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Cancer is a disease of cells characterized by a shift in the control mechanisms that govern cell proliferation and differentiation. Cells that have undergone neoplastic transformation often express normal fetal cell surface antigens or display other signs of apparent immaturity. Cancer cells may also exhibit qualitative or quantitative chromosomal abnormalities, including translocations and amplified gene sequences. Cancer cells proliferate excessively and form local tumors that can compress or invade adjacent normal structures. Within local tumors, a small subpopulation of cells can be described as tumor stem cells. These cells retain the ability to undergo repeated cycles of proliferation and can migrate to distant sites in the body to colonize various organs in the process called metastasis. Thus, tumor stem cells can express clonogenic (colony-forming) capabilities. Chromosomal abnormalities in tumor stem cells reflect their genetic instability, which leads to progressive selection of subclones that can survive more readily in the host’s multicellular environment. Abnormalities in various metabolic pathways and cellular components (e.g., expression of cell-surface drug transporters) accompany neoplastic progression. The invasive and metastatic processes, as well as metabolic abnormalities resulting from the cancer, cause illness and eventual death unless the neoplasm can be eradicated with treatment.

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A classification of anticancer drugs is presented in Figure 31–1. Initial division is based on whether the drugs affect DNA (action on DNA and action on mitotic spindle) or modulate hormonal activity (hormonal agents). Drugs affecting DNA may inhibit synthesis or directly damage DNA. As a group, anticancer drugs are more toxic than any other drugs because they act not only on neoplastic cells but also on normal cells that are in dividing or resting states. Therefore, the benefits of anticancer drugs must be carefully weighed against their risks.

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Figure 31–1.
Graphic Jump Location

Initial classification of anticancer drugs is based on location(s) of action. The first two classes affect DNA or mitosis, whereas the third class modulates hormonal influences on cancer cells. Subsequent divisions of anticancer drugs affecting DNA are based on whether the drug affects DNA directly, or alters DNA synthesis and replication. Drugs that modulate hormonal influence on cancer cells are subsequently divided into agonists or antagonists.

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The incidence, geographic distribution, and behavior of specific types of cancer are related to multiple factors, including gender, age, genetic make-up, and exposure to environmental carcinogens. Of these, environmental exposure is the only modifiable risk factor. Chemical carcinogens, particularly those in tobacco smoke, as well as azo dyes, aflatoxins, asbestos, and benzene have been clearly implicated in cancer induction in humans and animals. In the laboratory, potential environmental carcinogens can be identified by microbial mutagenesis and animal testing.

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Certain deoxyribonucleic acid (DNA) viruses and type C ribonucleic acid (RNA) viruses have been implicated as cancer-causing (oncogenic) agents in animals and humans. Oncogenic RNA viruses contain a reverse transcriptase that transcribes the RNA of the tumor virus ...

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