Evidence map›Paper›PMID 10490643›Full record

ArticleMolecular and cellular biology1999

Growth retardation, DNA repair defects, and lack of spermatogenesis in BRCA1-deficient mice.

V L Cressman, D C Backlund, A V Avrutskaya, S A Leadon, V Godfrey, B H Koller

RetractedErratum issuedAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Review
  2. Article
  3. Transcriptome Studies Reveal theAnimals : an open access journal from MDPI · 2023
    Article
  4. Article
  5. BRCA1 and BRCA2 Tumor Suppressor Function in Meiosis.Frontiers in cell and developmental biology · 2021
    Review
  6. Review
  7. Article
  8. Article
  9. Human ovarian tissue cortex surrounding benign and malignant lesions.Reproductive sciences (Thousand Oaks, Calif.) · 2014
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. DNA mismatch repair and infertility.Current opinion in urology · 2010
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

V L CressmanCurriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
D C Backlund
A V Avrutskaya
S A Leadon
V Godfrey
B H Koller

Funding

Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHARLES M PEROU · 1992 to 2026
$59.3M
TRANSCRIPTION COUPLED REPAIR OF EUKARYOTIC CELLSR01CA040453 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI LEADON, STEVEN A · 1985 to 2002
$629k
MODELS OF BREAST CANCERR03CA070490 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI KOLLER, BEVERLY H · 1996 to 1997
–
NCI NIH HHS CA40453NCI NIH HHS CA70490NCI NIH HHS IP50CA58223NCI NIH HHS P50 CA058223NCI NIH HHS R01 CA040453
6 · The paper itself

Abstract

BRCA1 is a nuclear phosphoprotein expressed in a broad spectrum of tissues during cell division. The inheritance of a mutant BRCA1 allele dramatically increases a woman's lifetime risk for developing both breast and ovarian cancers. A number of mouse lines carrying mutations in the Brca1 gene have been generated, and mice homozygous for these mutations generally die before day 10 of embryonic development. We report here the survival of a small number of mice homozygous for mutations in both the p53 and Brca1 genes. The survival of these mice is likely due to additional unknown mutations or epigenetic effects. Analysis of the Brca1(-/-) p53(-/-) animals indicates that BRCA1 is not required for the development of most organ systems. However, these mice are growth retarded, males are infertile due to meiotic failure, and the mammary gland of the female mouse is underdeveloped. Growth deficiency due to loss of BRCA1 was more thoroughly examined in an analysis of primary fibroblast lines obtained from these animals. Like p53(-/-) fibroblasts, Brca1(-/-) p53(-/-) cells proliferate more rapidly than wild-type cells; however, a high level of cellular death in these cultures results in reduced overall growth rates in comparison to p53(-/-) fibroblasts. Brca1(-/-) p53(-/-) fibroblasts are also defective in transcription-coupled repair and display increased sensitivity to DNA-damaging agents. We show, however, that after continued culture, and perhaps accelerated by the loss of BRCA1 repair functions, populations of Brca1(-/-) p53(-/-) fibroblasts with increased growth rates can be isolated. The increased survival of BRCA1-deficient fibroblasts in the absence of p53, and with the subsequent accumulation of additional growth-promoting changes, may mimic the events that occur during malignant transformation of BRCA1-deficient epithelia.

Indexed as

AnimalsBRCA1 ProteinCell CycleCell DeathCell Transformation, NeoplasticDNA DamageDNA RepairDrug ResistanceFemaleFibroblastsGenes, LethalGerm-Line MutationHomozygoteInfertility, MaleMaleMammary Glands, AnimalBRCA1 ProteinMutagensTumor Suppressor Protein p53

Identifiers

PMID10490643
PMCPMC84701

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.