Evidence map›Paper›PMID 39976799›Full record

ReviewMolecular biology reports2025

Focal adhesion kinase (FAK): emerging target for drug-resistant malignant tumors.

Jaya Aakriti, Megh Pravin Vithalkar, Swastika Maity, Krishnaprasad Baby, Prabhakara R Nagareddy, Yogendra Nayak

Abstract readReview
In one paragraph

Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

6 authors.

Jaya AakritiDepartment of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Madhava Nagar, Manipal, 576104, India.
Megh Pravin VithalkarDepartment of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Madhava Nagar, Manipal, 576104, India.
Swastika MaityDepartment of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Madhava Nagar, Manipal, 576104, India.
Krishnaprasad BabyDepartment of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Madhava Nagar, Manipal, 576104, India.
Prabhakara R NagareddyDepartment of Internal Medicine, Cardiovascular Section, University of Oklahoma Health Sciences Center (OUHSC), Oklahoma City, OK, USA.
Yogendra NayakDepartment of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Madhava Nagar, Manipal, 576104, India. yogendra.nayak@manipal.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant tumors associated with drug resistance present a significant challenge for clinicians and drug developers. Mutations and alterations within the tumor microenvironment frequently drive cancer cell invasion and metastasis. Despite identifying numerous molecular targets and lead compounds, achieving sustained efficacy remains challenging due to the rapid mutation rates and the emergence of resistance. Recently, Focal Adhesion Kinase (FAK), a non-receptor tyrosine kinase, has emerged as a promising target for inhibiting cancer progression, with several lead molecules advancing through clinical trials. FAK plays a critical role in cancer pathology by regulating cell adhesion, migration, proliferation, and survival. Its structure comprises three domains- the N-terminal FERM domain, kinase domain, and C-terminal focal adhesion targeting domain- contributing to its functional versatility. Ligands targeting the FERM and kinase domains can suppress cancer cell proliferation, invasion, and migration. The FERM domain, a member of the ezrin, radixin, and moesin family, is particularly noteworthy for its ligand-binding capabilities and potential to inhibit tumor growth. While FAK is a compelling anticancer target, challenges such as tissue-specific physiological variability and broad ligand specificity remain. This review provides a detailed analysis of FAK's role in cancer progression and explores emerging molecules targeting FAK as potential treatments for drug-resistant malignant tumors.

Indexed as

Drug Resistance, NeoplasmFocal Adhesion Protein-Tyrosine KinasesNeoplasmsAnimalsAntineoplastic AgentsCell AdhesionCell MovementCell ProliferationHumansMolecular Targeted TherapyProtein Kinase InhibitorsTumor MicroenvironmentAntineoplastic AgentsFocal Adhesion Protein-Tyrosine KinasesProtein Kinase InhibitorsCancerClinical trialsCombination therapyDefactinibFAK-inhibitorsFAK-structureFocal adhesion kinase

Identifiers

PMID39976799
PMCPMC11842479

What OpenQuestion holds

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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.