Evidence map›Paper›PMID 24469047›Full record

ArticleOncogene2015

Elafin drives poor outcome in high-grade serous ovarian cancers and basal-like breast tumors.

S I Labidi-Galy, A Clauss, V Ng, S Duraisamy, K M Elias, H-Y Piao, E Bilal, R A Davidowitz, Y Lu, G Badalian-Very and 7 more

Open access · greenAbstract read
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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

34 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Effect of ischemia-reperfusion injury on elafin levels in rat liver.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2024
    Article
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  8. Review
  9. Article
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  12. Roles of Antimicrobial Peptides in Gynecological Cancers.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  20. Review
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

17 authors at 5 institutions in 2 countries.

S I Labidi-Galy1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
A Clauss1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
V NgDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
S Duraisamy1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
K M Elias1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA [3] Division of Gynecologic Oncology, Brigham and Women's Hospital, Boston, MA, USA.
H-Y PiaoDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
E BilalThe Cancer Institute of New Jersey, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, New Brunswick, NJ, USA.
R A DavidowitzDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.
Y LuDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
G Badalian-Very1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA.
B GyörffyResearch Laboratory of Pediatrics and Nephrology, Hungarian Academy of Sciences, Budapest, Hungary.
U-B Kang1] Harvard Medical School, Boston, MA, USA [2] Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA, USA.
S Ficarro1] Harvard Medical School, Boston, MA, USA [2] Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA, USA.
S GanesanThe Cancer Institute of New Jersey, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, New Brunswick, NJ, USA.
G B MillsDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
J A Marto1] Harvard Medical School, Boston, MA, USA [2] Blais Proteomics Center, Dana-Farber Cancer Institute, Boston, MA, USA.
R Drapkin1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA [2] Harvard Medical School, Boston, MA, USA [3] Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA.ORCID 0000000269126977
Dana-Farber Cancer Institute · USHarvard University · USRutgers, The State University of New Jersey · USThe University of Texas MD Anderson Cancer Center · USHungarian Academy of Sciences · HU

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Transcriptional control of inhibitory synapse formationP01NS047572 · NINDS · DANA-FARBER CANCER INSTITUTE · PI STILES, CHARLES D · 2004 to 2013
$13.5M
Novel Serum, Plasma, and Urine Biomarkers of Ovarian CanP50CA105009 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI CRAMER, DANIEL WILLIAM · 2004 to 2010
$13.3M
Proteomic, Genomic, and Longitudinal Pathways to Ovarian Cancer Biomarker DiscoveryU01CA152990 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI BIRRER, MICHAEL, SKATES, STEVEN J · 2010 to 2021
$8.9M
Elafin as a biomarker in serous ovarian cancers and basal-like breast tumorsR21CA156021 · NCI · DANA-FARBER CANCER INST · PI DRAPKIN, RONNY I · 2013 to 2014
$406k
NCI NIH HHS P50 CA105009NCI NIH HHS P50-CA105009NCI NIH HHS R21 CA-156021NCI NIH HHS R21 CA156021NCI NIH HHS U01 CA-152990NCI NIH HHS U01 CA152990NINDS NIH HHS P01 NS047572
6 · The paper itself

Abstract

High-grade serous ovarian carcinoma (HGSOC) and basal-like breast cancer (BLBC) share many features including TP53 mutations, genomic instability and poor prognosis. We recently reported that Elafin is overexpressed by HGSOC and is associated with poor overall survival. Here, we confirm that Elafin overexpression is associated with shorter survival in 1000 HGSOC patients. Elafin confers a proliferative advantage to tumor cells through the activation of the MAP kinase pathway. This mitogenic effect can be neutralized by RNA interference, specific antibodies and a MEK inhibitor. Elafin expression in patient-derived samples was also associated with chemoresistance and strongly correlates with bcl-xL expression. We extended these findings into the examination of 1100 primary breast tumors and six breast cancer cell lines. We observed that Elafin is overexpressed and secreted specifically by BLBC tumors and cell lines, leading to a similar mitogenic effect through activation of the MAP kinase pathway. Here too, Elafin overexpression is associated with poor overall survival, suggesting that it may serve as a biomarker and therapeutic target in this setting.

Indexed as

bcl-X ProteinBlotting, WesternBreast NeoplasmsCell Line, TumorCell ProliferationCystadenocarcinoma, SerousElafinFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansImmunohistochemistryKaplan-Meier EstimateMAP Kinase Signaling SystemMCF-7 CellsOutcome Assessment, Health Carebcl-X ProteinElafin

Identifiers

PMID24469047
PMCPMC4112176
OpenAlexW2015939473

What OpenQuestion holds

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Registered trials

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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.