Evidence map›Paper›PMID 29293502›Full record

ArticlePLoS computational biology2018

Integration of pan-cancer transcriptomics with RPPA proteomics reveals mechanisms of epithelial-mesenchymal transition.

Simon Koplev, Katie Lin, Anders B Dohlman, Avi Ma'ayan

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  18. Multi-omics Integration Analysis Robustly Predicts High-Grade Patient Survival and Identifies CPT1B Effect on Fatty Acid Metabolism in Bladder Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
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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

4 authors at 1 institution in 1 country.

Simon KoplevDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, United States of America.
Katie LinDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, United States of America.
Anders B DohlmanDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, United States of America.
Avi Ma'ayanDepartment of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, United States of America.ORCID 0000-0002-6904-1017
Icahn School of Medicine at Mount Sinai · US

Funding

Data Coordination and Integration Center for LINCS-BD2KU54HL127624 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MA'AYAN, AVI, SCHURER, STEPHAN C · 2014 to 2019
$23.5M
User Interface PortalU54CA189201 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DUDLEY, JOEL THOMAS, MA'AYAN, AVI · 2014 to 2017
$1.9M
Expression2Kinases: mRNA Profiling Linked to Multiple Upstream Regulatory LayersR01GM098316 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MA'AYAN, AVI · 2012 to 2015
$1.3M
NCI NIH HHS U54 CA189201NHLBI NIH HHS U54 HL127624NIGMS NIH HHS R01 GM098316NIH HHS R01GM098316NIH HHS U54CA189201NIH HHS U54HL127624
6 · The paper itself

Abstract

Integrating data from multiple regulatory layers across cancer types could elucidate additional mechanisms of oncogenesis. Using antibody-based protein profiling of 736 cancer cell lines, along with matching transcriptomic data, we show that pan-cancer bimodality in the amounts of mRNA, protein, and protein phosphorylation reveals mechanisms related to the epithelial-mesenchymal transition (EMT). Based on the bimodal expression of E-cadherin, we define an EMT signature consisting of 239 genes, many of which were not previously associated with EMT. By querying gene expression signatures collected from cancer cell lines after small-molecule perturbations, we identify enrichment for histone deacetylase (HDAC) inhibitors as inducers of EMT, and kinase inhibitors as mesenchymal-to-epithelial transition (MET) promoters. Causal modeling of protein-based signaling identifies putative drivers of EMT. In conclusion, integrative analysis of pan-cancer proteomic and transcriptomic data reveals key regulatory mechanisms of oncogenic transformation.

Indexed as

Antigens, CDCadherinsCarcinogenesisCell Line, TumorComputational BiologyEpithelial-Mesenchymal TransitionHistone Deacetylase InhibitorsHumansModels, GeneticModels, StatisticalNeoplasmsPhosphorylationProtein Array AnalysisProtein Kinase InhibitorsProteomicsRNA, MessengerAntigens, CDCadherinsCDH1 protein, humanHistone Deacetylase InhibitorsProtein Kinase InhibitorsRNA, MessengerRNA, Neoplasm

Identifiers

PMID29293502
PMCPMC5766255
OpenAlexW2781983082

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.