Evidence map›Paper›PMID 22617326›Full record

ArticleCancer research2012

Perturbation of Rb, p53, and Brca1 or Brca2 cooperate in inducing metastatic serous epithelial ovarian cancer.

Ludmila Szabova, Chaoying Yin, Sujata Bupp, Theresa M Guerin, Jerome J Schlomer, Deborah B Householder, Maureen L Baran, Ming Yi, Yurong Song, Wenping Sun and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
16.4field-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

83 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
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  8. Interplay between altered metabolism and DNA damage and repair in ovarian cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Harnessing preclinical models for the interrogation of ovarian cancer.Journal of experimental & clinical cancer research : CR · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

23 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

14 authors at 5 institutions in 1 country.

Ludmila SzabovaCenter for Advanced Preclinical Research, Advanced Biomedical Computing Center, SAIC at Frederick National Laboratory for Cancer Research, Mouse Cancer Genetics Program, NCI-Frederick, Frederick, Maryland 21702, USA.
Chaoying Yin
Sujata Bupp
Theresa M Guerin
Jerome J Schlomer
Deborah B Householder
Maureen L Baran
Ming Yi
Yurong Song
Wenping Sun
Jonathan E McDunn
Philip L Martin
Terry Van Dyke
Simone Difilippantonio
Metabolon (United States) · USFrederick National Laboratory for Cancer Research · USScience Applications International Corporation (United States) · USUniversity of North Carolina at Chapel Hill · USCancer Genetics (United States) · US

Funding

Center for Applied Preclinical Research (CAPR)ZICBC011137 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VAN DYKE, TERRY · 2009 to 2015
$7.5M
Validation of, and therapeutic evaluation in ovarian cancer GEM modelsZIABC011353 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VAN DYKE, TERRY · 2010 to 2015
$5.7M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

The majority of human high-grade serous epithelial ovarian cancer (SEOC) is characterized by frequent mutations in p53 and alterations in the RB and FOXM1 pathways. A subset of human SEOC harbors a combination of germline and somatic mutations as well as epigenetic dysfunction for BRCA1/2. Using Cre-conditional alleles and intrabursal induction by Cre-expressing adenovirus in genetically engineered mice, we analyzed the roles of pathway perturbations in epithelial ovarian cancer initiation and progression. Inactivation of RB-mediated tumor suppression induced surface epithelial proliferation with progression to stage I carcinoma. Additional biallelic inactivation and/or missense p53 mutation in the presence or absence of Brca1/2 caused progression to stage IV disease. As in human SEOC, mice developed peritoneal carcinomatosis, ascites, and distant metastases. Unbiased gene expression and metabolomic profiling confirmed that Rb, p53, and Brca1/2-triple mutant tumors aligned with human SEOC, and not with other intraperitoneal cancers. Together, our findings provide a novel resource for evaluating disease etiology and biomarkers, therapeutic evaluation, and improved imaging strategies in epithelial ovarian cancer.

Indexed as

AnimalsBRCA1 ProteinBRCA2 ProteinCarcinoma, Ovarian EpithelialDisease Models, AnimalFemaleGene DeletionImmunohistochemistryMiceMice, TransgenicMutationNeoplasm MetastasisNeoplasms, Glandular and EpithelialOvarian NeoplasmsRetinoblastoma ProteinTumor Suppressor Protein p53BRCA1 ProteinBRCA2 ProteinRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID22617326
PMCPMC3421072
OpenAlexW2130330160

What OpenQuestion holds

Textmetadata
LicenceTDM
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.