PTK2
Overview
PTK2 (Protein Tyrosine Kinase 2), also known as Focal Adhesion Kinase (FAK), encodes a non-receptor tyrosine kinase that regulates cell adhesion, migration, invasion, and survival downstream of integrin and growth factor receptor signaling. PTK2 copy gain and overexpression have been described in several squamous cell carcinomas and are associated with increased invasiveness and poor prognosis.
Alterations observed in the corpus
- Copy gain with high expression in 14% (5/35) of oral squamous cell carcinoma (OSCC) tumors; identified as a candidate therapeutic target in HNSCC PMID:23619168
- Overexpressed in the immune-excluded HCC subclass; oncogenic PTK2 (FAK) pathway activity is associated with poor T-cell infiltration and immune exclusion in HCC PMID:24798001
Cancer types (linked)
- OCSC / HNSC (Oral/Head and Neck Squamous Cell Carcinoma): PTK2 (FAK) copy gain with high mRNA expression in 14% of OSCC; included among the 80% of tumors harboring at least one targetable gene alteration PMID:23619168
Co-occurrence and mutual exclusivity
- PTK2 copy gain co-occurs with SRC-family kinase alterations (SRC, LYN, YES1 collectively in 29% of OSCC) as part of the broader targetable kinase landscape in OSCC PMID:23619168
Therapeutic relevance
- PTK2 (FAK) is a candidate drug target in OSCC; FAK inhibitors are in clinical development. The OSCC study identifies PTK2 copy gain + high expression (14% of tumors) as a rationale for FAK-directed therapy PMID:23619168
Open questions
- Clinical validation of PTK2 copy gain as a predictive biomarker for FAK inhibitor response in HNSCC is not addressed in this cohort.
Sources
This page was processed by crosslinker on 2026-05-09. - PMID:24798001
This page was processed by wiki-cli on 2026-05-11.