Evidence map›Paper›PMID 27396341›Full record

ArticleCell reports2016

Anti-Müllerian Hormone Signaling Regulates Epithelial Plasticity and Chemoresistance in Lung Cancer.

Tim N Beck, Vlad A Korben, Alexander E Kudinov, Rachel Georgopoulos, Nehal R Solanki, Magda Andrews-Hoke, Timothy M Kistner, David Pépin, Patricia K Donahoe, Emmanuelle Nicolas and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 71 citations in OpenAlex.

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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

16 authors at 9 institutions in 2 countries.

Tim N BeckProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Program in Molecular and Cell Biology and Genetics, Drexel University College of Medicine, Philadelphia, PA 19129, USA.
Vlad A KorbenProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Medical Department, Novosibirsk State University, Novosibirsk 630090, Russia.
Alexander E KudinovProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Rachel GeorgopoulosTemple University School of Medicine, Philadelphia, PA 19140, USA.
Nehal R SolankiImmune Cell Development and Host Defense Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Program in Microbiology and Immunology, Drexel University College of Medicine, Philadelphia, PA 19129, USA.
Magda Andrews-HokeYale University, New Haven, CT 06520, USA.
Timothy M KistnerJohns Hopkins University, Baltimore, MD 21218, USA.
David PépinPediatric Surgical Research Laboratories, Massachusetts General Hospital and Department of Surgery, Harvard Medical School, Boston, MA 02114, USA.
Patricia K DonahoePediatric Surgical Research Laboratories, Massachusetts General Hospital and Department of Surgery, Harvard Medical School, Boston, MA 02114, USA.
Emmanuelle NicolasProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Margret B EinarsonProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Yan ZhouDepartment of Biostatistics and Bioinformatics, Fox Chase Cancer Center, Philadelphia, PA 19140, USA.
Yanis BoumberProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
David A ProiaSynta Pharmaceuticals, Lexington, MA 02421, USA.
Ilya G SerebriiskiiProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Kazan Federal University, 420000 Kazan, Russian Federation.
Erica A GolemisProgram in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA; Program in Molecular and Cell Biology and Genetics, Drexel University College of Medicine, Philadelphia, PA 19129, USA. Electronic address: erica.golemis@fccc.edu.
Fox Chase Cancer Center · USDrexel University · USHarvard University · USJohns Hopkins University · USMassachusetts General Hospital · USNovosibirsk State Medical University · RUSynta Pharmaceuticals (United States) · USTemple University · USYale University · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Eric Andrew Ross · 1985 to 2026
$138.8M
Therapeutic Micro RNA Strategies for Ovarian CancerP50CA083638 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI BOOKMAN, MICHAEL A, CAIRNS, PAUL · 1999 to 2013
$33.6M
Novel Targets in Endocrine ResponsivenessU54CA149147 · NCI · GEORGETOWN UNIVERSITY · PI WEINER, LOUIS M. · 2010 to 2014
$6.9M
Msi2 regulates the aggressiveness of Non-Small Cell Lung Cancer (NSCLC)R21CA191425 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2016 to 2017
$427k
A Role for AMH Autocrine Signaling in NSCLCR21CA181287 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 2014 to 2015
$421k
Characterization of AMH as part of a novel TGF-beta signaling loopF30CA180607 · NCI · DREXEL UNIVERSITY · PI BECK, TIM NICO · 2014 to 2017
$163k
NCI NIH HHS F30 CA180607NCI NIH HHS P30 CA006927NCI NIH HHS P50 CA083638NCI NIH HHS R21 CA181287NCI NIH HHS R21 CA191425NCI NIH HHS U54 CA149147
6 · The paper itself

Abstract

Anti-Müllerian hormone (AMH) and its type II receptor AMHR2, both previously thought to primarily function in gonadal tissue, were unexpectedly identified as potent regulators of transforming growth factor (TGF-β)/bone morphogenetic protein (BMP) signaling and epithelial-mesenchymal transition (EMT) in lung cancer. AMH is a TGF-β/BMP superfamily member, and AMHR2 heterodimerizes with type I receptors (ALK2, ALK3) also used by the type II receptor for BMP (BMPR2). AMH signaling regulates expression of BMPR2, ALK2, and ALK3, supports protein kinase B-nuclear factor κB (AKT-NF-κB) and SMAD survival signaling, and influences BMP-dependent signaling in non-small cell lung cancer (NSCLC). AMH and AMHR2 are selectively expressed in epithelial versus mesenchymal cells, and loss of AMH/AMHR2 induces EMT. Independent induction of EMT reduces expression of AMH and AMHR2. Importantly, EMT associated with depletion of AMH or AMHR2 results in chemoresistance but sensitizes cells to the heat shock protein 90 (HSP90) inhibitor ganetespib. Recognition of this AMH/AMHR2 axis helps to further elucidate TGF-β/BMP resistance-associated signaling and suggests new strategies for therapeutic targeting of EMT.

Indexed as

AnimalsAnti-Mullerian HormoneBone Morphogenetic Protein Receptors, Type IICarcinoma, Non-Small-Cell LungCell PlasticityDrug Resistance, NeoplasmEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression RegulationHeat-Shock ProteinsLung NeoplasmsMesenchymal Stem CellsMiceMice, SCIDNF-kappa BReceptors, PeptideAnti-Mullerian Hormoneanti-Mullerian hormone receptorBone Morphogenetic Protein Receptors, Type IIHeat-Shock ProteinsNF-kappa BReceptors, PeptideReceptors, Transforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID27396341
PMCPMC4956518
OpenAlexW2466883271

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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.