A targeted cancer therapy is a drug that treats cancer by interacting with a specific molecule that is, for example, involved in the growth, progression or spread of cancer. As research continues into the mechanisms behind different lung cancer tumors, the variety of potential therapeutic targets is continually increasing.
Unlike chemotherapy, targeted therapies are specifically directed toward a particular type of cell, as they home in on a particular feature of the cancer cell. As a result, the side effects can differ and often are less severe. Targeted therapies also differ in their mechanism of action. In general, chemotherapy is “cytotoxic,” meaning that it kills the cells, whereas targeted therapies are generally “cytostatic.” That means they do not tend to kill the cancer cells directly, but instead act to trigger the immune system to destroy the cancer, carry a toxin directly to the cancer cell, or block cell growth and proliferation.
Following are examples of the various targeted therapies:
Like normal cells, cancer cells require a network of blood vessels to keep a flow of nutrients to feed the tumor. By blocking the growth of blood vessels (or angiogenesis) the cancer may be prevented from growing. Two examples of this type of therapy are Avastin (bevacizumab) and Cyramza (ramucirumab). These act on the vascular endothelial growth factor (VEGF) pathway. Avastin directly blocks the VEGF protein, which is required to send signals to trigger blood vessel growth, while Cyramza acts to block the receptors that can sense VEGF, preventing the signal for blood vessel formation from being transmitted.
EGFR (or HER-1), is a type of protein called a tyrosine kinase. It is involved in sending signals that trigger a cell to divide or grow. Many lung cancer tumors have a mutation in the gene encoding for EGFR. These tumors are called EGFR-positive tumors. The mutation results in increased protein activity triggering cancer cell growth and proliferation. EGFR can be targeted by tyrosine-kinase inhibitors (TKIs), a therapy that blocks the action of EGFR and reduces tumor growth. EGFR over-activity can be caused by several different mutations, and some therapies are more effective on certain mutations.
Tarceva (erlotinib), Gilotrif (afatinib) and Iressa (gefitinib) have been approved for the treatment of advanced EGFR-positive non-small cell lung cancer (NSCLC) tumors. Tagrisso (osimertinib) is indicated for the treatment of EGFR-positive tumors that carry a mutation called T790M, and Portrazza (necitumumab) is indicated for squamous cell NSCLC patients.
About 5 percent of NSCLC tumors are “ALK-positive.” This indicates there has been an abnormal rearrangement in the anaplastic lymphoma kinase (ALK) gene sequence. This is more common in non-smokers and can be associated with an increased risk of the cancer spreading to the brain. There are several treatments targeted toward treating tumors with this abnormality, including Xalkori (crizotinib), Zykadia (ceritinib), Alecensa (alectinib), and Alunbrig (brigatinib).
Immune system checkpoint inhibitors
Some cancer cells can use the systems that are in place to protect healthy cells from being attacked by the body’s own immune system. Some targeted therapies act to remove immune system checkpoint pathways, allowing the body’s defenses (the cytotoxic T-cells) to identify and kill the abnormal cancer cells. This also can be referred to as an immunotherapy. Currently approved immunotherapy drugs are Opdivo (nivolumab), Keytruda (pembrolizumab), and Tecentriq (atezolizumab). These all act on the programmed cell death 1 (PD-1) pathway.
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