How do fibroblast growth factor inhibitors like gefitinib function in cancer therapy?

Gefitinib functions in cancer therapy primarily by selectively inhibiting the tyrosine kinase activity of the epidermal growth factor receptor (EGFR). This receptor plays a critical role in the signaling pathways that regulate cell division, proliferation, and survival. In many cancers, especially non-small cell lung cancer, mutations in the EGFR gene lead to constitutive activation of the receptor, promoting uncontrolled tumor growth.

By targeting and inhibiting the tyrosine kinase domain of EGFR, gefitinib disrupts these signaling pathways, resulting in reduced proliferation and survival of cancer cells. This mechanism directly addresses the enhanced signaling output from mutated or overexpressed EGFR in tumors, leading to a therapeutic effect.

The other potential actions described in the choices, such as promoting apoptosis, enhancing immune response, or blocking angiogenesis, do not accurately reflect the primary mechanism of gefitinib. Instead, the key action is its targeted inhibition of EGFR, which is crucial for the drug's efficacy in treating specific types of cancer associated with EGFR dysregulation.