Evidence map›Paper›PMID 37588236›Full record

ReviewGenes & diseases2024

Cancer cell cycle heterogeneity as a critical determinant of therapeutic resistance.

Ebrahim H Maleki, Ahmad Reza Bahrami, Maryam M Matin

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
26.7field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 116 citations in OpenAlex.

  1. The logarithmic phase as a therapeutic direction: evaluating pharmacological strategies against cancer progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Single-cell transcriptomic analysis reveals cellular heterogeneity and prognostic subtypes in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  8. Article
  9. Network pharmacology reveals thatGenes & diseases · 2026
    Article
  10. Review
  11. Single-cell hit calling in high-content imaging screens with Buscar.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

10 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Ebrahim H MalekiDepartment of Biology, Faculty of Science, Ferdowsi University of Mashhad, 9177948974 Mashhad, Iran.
Ahmad Reza BahramiDepartment of Biology, Faculty of Science, Ferdowsi University of Mashhad, 9177948974 Mashhad, Iran.
Maryam M MatinDepartment of Biology, Faculty of Science, Ferdowsi University of Mashhad, 9177948974 Mashhad, Iran.
Academic Center for Education, Culture and Research · IRFerdowsi University of Mashhad · IRJagiellonian University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intra-tumor heterogeneity is now arguably one of the most-studied topics in tumor biology, as it represents a major obstacle to effective cancer treatment. Since tumor cells are highly diverse at genetic, epigenetic, and phenotypic levels, intra-tumor heterogeneity can be assumed as an important contributing factor to the nullification of chemotherapeutic effects, and recurrence of the tumor. Based on the role of heterogeneous subpopulations of cancer cells with varying cell-cycle dynamics and behavior during cancer progression and treatment; herein, we aim to establish a comprehensive definition for adaptation of neoplastic cells against therapy. We discuss two parallel and yet distinct subpopulations of tumor cells that play pivotal roles in reducing the effects of chemotherapy: "resistant" and "tolerant" populations. Furthermore, this review also highlights the impact of the quiescent phase of the cell cycle as a survival mechanism for cancer cells. Beyond understanding the mechanisms underlying the quiescence, it provides an insightful perspective on cancer stem cells (CSCs) and their dual and intertwined functions based on their cell cycle state in response to treatment. Moreover, CSCs, epithelial-mesenchymal transformed cells, circulating tumor cells (CTCs), and disseminated tumor cells (DTCs), which are mostly in a quiescent state of the cell cycle are proved to have multiple biological links and can be implicated in our viewpoint of cell cycle heterogeneity in tumors. Overall, increasing our knowledge of cell cycle heterogeneity is a key to identifying new therapeutic solutions, and this emerging concept may provide us with new opportunities to prevent the dreadful cancer recurrence.

Indexed as

Cancer stem cells (CSCs)CarcinomaCell cycle heterogeneityQuiescenceTherapy resistanceTherapy toleranceTumor dormancy

Identifiers

PMID37588236
PMCPMC10425754
OpenAlexW4316041915

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.