Evidence map›Paper›PMID 19379143›Full record

ReviewJournal of cellular and molecular medicine2009

Polymorphisms in p53 and the p53 pathway: roles in cancer susceptibility and response to treatment.

Roman Hrstka, Philip J Coates, Borivoj Vojtesek

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
2.2field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Review
  7. Association ofBiomedicines · 2023
    Article
  8. Article
  9. Alterations in p53 Influence hTERT, VEGF and MMPs Expression in Oral Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  10. Association ofBioMed research international · 2022
    Article
  11. Article
  12. Current understanding of gliomagenesis: from model to mechanism.International journal of medical sciences · 2022
    Review
  13. Characterization and strong risk association ofWorld journal of gastrointestinal oncology · 2020
    Article
  14. Article
  15. Bioscience reports · 2019
    Article
  16. Oncology letters · 2018
    Article
  17. Article
  18. TheAging · 2017
    Article
  19. Article
  20. Article
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 2 institutions in 2 countries.

Roman HrstkaDepartment of Oncological and Experimental Pathology, Masaryk Memorial Cancer Institute, Zlutý Kopec, Brno, Czech Republic.
Philip J Coates
Borivoj Vojtesek
Masaryk Memorial Cancer Institute · CZUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumour suppressor protein lies at the crossroads of multiple cellular response pathways that control the fate of the cell in response to endogenous or exogenous stresses and inactivation of the p53 tumour suppressor signalling pathway is seen in most human cancers. Such aberrant p53 activity may be caused by mutations in the TP53 gene sequence producing truncated or inactive mutant proteins, or by aberrant production of other proteins that regulate p53 activity, such as gene amplification and overexpression of MDM2 or viral proteins that inhibit or degrade p53. Recent studies have also suggested that inherited genetic polymorphisms in the p53 pathway influence tumour formation, progression and/or response to therapy. In some cases, these variants are clearly associated with clinico-pathological variables or prognosis of cancer, whereas in other cases the evidence is less conclusive. Here, we review the evidence that common polymorphisms in various aspects of p53 biology have important consequences for overall tumour susceptibility, clinico-pathology and prognosis. We also suggest reasons for some of the reported discrepancies in the effects of common polymorphisms on tumourigenesis, which relate to the complexity of effects on tumour formation in combination with other oncogenic changes and other polymorphisms. It is likely that future studies of combinations of polymorphisms in the p53 pathway will be useful for predicting tumour susceptibility in the human population and may serve as predictive biomarkers of tumour response to standard therapies.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAmino Acid SequenceAnimalsExonsHumansMutationNeoplasmsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID19379143
PMCPMC3822507
OpenAlexW2072224532

What OpenQuestion holds

Textmetadata
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.