Clinical cancer chemotherapy uses low-molecular-mass agents to destroy rapidly dividing cells (see 7.02 Principles of Chemotherapy and Pharmacology). This strategy was initially dominated by genotoxic drugs that target the integrity of the cell's genetic material. Currently, more than 100 chemotherapeutic drugs are used either alone or in combination regimes. The mechanism of action of these anticancer drugs is very broad and expands from the initial DNA interactive agents, which interfere with the growth of cancer cells by reacting with DNA to block its replication, to the most recent targeted therapeutic drugs, which block components of deregulated signal transduction pathways. (Other types of chemotherapy medications include antimetabolites (see 7.03 Antimetabolites), antitumor antibiotics, mitotic inhibitors, hormonal therapies, nitrosoureas.) Cancer chemotherapy offers a unique advantage over the other treatment modalities: it can treat the entire body, even the cells that may have escaped from the primary tumor(s). Chemotherapy is often used in conjunction with other treatments to improve its efficiency, and in this case, patients may receive neoadjuvant chemotherapy to reduce the size of the tumor before surgery or radiation, or adjuvant chemotherapy to eliminate cancer cells that might linger following earlier treatment. Normal cells that divide quickly (e.g., those of bone marrow or the reproductive system) are also affected by chemotherapy and substantial drug discovery efforts have been devoted in the past few years to the identification of more effective agents with better side effect profiles. One of the main issues with this approach is the development of drug resistance, and in order to overcome this problem, combinations of different agents and dosage regimes are often used to maximize benefit for the patient (see 7.02 Principles of Chemotherapy and Pharmacology).
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