How does chemotherapy work? - Hyunsoo Joshua No
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Chemotherapy is one of the many tools used by physicians for cancer treatment, sitting under a class of medications called “systemic therapies.” Systemic therapies are treatments that use substances that travel through the bloodstream. Along with chemotherapy, other treatments within this modality are targeted therapies, immunotherapy, and hormonal therapy. Systemic treatments are one of the three major modalities that physicians need to treat cancer, along with radiation therapy, and surgery.
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Chemotherapy has 6 medication classes under its belt, including alkylating agents, plant alkaloids, anti-metabolites, anti-neoplastic antibiotics, topoisomerase inhibitors, and “other,” a catch-all category including medications such as microtubule stabilizers. All these classes operate with their own unique mechanisms of action. Despite the varying mechanistic actions, the over-arching principle of these medications are similar. They rely on the differential toxicity of normal cells and tumor cells. Essentially, cytotoxic agents cause harm to all cells, however, given cancer cells predilection for a higher growth rate, along with a stronger dependence on available biomolecules to continue their rapid, uncontrolled growth- they receive the largest impact from these agents. The ability for normal cells to repair the damage elicited from chemotherapies is the key to allowing patients to tolerate these treatments and survive.
The future of systemic therapies is bright, with promising targeted therapies and immunotherapies capitalizing on our ability to better understand specific gene mutations of cancers, as well as the driving factors for carcinogenesis. This has led to the development of more effective, cell-specific therapies, while often times sparing many of the traditional side effects of non-specific cytotoxic therapies. For example, an understanding in the “Philadelphia Chromosome,” where a piece of chromosome 9 and chromosome 22 trade places leading to the formation of a “BCR-ABL” gene, led to the better understanding of the development of chronic myelogenous leukemia, or CML, and how to best treat it. This chromosomal translocation phenomenon causes permanently active tyrosine-kinases, an important mediator in signal transduction for cell proliferation and growth, and a key component in developing CML. This understanding allowed for the development and trials of targeted medications, like Imatinib, a member of a class of medications called “tyrosine kinase inhibitors,” to effectively turn off the downstream signaling pathways that were enabled by the BCR-ABL gene. This lead to incredible survival rates for those with CML, historically with a 5-year survival at 22% in the mid-1970s, to 90% today. The future of systemic therapies and optimized dosing of currently available therapies continue to offer growing promises in the fight against cancer.
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