Evidence map›Paper›PMID 24065105›Full record

ReviewInternational journal of molecular sciences2013

The consequence of oncomorphic TP53 mutations in ovarian cancer.

Pavla Brachova, Kristina W Thiel, Kimberly K Leslie

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022
    Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. TP53 mutations and MDM2 polymorphisms in breast and ovarian cancers: amelioration by drugs and natural compounds.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. SNPs Give LACTB Oncogene-Like Functions and Prompt Tumor Progression via Dual-Regulating p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  12. Review
  13. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  14. Doxorubicin catalyses self-assembly of p53 by phase separation.Current research in structural biology · 2024
    Article
  15. Article
  16. Gain-of-function p53Scientific reports · 2023
    Article
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Pavla BrachovaMolecular and Cellular Biology Program, University of Iowa, Iowa City, IA 52242, USA. kimberly-leslie@uiowa.edu.
Kristina W Thiel
Kimberly K Leslie
University of Iowa · US

Funding

Targeted Therapy for Endometrial CancerR01CA099908 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LESLIE, KIMBERLY K. · 2002 to 2023
$5.8M
NCI NIH HHS R01 CA099908NCI NIH HHS R01CA99908-7
6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecological malignancy, with an alarmingly poor prognosis attributed to late detection and chemoresistance. Initially, most tumors respond to chemotherapy but eventually relapse due to the development of drug resistance. Currently, there are no biological markers that can be used to predict patient response to chemotherapy. However, it is clear that mutations in the tumor suppressor gene TP53, which occur in 96% of serous ovarian tumors, alter the core molecular pathways involved in drug response. One subtype of TP53 mutations, widely termed gain-of-function (GOF) mutations, surprisingly converts this protein from a tumor suppressor to an oncogene. We term the resulting change an oncomorphism. In this review, we discuss particular TP53 mutations, including known oncomorphic properties of the resulting mutant p53 proteins. For example, several different oncomorphic mutations have been reported, but each mutation acts in a distinct manner and has a different effect on tumor progression and chemoresistance. An understanding of the pathological pathways altered by each mutation is necessary in order to design appropriate drug interventions for patients suffering from this deadly disease.

Indexed as

AnimalsFemaleGene Knockout TechniquesHumansMutationOvarian NeoplasmsTranscriptomeTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID24065105
PMCPMC3794832
OpenAlexW2049497373

What OpenQuestion 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 OpenQuestion graph.