Evidence mapPaperPMID 41160113Full record

ReviewHandbook of experimental pharmacology2026

GPCR Biased Signaling in Cancer.

Ariella C Avigad, Melody Zhou, Chengyu Sun, Levin Ma, Xue Li, Rosie J Blodgett, Vera S Donnenberg, Albert D Donnenberg, Patrick L Wagner, David L Bartlett and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Handbook of experimental pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Ariella C Avigad *Allegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Melody Zhou *Allegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Chengyu Sun *Allegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Levin MaAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Xue LiAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Rosie J BlodgettAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Vera S DonnenbergDepartment of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Albert D DonnenbergAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Patrick L WagnerAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
David L BartlettAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA.
Kunhong XiaoAllegheny Health Network Cancer Institute, Allegheny Health Network, Pittsburgh, PA, USA. kunhongkevin.xiao@ahn.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) represent the largest family of cell surface receptors. They orchestrate various signaling pathways, playing a central role in regulating various physiological and pathophysiological processes. Dysregulation of GPCR signaling has been intricately linked to cancer pathogenesis, including tumor growth, angiogenesis, metastasis, and immune modulation. Biased GPCR signaling occurs when a ligand preferentially activates one signaling pathway over another, leading to distinct cellular outcomes. In cancer, biased GPCR signaling represents a complex, dynamic phenomenon, significantly influencing cancer development, progression, and treatment resistance. This chapter reviews recent advances in our understanding of GPCR biased signaling in various aspects of cancer biology and explores its therapeutic potential. Given the fragmented nature of existing evidence, we integrate available literature with findings from our own proteomics studies on GPCR and β-arrestin function to provide a preliminary framework for understanding β-arrestin-mediated signaling in cancer. While this overview may capture only a limited snapshot of the broader landscape, it provides a valuable foundation for generating new hypotheses and guiding future research and drug discovery efforts in oncology.

Indexed as

NeoplasmsReceptors, G-Protein-CoupledSignal TransductionAnimalsAntineoplastic Agentsbeta-ArrestinsHumansAntineoplastic Agentsbeta-ArrestinsReceptors, G-Protein-CoupledCancerGPCRGPCR biased signalingβ-arrestinβ-arrestin-mediated signaling

Identifiers

PMID41160113

What Socratic holds

Textmetadata
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 Socratic graph.