Evidence map›Paper›PMID 31318969›Full record

ReviewJournal of molecular cell biology2019

Mutant p53-a potential player in shaping the tumor-stroma crosstalk.

Yan Stein, Ronit Aloni-Grinstein, Varda Rotter

Abstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
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  9. Elevated expression ofFrontiers in molecular biosciences · 2024
    Article
  10. The prognostic significance and immune characteristics of bone morphogenetic proteins (BMPs) family: A pan-cancer multi-omics analysis.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024
    Article
  11. Identification of enhancer RNATranslational cancer research · 2023
    Article
  12. p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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.

Yan SteinDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Ronit Aloni-GrinsteinDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Varda RotterDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 7610001, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A plethora of studies suggest that the non-transformed cellular and non-cellular components of the tumor, collectively known as the tumor microenvironment, have a significant impact on the tumorigenic process. It was suggested that the microenvironment, which initially restricts tumor development, is recruited by the tumor and maintains a crosstalk that further promotes cancer progression. Indeed, many of the molecules that participate in the tumor-stroma crosstalk have been characterized. However, the crucial factors that are responsible for the initiation of this crosstalk or the 'recruitment' process remain poorly understood. We propose that oncogenes themselves may influence the 'recruitment' of the stromal cells, while focusing on mutant p53. Apart from losing its tumor-suppressing properties, mutant p53 gains novel oncogenic functions, a phenomenon dubbed mutant p53 gain of function (GOF). Here, we discuss possible ways in which mutant p53 may modulate the microenvironment in order to promote tumorigenesis. We thus propose that mutant p53 may serve as a key player in the modulation of the tumor-stroma crosstalk in a way that benefits the tumor. Further elucidation of these 'recruitment' processes, dictated by mutant p53, may be utilized for tailoring personalized therapeutic approaches for patients with tumors that harbor p53 mutation.

Indexed as

CarcinogenesisGain of Function MutationGene Expression Regulation, NeoplasticTumor Suppressor Protein p53AnimalsHumansTumor MicroenvironmentTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID31318969
PMCPMC6736352

What OpenQuestion holds

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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.