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Targeted cancer therapies use drugs designed to attack specific molecular structures present only in cancer cells, whereas traditional chemotherapy and radiotherapy are non-selective and damage both cancer and normal cells. This selectivity allows targeted therapies to reduce side effects while maintaining effectiveness. Targeted approaches exploit molecular differences between cancer and healthy cells to achieve higher precision in treatment.

In chronic myeloid leukemia, chromosomal translocation fuses the BCR and ABL1 genes, producing an abnormal BCR/ABL1 fusion protein that drives uncontrolled cell proliferation. Imatinib mesylate is a kinase inhibitor that specifically blocks this fusion protein's activity and downstream signaling pathways. The drug achieves a 90% response rate because healthy cells contain redundant tyrosine kinases that compensate for ABL1 inhibition.

Cancer cells with inactive BRCA1 and BRCA2 tumor suppressor genes rely on PARP enzyme for DNA repair and survival. PARP inhibitors block this alternative repair pathway, permanently preventing DNA repair in these cancer cells. Healthy cells remain unaffected because they possess active BRCA1 and BRCA2 DNA repair pathways that provide alternative repair mechanisms.

Monoclonal antibodies target tumor-specific proteins or receptors on cancer cells. For example, trastuzumab inhibits overexpressed HER2 receptor tyrosine kinase in some breast cancer patients. However, since normal cells also express HER2, this therapy can affect healthy cells and cause side effects, demonstrating that even targeted approaches require careful consideration of normal cell expression patterns.

Angiogenesis inhibitors, such as bevacizumab, block the formation of new blood vessels by binding circulating vascular endothelial growth factors. Since tumors require oxygen and nutrients from blood vessels to grow, preventing angiogenesis starves cancer cells of essential resources. This approach targets the tumor microenvironment rather than cancer cells directly, offering a distinct mechanism for restricting tumor cell growth.

Signal transduction inhibitors target abnormal pathways that drive uncontrolled cancer cell growth and proliferation. These drugs inhibit surface receptors or downstream effectors like kinases. Gefitinib, an EGFR inhibitor, exemplifies this approach by successfully treating non-small cell lung cancer where epidermal growth factor receptor is abnormally expressed, blocking the aberrant signals that promote cancer cell survival.

Proteasome inhibitors block the ubiquitin-proteasome pathway, which plays crucial roles in apoptosis, cell survival, cell-cycle progression, and DNA repair. Drugs like bortezomib, carfilzomib, and ixazomib are successfully used because cancer cells in myeloma and mantle-cell lymphoma depend heavily on proteasome function for survival. Inhibiting this pathway triggers cancer cell death while exploiting cancer cells' heightened dependence on proteasome activity.