Evidence map›Paper›PMID 31765370›Full record

ArticlePLoS biology2019

GPCRs show widespread differential mRNA expression and frequent mutation and copy number variation in solid tumors.

Krishna Sriram, Kevin Moyung, Ross Corriden, Hannah Carter, Paul A Insel

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 74 citations in OpenAlex.

  1. An Itch Receptor Drives Melanoma.bioRxiv : the preprint server for biology · 2026
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  11. GPCRs and fibroblast heterogeneity in fibroblast-associated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Review
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  15. Active GαMolecular and cellular biology · 2023
    Article
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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

5 authors at 1 institution in 1 country.

Krishna SriramDepartment of Pharmacology, University of California, San Diego, California, United States of America.ORCID 0000-0002-2385-3626
Kevin MoyungDepartment of Pharmacology, University of California, San Diego, California, United States of America.
Ross CorridenDepartment of Pharmacology, University of California, San Diego, California, United States of America.
Hannah CarterDepartment of Medicine, University of California, San Diego, California, United States of America.
Paul A InselDepartment of Pharmacology, University of California, San Diego, California, United States of America.
University of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are the most widely targeted gene family for Food and Drug Administration (FDA)-approved drugs. To assess possible roles for GPCRs in cancer, we analyzed The Cancer Genome Atlas (TCGA) data for mRNA expression, mutations, and copy number variation (CNV) in 20 categories and 45 subtypes of solid tumors and quantified differential expression (DE) of GPCRs by comparing tumors against normal tissue from the Gene Tissue Expression Project (GTEx) database. GPCRs are overrepresented among coding genes with elevated expression in solid tumors. This analysis reveals that most tumor types differentially express >50 GPCRs, including many targets for approved drugs, hitherto largely unrecognized as targets of interest in cancer. GPCR mRNA signatures characterize specific tumor types and correlate with expression of cancer-related pathways. Tumor GPCR mRNA signatures have prognostic relevance for survival and correlate with expression of numerous cancer-related genes and pathways. GPCR expression in tumors is largely independent of staging, grading, metastasis, and/or driver mutations. GPCRs expressed in cancer cell lines largely parallel GPCR expression in tumors. Certain GPCRs are frequently mutated and appear to be hotspots, serving as bellwethers of accumulated genomic damage. CNV of GPCRs is common but does not generally correlate with mRNA expression. Our results suggest a previously underappreciated role for GPCRs in cancer, perhaps as functional oncogenes, biomarkers, surface antigens, and pharmacological targets.

Indexed as

DNA Copy Number VariationsGene DosageGenomicsMutationMutation RateNeoplasmsReceptors, G-Protein-CoupledRNA, MessengerReceptors, G-Protein-CoupledRNA, Messenger

Identifiers

PMID31765370
PMCPMC6901242
OpenAlexW2990970256

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.