for the development and malignant progression of colorectal cancer in primary sites. Genetic mouse model studies have revealed combinations of driver gene mutations that induce phenotypic changes in tumors toward malignancy. However, cancer evolution is regulated by not only genetic alterations but also nongenetic mechanisms. For example, certain populations of metastatic cancer cells show a loss of malignant characteristics even after the accumulation of driver mutations, and such cells are eliminated in a negative selection manner. Furthermore, a polyclonal metastasis model has recently been proposed, in which cell clusters consisting of genetically heterogeneous cells break off from the primary site, disseminate to distant organs, and develop into heterogenous metastatic tumors. Such nongenetic mechanisms for malignant progression have been elucidated using genetically engineered mouse models as well as organoid transplantation experiments. In this review article, we discuss the role of genetic alterations in the malignant progression of primary intestinal tumors and nongenetic mechanisms for negative selection and polyclonal metastasis, which we learned from model studies.

Indexed as

Colorectal NeoplasmsAnimalsMiceMutationcancer evolutionmouse modelmultistep tumorigenesisorganoidpolyclonal metastasis

Identifiers

PMID37357016
PMCPMC10475778
OpenAlexW4381948333

What OpenQuestion holds

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LicenceCC BY-NC
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.