Evidence map›Paper›PMID 8506342›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

p53 gene mutations and protein accumulation in human ovarian cancer.

J Kupryjańczyk, A D Thor, R Beauchamp, V Merritt, S M Edgerton, D A Bell, D W Yandell

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 299 citations in OpenAlex.

  1. 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
  2. The Clinical Significance ofInternational journal of molecular sciences · 2024
    Article
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  7. The Putative Role ofJournal of Cancer · 2017
    Review
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  19. Precursors of endometrial and ovarian carcinoma.Virchows Archiv : an international journal of pathology · 2010
    Review
  20. Article

8 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

7 authors at 3 institutions in 1 country.

J KupryjańczykDepartment of Pathology, Harvard Medical School, Boston, MA.
A D Thor
R Beauchamp
V Merritt
S M Edgerton
D A Bell
D W Yandell
Harvard University · USCancer Genetics (United States) · USMassachusetts General Hospital · US

Funding

TRANSFORMING GENES EXPRESSION IN BREAST CANCERP01CA044768 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI BENZ, CHRISTOPHER · 1987 to 2000
$890k
NCI NIH HHS CA-44768
6 · The paper itself

Abstract

Mutations of the p53 gene on chromosome 17p are a common genetic change in the malignant progression of many cancers. We have analyzed 38 malignant tumors of ovarian or peritoneal müllerian type for evidence of p53 variations at either the DNA or protein levels. Genetic studies were based on single-strand conformation polymorphism analysis and DNA sequencing of exons 2 through 11 of the p53 gene; mutations were detected in 79% of the tumors. These data show a statistically significant association between mutations at C.G pairs and a history of estrogen therapy. Two of 20 patients whose normal tissue could be studied carried germ-line mutations of p53. Immunohistochemical analysis of the p53 protein was carried out using monoclonal antibody PAb1801. Ninety-six percent of the missense mutations were associated with abnormal accumulation of p53 protein, but nonsense mutations, a splicing mutation, and most deletions did not result in p53 protein accumulation. A statistically significant association between p53 protein accumulation in poorly differentiated stage III serous carcinomas and small primary tumor size at diagnosis was found, perhaps suggesting that p53 protein accumulation accelerates the metastatic spread from a primary tumor. Overall, our findings indicate that alterations of p53 play a major role in ovarian cancer, including predisposition to the disease in some patients, and suggest a possible mechanism for somatic mutations leading to this cancer.

Indexed as

Chromosomes, Human, Pair 17Genes, p53Point MutationAmino Acid SequenceBase SequenceCodonDNA, NeoplasmExonsFemaleHumansImmunohistochemistryNeoplasm MetastasisNeoplasm StagingOvarian NeoplasmsPolymerase Chain ReactionTumor Suppressor Protein p53CodonDNA, NeoplasmTumor Suppressor Protein p53

Identifiers

PMID8506342
PMCPMC46633
OpenAlexW1966143946

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.