Evidence map›Paper›PMID 10623666›Full record

ArticleThe American journal of pathology2000

p53 mutations and expression in breast carcinoma in situ.

J Lukas, N Niu, M F Press

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Elucidating cooperative genetic events in DCIS progression in mutantProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Intratumoral Heterogeneity in Ductal Carcinoma In Situ: Chaos and Consequence.Journal of mammary gland biology and neoplasia · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Mutations in p53, p53 protein overexpression and breast cancer survival.Journal of cellular and molecular medicine · 2009
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

J LukasDepartment of Pathology, University of Southern California School of Medicine, Los Angeles, California, USA.
N Niu
M F Press
University of Southern California · US

Funding

PATHOBIOLOGY OF BREAST CANCER AND HORMONE RECEPTORSR01CA048780 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI PRESS, MICHAEL F · 1988 to 2003
$1.1M
SPECIALIZED PROGRAM OF RESEARCH EXCELLENCE/BREAST CANCERP20CA058197 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SLAMON, DENNIS J · 1992 to 1994
–
NCI NIH HHS CA48780NCI NIH HHS CA58197NCI NIH HHS R01 CA048780NCRR NIH HHS M01RR43
6 · The paper itself

Abstract

The p53 tumor suppressor gene is altered in approximately half of human cancers. Although p53 mutations are common in invasive breast carcinoma, few have been identified in breast carcinoma in situ (intraductal breast carcinomas). Most studies of p53 in breast carcinoma in situ are immunohistochemical studies of p53 staining in paraffin-embedded tissue sections. Few studies have isolated the tumor cells and subjected them to DNA sequence analysis. The current study was undertaken to characterize p53 in a cohort of breast carcinoma in situ cases, both with and without invasive disease. Fifty-eight frozen breast biopsy samples were used for these investigations. Twenty-seven cases had only ductal carcinoma in situ (CIS) and 31 cases had evidence of both invasive and in situ carcinoma. DNA sequence alterations in exons 2 through 11 of p53 were screened by the single-strand conformational polymorphism technique. Exons with altered mobility were sequenced. Among breast CIS cases without invasive disease, 22% had p53 mutations and 7% had DNA sequence alterations of unknown significance. Analysis of breast CIS with concurrent invasive disease demonstrated p53 mutations in 19% of cases and one (3%) DNA alteration of unknown significance. Each carcinoma having a p53 mutation in the breast CIS component had the identical mutation in the invasive component of the same tumor indicating a clonal relationship between the two tumor components. p53 protein overexpression was identified in 22% of pure intraductal breast carcinomas and in 35% of breast CIS with invasive disease. Comparison of immunostaining and DNA sequence alterations showed a significant association between overexpression and mutations (P = 0. 0037) in cases of CIS without invasion, and similarly between overexpression and mutations in cases of CIS with invasion (P = 0. 007). p53 mutations and p53 overexpression were relatively common in intraductal breast carcinomas but were not observed in adjacent normal breast lobules or ducts in 9 cases available for DNA analysis. The frequency of p53 alterations when comparing breast CIS with and without an invasive component indicated that p53 mutations usually occur before invasion during the progression of breast cancer, as is observed for a number of other adult solid tumors.

Indexed as

MutationBase SequenceBreast NeoplasmsCarcinoma in SituDNA Mutational AnalysisDNA, NeoplasmFemaleHumansMolecular Sequence DataNeoplasm InvasivenessPolymorphism, Single-Stranded ConformationalTumor Suppressor Protein p53DNA, NeoplasmTumor Suppressor Protein p53

Identifiers

PMID10623666
PMCPMC1868634
OpenAlexW2030234723

What OpenQuestion holds

Textmetadata
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Registered trials

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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.