Targeted cancer therapies are a type of treatment that uses drugs or other substances to identify and attack specific types of cancer cells without harming normal cells. These therapies work differently than traditional chemotherapy or radiation therapies by focusing specifically on cancer-driving abnormalities. Some common targeted cancer therapies include monoclonal antibodies, tyrosine kinase inhibitors, angiogenesis inhibitors, PARP inhibitors and immunotherapies. Monoclonal Antibody Therapies Monoclonal antibodies are laboratory-produced molecules that can precisely bind to cancer cells and stop their growth and spread. They work by attaching to specific proteins on cancer cell surfaces and interfering with the signals cancer needs to grow and survive. Some antibodies deliver cytotoxic drugs or radioactive particles directly to tumor sites to kill cancer cells from within. Popular monoclonal antibody drugs include trastuzumab (Herceptin) for breast cancer, rituximab (Rituxan) for lymphoma, bevacizumab (Avastin) for various cancers and cetuximab (Erbitux) for colorectal cancer. Antibody drugs often cause fewer side effects than chemotherapy since they only target cancer cells without harming healthy ones. Research continues to develop more targeted monoclonal antibodies for additional cancer types. Tyrosine Kinase Inhibitors The Targeted Cancer Therapies are enzymes inside cells that help transmit signals from growth factor receptors on the cell surface to the cell's nucleus. Cancer cells sometimes develop mutations that over-activate tyrosine kinase enzymes, spurring uncontrolled growth. Tyrosine kinase inhibitors are targeted drugs that block signals from mutated or over-active tyrosine kinases to cut off the fuel supply cancer needs. Examples include imatinib (Gleevec) for chronic myeloid leukemia, erlotinib (Tarceva) and gefitinib (Iressa) for lung cancer, and lapatinib (Tykerb) for breast cancer. These drugs are often very effective as they directly shut down problematic tyrosine kinase signals driving the tumor. Angiogenesis Inhibitors All tumors require a network of new blood vessels, called angiogenesis, to deliver oxygen and nutrients to fuel rapid growth beyond a limited size. Angiogenesis inhibitors work by choking off this blood supply. The drug bevacizumab is a prime example in this class. It targets vascular endothelial growth factor (VEGF), a protein that tumors secrete to stimulate new blood vessel formation. By blocking VEGF, bevacizumab starves tumors of the oxygen and nourishment needed to thrive and spread. It is approved for certain cancers like colorectal cancer in combination with chemotherapy. PARP Inhibitors DNA damage repair pathways help maintain genomic stability and prevent cancer-causing mutations. One such pathway utilizes poly ADP-ribose polymerase (PARP) enzymes. PARP inhibitors block these enzymes, rendering cancer cells that already have deficient DNA repair mechanisms much less able to fix genomic damage and more prone to cell death. This targeted approach is effective in some breast cancers and ovarian cancers with BRCA1/BRCA2 mutations that rob cells of effective homologous recombination repair. Popular PARP inhibitors include olaparib and rucaparib. Cancer Immunotherapies The immune system naturally surveils for and destroys developing tumors, but cancer can evolve ways to evade immune detection. Cancer immunotherapies aim to reawaken and leverage the body's immune cells, like T cells, to better recognize and attack cancer as the invader it is. Immune checkpoint inhibitors prevent cancer from putting the brakes on activated T cells. Popular checkpoint inhibitors target CTLA-4 and PD-1/PD-L1 pathways to release T cell brakes and empower anti-tumor responses. Other immunotherapies use chimeric antigen receptor (CAR) T cell therapy to reprogram a patient's own T cells to homes in on tumors. Immunotherapies are becoming a revolution in cancer care, producing durable remissions in some patients with advanced disease. Optimizing Targeted Therapies The targeted cancer therapies revolution is transforming the way oncologists and patients approach cancer treatment. While each targeted drug specifically inhibits a molecular abnormality or weak spot, more complex tumors have proved harder to tackle with single agents alone. Thus, combining targeted drugs or using them with immunotherapy or chemotherapy is often needed to improve outcomes. Much progress also remains to be made in matching the right drug to the right patient based on their individual tumor’s unique molecular fingerprint. Advances in genetic testing of tumors are helping to better select optimal targeted therapies, doses and sequences for each cancer patient. Overall, targeted therapies represent a new era of customized, mechanism-focused treatment that offers profound hope, especially when paired with immune therapies, to conquer even some of the most challenging and treatment-resistant cancers.
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