Evidence map›Paper›PMID 40690563›Full record

ReviewJournal of cellular and molecular medicine2025

The Role of p66Shc in Cancer: Molecular Mechanisms and Therapeutic Implications.

Davood Zaeifi, Khadijeh Jamialahmadi, Gholamreza Karimi

Abstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

3 authors.

Davood ZaeifiDepartment of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Khadijeh JamialahmadiDepartment of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Gholamreza KarimiPharmaceutical Research Center, Institute of Pharmaceutical Technology, Faculty of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID 0000-0002-1273-5448

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p66Shc is a redox-sensitive and pro-apoptotic adaptor protein that regulates oxidative stress and mitochondrial apoptosis. It is the largest of three isoforms encoded by the proto-oncogene ShcA (Src collagen homologue A). Members of the ShcA family are capable of recruiting various signalling molecules and are involved in several cellular pathways, including proliferation, growth and survival. Increasing evidence highlights the p66Shc role in various tumourigenic processes, such as cell expansion, progression, metastasis and metabolic reprogramming. This review summarises current knowledge on the role of p66Shc in cancer, explains the molecular mechanisms underlying the effects of this protein, and considers therapeutic prospects aimed at targeting it. Emerging therapeutic strategies, including small-molecule inhibitors and gene-editing approaches, are discussed alongside challenges in clinical translation.

Indexed as

NeoplasmsSrc Homology 2 Domain-Containing, Transforming Protein 1AnimalsApoptosisCell ProliferationHumansProto-Oncogene MasSignal TransductionMAS1 protein, humanProto-Oncogene MasSHC1 protein, humanSrc Homology 2 Domain-Containing, Transforming Protein 1cancerp66Shcreactive oxygen speciessignalling pathway

Identifiers

PMID40690563
PMCPMC12279043

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.