Evidence map›Paper›PMID 26234182›Full record

ArticleNature communications2015

An apoptosis-enhancing drug overcomes platinum resistance in a tumour-initiating subpopulation of ovarian cancer.

D M Janzen, E Tiourin, J A Salehi, D Y Paik, J Lu, M Pellegrini, S Memarzadeh

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Nature communications, 2015. 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 It has been retracted, and should not be counted.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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
13.5field-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

38 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Lgr6Genes & diseases · 2026
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  10. Computational modeling of ovarian cancer dynamics suggests optimal strategies for therapy and screening.Proceedings of the National Academy of Sciences of the United States of America · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

D M JanzenDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
E TiourinDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
J A SalehiDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
D Y PaikDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
J LuDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, California 90095, USA.
M PellegriniDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, California 90095, USA.
S MemarzadehDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
University of California, Los Angeles · USBroad Center · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Pathobiology and Mechanism of Progesterone Resistance in Human Endometrial CancerR01CA183877 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MEMARZADEH, SANAZ · 2015 to 2019
$1.8M
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NCI NIH HHS R01 CA183877NCI NIH HHS R01CA183877
6 · The paper itself

Abstract

High-grade serous ovarian cancers (HGSCs) are deadly malignancies that relapse despite carboplatin chemotherapy. Here we show that 16 independent primary HGSC samples contain a CA125-negative population enriched for carboplatin-resistant cancer initiating cells. Transcriptome analysis reveals upregulation of homologous recombination DNA repair and anti-apoptotic signals in this population. While treatment with carboplatin enriches for CA125-negative cells, co-treatment with carboplatin and birinapant eliminates these cells in HGSCs expressing high levels of the inhibitor of apoptosis protein cIAP in the CA125-negative population. Birinapant sensitizes CA125-negative cells to carboplatin by mediating degradation of cIAP causing cleavage of caspase 8 and restoration of apoptosis. This co-therapy significantly improves disease-free survival in vivo compared with either therapy alone in tumour-bearing mice. These findings suggest that therapeutic strategies that target CA125-negative cells may be useful in the treatment of HGSC.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCA-125 AntigenCarboplatinCaspase 8DipeptidesDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIndolesInhibitor of Apoptosis ProteinsMembrane ProteinsMicebirinapantCA-125 AntigenCarboplatinCASP8 protein, humanCaspase 8DipeptidesIndolesInhibitor of Apoptosis ProteinsMembrane ProteinsMUC16 protein, human

Identifiers

PMID26234182
PMCPMC4532886
OpenAlexW1781170077

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.