FAK in cancer: mechanistic findings and clinical applications
By Florian J Sulzmaier, C. Jean, D. Schlaepfer. Nature Reviews. Cancer, 2014
1,253 citations recorded by the source corpus.
Focal adhesion kinase (FAK) is a cytoplasmic protein tyrosine kinase that is overexpressed and activated in several advanced-stage solid cancers. FAK promotes tumour progression and metastasis through effects on cancer cells, as well as stromal cells of the tumour microenvironment. The kinase-dependent and kinase-independent functions of FAK control cell movement, invasion, survival, gene expression and cancer stem cell self-renewal. Small molecule FAK inhibitors decrease tumour growth and metastasis in several preclinical models and have initial clinical activity in patients with limited adverse events. In this Review, we discuss FAK signalling effects on both tumour and stromal cell biology that provide rationale and support for future therapeutic opportunities.
Subfields: Cancer Research, Cell Biology, Immunology and Allergy
View Paper: https://www.semanticscholar.org/paper/a1c2ae93d1b64831682158115e1d74774ade23c7
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
In Cell Biology
In Immunology and Allergy
Citations in the corpus
- The delivery of therapeutic oligonucleotides (2016, background): “They also directly generate intracellular signals themselves, primarily through focal adhesion kinase (88).”
- FAP Promotes Immunosuppression by Cancer-Associated Fibroblasts in the Tumor Microenvironment via STAT3-CCL2 Signaling. (2016, background): “uPAR is reported to frequently cause activation of FAK, an important upstream signaling molecule that drives various tumor-promoting signaling pathways(20,21).”