Evidence mapPaperPMID 41013839Full record

ReviewHereditas2025

Cancer cell plasticity and therapeutic resistance: mechanisms, crosstalk, and translational perspectives.

Saeid Ghorbian

Abstract readReview
In one paragraph

Review in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. 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

1 author.

Saeid GhorbianDepartment of Bilogy, Ta.C., Islamic Azad University, Tabriz, Iran. saeid.ghorbian@iau.ac.ir.ORCID http://orcid.org/0000-0003-0780-3159

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to targeted cancer therapies is a significant barrier to favorable treatment outcomes. Malignant cells can tolerate and resist drug treatments due to their biological flexibility. Specifically, slow-cycling drug-resistant cells may achieve permanent resistance to the treatment or restore sensitivity upon cessation of therapy. Enhancing cancer treatment methodologies necessitates a deeper understanding of the adaptability of tumor cells. Drug resistance and cellular heterogeneity are closely associated with cancer cell adaptability. Alterations in cellular signaling, interactions with the tumor microenvironment, and genetic and epigenetic alterations are all implicated. Analyzing these pathways will enhance our understanding of how cancer cells evolve and evade treatment. Two effective strategies to address cancer cell adaptability are to target specific biological pathways and to employ combination therapies. The progression of cancer therapy methodologies relies on comprehending and exploring the concept of cancer cell adaptability. Understanding tumor heterogeneity and drug resistance necessitates identifying the cellular, molecular, and genetic processes that govern cancer cell plasticity. This understanding enables the development of more personalized and effective cancer therapies, leading to improved treatment outcomes. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Cell PlasticityDrug Resistance, NeoplasmNeoplasmsAntineoplastic AgentsEpigenesis, GeneticHumansSignal TransductionTumor MicroenvironmentAntineoplastic AgentsCancer plasticityCancer stem cellDrug resistancesTumor heterogeneity

Identifiers

PMID41013839
PMCPMC12465352

What Socratic holds

Textmetadata
LicenceCC BY
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.