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Targeting FAK in anticancer combination therapies
John C Dawson1, Alan Serrels2, Dwayne G Stupack3
1Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. john.c.dawson@ed.ac.uk.
Nature Reviews. Cancer
|March 18, 2021
Summary
Focal adhesion kinase (FAK) inhibitors show promise in cancer therapy. Preclinical data suggest FAK inhibitors are most effective when combined with other treatments to overcome drug resistance in solid tumors.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase and adaptor protein.
- FAK regulates cell adhesion, migration, and survival.
- FAK is frequently overexpressed in various cancers, making it a significant therapeutic target.
Purpose of the Study:
- To review preclinical evidence on FAK's role in anticancer therapeutic resistance.
- To evaluate the potential of FAK inhibitors as combination therapies.
Main Methods:
- Literature review of preclinical studies.
- Analysis of FAK's involvement in resistance mechanisms.
- Evaluation of FAK inhibitors in combination therapy models.
Main Results:
- FAK overexpression is linked to resistance against chemotherapy and targeted therapy.
- FAK inhibition can sensitize solid tumors to existing treatments.
- Combining FAK inhibitors with immunotherapy may enhance anti-tumor immune responses.
Conclusions:
- FAK plays a critical role in the development of therapeutic resistance in cancer.
- FAK inhibitors are likely to be most effective as part of combination strategies.
- Targeting FAK in combination therapies holds potential for selected patient populations with solid tumors.
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