Evidence map›Paper›PMID 11709723›Full record

ArticleOncogene2001

Multiple genetic changes are associated with mammary tumorigenesis in Brca1 conditional knockout mice.

S G Brodie, X Xu, W Qiao, W M Li, L Cao, C X Deng

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

97 citing papers in PubMed, 190 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. HumanLife science alliance · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. BRCA1 Antibodies Matter.International journal of biological sciences · 2021
    Article
  12. Article
  13. Article
  14. Preclinical evaluation of radiation therapy ofInternational journal of biological sciences · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Establishment and Characterization of a Brca1International journal of molecular sciences · 2020
    Article
  19. Review
  20. BRCA1/BARD1-dependent ubiquitination of NF2 regulates Hippo-YAP1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

37 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

6 authors at 2 institutions in 1 country.

S G BrodieGenetics of Development and Disease Branch, 10/9N105, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
X Xu
W Qiao
W M Li
L Cao
C X Deng
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Brca1 in development and tumorigenesisZIADK056001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 2009 to 2012
$2.2M
Fibroblast Growth Factor ReceptorZ01DK056001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 1999 to 2008
$1.0M
6 · The paper itself

Abstract

Germline mutations in the tumor suppressor gene BRCA1 predispose women to breast cancer, however somatic mutations in the gene are rarely detected in sporadic cancers. To understand this phenomenon, we examined mouse models carrying conditional disruption of Brca1 in mammary epithelium in either p53 wild type (wt) or heterozygous backgrounds. Although a p53(+/-) mutation significantly accelerated tumorigenesis, both strains developed mammary tumors in a stochastic fashion, suggesting that multiple factors, in addition to p53 mutations, may be involved in Brca1 related tumorigenesis. A unique feature of Brca1 mammary tumors is their highly diverse histopathology accompanied by severe chromosome abnormalities. The tumors also display extensive genetic/molecular alterations, including overexpression of ErbB2, c-Myc, p27 and Cyclin D1 in the majority of tumors, while they were virtually ERalpha and p16 negative. Translocations involving p53 were also identified which lead to abnormal RNA and protein products. In addition, we generated cell lines from mammary tumors and found that the cells retained many of the genetic changes found in the primary tumors, suggesting that these genes may be players in Brca1-associated tumorigenesis. Despite their distinct morphology, all cultured tumor cells were Tamoxifen resistant but highly sensitive to Doxorubicin or gamma-irradiation, suggesting that these methods would be effective in treatment of this disease.

Indexed as

Genes, BRCA1Muscle ProteinsAnimalsAntineoplastic AgentsAntineoplastic Agents, HormonalBlotting, NorthernBlotting, WesternCDC2 Protein KinaseCell LineCyclin ACyclin BCyclin B1Cyclin D1Cyclin-Dependent Kinase Inhibitor p16Cyclin EDose-Response Relationship, DrugAntineoplastic AgentsAntineoplastic Agents, HormonalCcnb1 protein, mouseCDC2 Protein KinaseCyclin ACyclin BCyclin B1Cyclin D1Cyclin-Dependent Kinase Inhibitor p16Cyclin EDoxorubicinErb-b2 Receptor Tyrosine KinasesMicrofilament ProteinsMuscle ProteinsProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Tagln protein, mouseTamoxifen

Identifiers

PMID11709723
OpenAlexW1993337285

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.