Evidence map›Paper›PMID 27529230›Full record

ReviewInternational journal of molecular sciences2016

G Protein-Coupled Receptors in Cancer.

Rachel Bar-Shavit, Myriam Maoz, Arun Kancharla, Jeetendra Kumar Nag, Daniel Agranovich, Sorina Grisaru-Granovsky, Beatrice Uziely

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 1 pooled it
12.9field-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

122 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

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62 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Rachel Bar-ShavitSharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. Rachelbar@ekmd.huji.ac.il.
Myriam MaozSharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. Myriamm@hadassah.org.il.
Arun KancharlaSharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. kancharlarn@gmail.com.
Jeetendra Kumar NagSharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. jeetendr.nag@mail.huji.ac.il.
Daniel AgranovichSharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. Danyaag@gmail.com.
Sorina Grisaru-GranovskyDepartment of Obstetrics and Gynecology, Shaare-Zedek Medical Center, Jerusalem 91031, Israel. sorina@szmc.org.il.
Beatrice UzielySharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem 91120, Israel. Beatrice@hadassah.org.il.
Hadassah Medical Center · ILShaare Zedek Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the fact that G protein-coupled receptors (GPCRs) are the largest signal-conveying receptor family and mediate many physiological processes, their role in tumor biology is underappreciated. Numerous lines of evidence now associate GPCRs and their downstream signaling targets in cancer growth and development. Indeed, GPCRs control many features of tumorigenesis, including immune cell-mediated functions, proliferation, invasion and survival at the secondary site. Technological advances have further substantiated GPCR modifications in human tumors. Among these are point mutations, gene overexpression, GPCR silencing by promoter methylation and the number of gene copies. At this point, it is imperative to elucidate specific signaling pathways of "cancer driver" GPCRs. Emerging data on GPCR biology point to functional selectivity and "biased agonism"; hence, there is a diminishing enthusiasm for the concept of "one drug per GPCR target" and increasing interest in the identification of several drug options. Therefore, determining the appropriate context-dependent conformation of a functional GPCR as well as the contribution of GPCR alterations to cancer development remain significant challenges for the discovery of dominant cancer genes and the development of targeted therapeutics.

Indexed as

AnimalsHumansNeoplasmsReceptors, G-Protein-CoupledSignal TransductionReceptors, G-Protein-CoupledcancerCXCR4G protein-coupled receptors (GPCRs)Hippo/YAPLPA(1-6)oncogenesPH-domainproteaseprotease-activated receptorprotease-activated receptors (PARs)Wnt/β-catenin

Identifiers

PMID27529230
PMCPMC5000717
OpenAlexW2507856777

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.