Evidence map›Paper›PMID 35229974›Full record

ReviewJournal of cellular and molecular medicine2022

JAK-STAT core cancer pathway: An integrative cancer interactome analysis.

Fettah Erdogan, Tudor Bogdan Radu, Anna Orlova, Abdul Khawazak Qadree, Elvin Dominic de Araujo, Johan Israelian, Peter Valent, Satu M Mustjoki, Marco Herling, Richard Moriggl and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
11.6field-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

66 citing papers in PubMed, 116 citations in OpenAlex.

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6 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

11 authors at 5 institutions in 4 countries.

Fettah ErdoganDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Tudor Bogdan RaduDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Anna OrlovaInstitute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria.
Abdul Khawazak QadreeDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Elvin Dominic de AraujoDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.ORCID 0000-0003-0716-2830
Johan IsraelianDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Peter ValentDivision of Hematology and Hemostaseology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria.
Satu M MustjokiTranslational Immunology Research Program and Department of Clinical Chemistry and Hematology, University of Helsinki, Helsinki, Finland.
Marco HerlingDepartment of Hematology, Cellular Therapy, and Hemostaseology, University of Leipzig, Leipzig, Germany.
Richard MorigglInstitute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria.
Patrick Thomas GunningDepartment of Chemical and Physical Sciences, University of Toronto Mississauga, Mississauga, Ontario, Canada.ORCID 0000-0003-0654-735X
University of Toronto · CAUniversity of Veterinary Medicine Vienna · ATLeipzig University · DEMedical University of Vienna · ATUniversity of Helsinki · FI

Funding

Austrian Science Fund FWF I 4157European Research Council
6 · The paper itself

Abstract

Through a comprehensive review and in silico analysis of reported data on STAT-linked diseases, we analysed the communication pathways and interactome of the seven STATs in major cancer categories and proposed rational targeting approaches for therapeutic intervention to disrupt critical pathways and addictions to hyperactive JAK/STAT in neoplastic states. Although all STATs follow a similar molecular activation pathway, STAT1, STAT2, STAT4 and STAT6 exert specific biological profiles associated with a more restricted pattern of activation by cytokines. STAT3 and STAT5A as well as STAT5B have pleiotropic roles in the body and can act as critical oncogenes that promote many processes involved in cancer development. STAT1, STAT3 and STAT5 also possess tumour suppressive action in certain mutational and cancer type context. Here, we demonstrated member-specific STAT activity in major cancer types. Through systems biology approaches, we found surprising roles for EGFR family members, sex steroid hormone receptor ESR1 interplay with oncogenic STAT function and proposed new drug targeting approaches of oncogenic STAT pathway addiction.

Indexed as

NeoplasmsSTAT Transcription FactorsCytokinesErbB ReceptorsHumansCytokinesErbB ReceptorsSTAT Transcription Factorsblood cancerbreast cancercolorectal cancersJAK/STAT pathway in cancersliver cancerslung cancerprotein-protein interactionssystems medicine

Identifiers

PMID35229974
PMCPMC8980946
OpenAlexW4214706655

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.