ALK: a tyrosine kinase target for cancer therapy
Dramatic and often prolonged responses are seen in patients with ALK alterations when treated with ALK inhibitors.
The anaplastic lymphoma kinase (ALK) gene, normally expressed in brain and small intestine, can be oncogenically altered in multiple malignancies including non‑small‑cell lung cancer (NSCLC) and anaplastic large‑cell lymphoma (ALCL). Chromosomal rearrangements that produce ALK fusion proteins (e.g., EML4‑ALK) and activating point mutations lead to ligand‑independent kinase activation. Patients harboring such ALK alterations exhibit dramatic and often prolonged clinical responses to ALK‑targeted tyrosine‑kinase inhibitors. Crizotinib, ceritinib, and alectinib are FDA‑approved for metastatic NSCLC positive for ALK fusions, and ongoing development of next‑generation inhibitors seeks to overcome universal resistance mechanisms.
Clinical targeting of ALK represents a paradigm for precision oncology, delivering significant survival benefit in NSCLC and other ALK‑driven malignancies, while highlighting the emergence of resistance as a therapeutic challenge.
Bizonyítékszint: Korai humán adat. Kis vagy feltáró emberi adat.
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