Evidence map›Paper›PMID 40806457›Full record

ReviewInternational journal of molecular sciences2025

TGF-β Signaling in Cancer: Mechanisms of Progression and Therapeutic Targets.

Elżbieta Cecerska-Heryć, Adrianna Jerzyk, Małgorzata Goszka, Aleksandra Polikowska, Julita Rachwalska, Natalia Serwin, Bartosz Wojciuk, Barbara Dołęgowska

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

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  11. Synthesis and Anticancer Activity of New Quinazolin-4(3Pharmaceuticals (Basel, Switzerland) · 2026
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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

8 authors.

Elżbieta Cecerska-HeryćDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.ORCID 0000-0002-7313-7193
Adrianna JerzykDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.
Małgorzata GoszkaDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.
Aleksandra PolikowskaDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.
Julita RachwalskaDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.
Natalia SerwinDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.ORCID 0000-0002-1769-2037
Bartosz WojciukDepartment of Immunological Diagnostics, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.ORCID 0000-0002-2990-0323
Barbara DołęgowskaDepartment of Laboratory Medicine, Pomeranian Medical University of Szczecin, Powstancow Wielkopolskich 72, 70-111 Szczecin, Poland.ORCID 0000-0003-3138-1013

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) is a key protein family member that includes activins, inhibins, and bone morphogenetic proteins (BMPs). It is essential in numerous biological processes, such as chemotaxis, apoptosis, differentiation, growth, and cell migration. TGF-β receptors initiate signaling through two primary pathways: the canonical pathway involving Smad proteins and non-canonical pathways that utilize alternative signaling mechanisms. When TGF-β signaling is disrupted, it has been shown to contribute to the development of various diseases, including cancer. Initially, TGF-β effectively inhibits the cell cycle and promotes apoptosis. However, its role can transition to facilitating tumor growth and metastasis as the disease progresses. Moreover, TGF-β drives cancer progression through epithelial-mesenchymal transition (EMT), modulation of factor expression, and evasion of immune responses. This complexity establishes the need for further research, particularly into pharmacological agents targeting TGF-β, which are emerging as promising therapeutic options. Current clinical and preclinical studies are making significant strides toward mitigating the adverse effects of TGF-β. This underscores the critical importance of understanding its underlying mechanisms to enhance treatment effectiveness and improve survival rates for cancer patients.

Indexed as

NeoplasmsSignal TransductionTransforming Growth Factor betaAnimalsDisease ProgressionEpithelial-Mesenchymal TransitionHumansMolecular Targeted TherapyTransforming Growth Factor betabreast cancercolorectal cancerlung cancerplatelet growth factorsTGF-β

Identifiers

PMID40806457
PMCPMC12347881

What OpenQuestion holds

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Registered trials

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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.