Evidence map›Paper›PMID 25132263›Full record

ArticleOncogene2015

BRCA1-IRIS inactivation sensitizes ovarian tumors to cisplatin.

B T Paul, Z Blanchard, M Ridgway, W M ElShamy

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Nephroprotective Potential of LyophilizedJournal of nutrition and metabolism · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Targeting mRNA processing as an anticancer strategy.Nature reviews. Drug discovery · 2020
    Review
  9. Article
  10. TheGenes · 2019
    Article
  11. BRCA1-No Matter How You Splice It.Cancer research · 2019
    Review
  12. Article
  13. Article
  14. BRCA1-IRIS promotes human tumor progression through PTEN blockade and HIF-1α activation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

B T PaulCancer Institute and Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, USA.
Z BlanchardCancer Institute and Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, USA.
M RidgwayDepartment of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, USA.
W M ElShamyCancer Institute and Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, USA.
University of Mississippi Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the first in mortalities among gynecologic cancers in the United States, often due to late diagnosis and/or acquired platinum-resistant recurrences. This study investigates whether BRCA1-IRIS is a novel treatment target for ovarian cancers and in platinum-resistant recurrences. Here we show that more than half of the ovarian cancer samples analyzed showed BRCA1-IRIS and survivin overexpression and lacked nuclear FOXO3a expression. Normal ovarian epithelial cells overexpressing BRCA1-IRIS formed metastasis in mice when injected in the peritoneal cavity, whereas aggressive ovarian cancer cell lines failed to form tumors or metastases in mice when BRCA1-IRIS was silenced in them. We show that BRCA1-IRIS activates two autocrine signaling loops, brain-derived neurotrophic factor/tyrosine kinase B receptor (BDNF/TrkB) and neuregulin 1 (NRG1)/ErbB2. These loops are involved in anoikis resistance and metastasis promotion. These loops operate in several ovarian cancer cell lines, and BRCA1-IRIS silencing or inactivation using a novel inhibitory peptide renders both non-functional and promoted cell death. In a mouse xenograft model, BRCA1-IRIS inactivation using this novel inhibitory peptide resulted in significant reduction in ovarian tumor growth. More importantly, this treatment sensitized ovarian tumors to low cisplatin concentrations. Taken together, these data strongly suggest that BRCA1-IRIS and/or BDNF/TrkB and NRG1/ErbB2 could serve as rational therapeutic targets for advanced ovarian cancers.

Indexed as

AnimalsAnoikisAntineoplastic AgentsBRCA1 ProteinCell Line, TumorCell ProliferationCell SurvivalCisplatinDrug Resistance, NeoplasmFemaleForkhead Box Protein O3Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsMiceAntineoplastic AgentsBIRC5 protein, humanBRCA1 ProteinBRCA1 protein, humanCisplatinForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanInhibitor of Apoptosis ProteinsPeptidesSurvivin

Identifiers

PMID25132263
OpenAlexW1984763444

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.