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John E. Woods, MD

Arch Surg. 1976;111(10):1055-1056.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Chemotherapy as a practical and useful tool in the treatment of cancer has developed only in the past four decades. The polyfunctional alkaloids became available in the 1940s; the folic acid antagonists, purine analogs, and adrenal corticosteroids in the 1950s; and an ever-increasing number of agents in the 1960s and 1970s, including the progestins, Vinca alkaloids, nitrosoureas, hydroxyurea, cytarabine (cystosine arabinoside), daunorubicin, asparaginase, procarbazine, and the antibiotics actinomycin, bleomycin, and doxorubicin, to name the more commonly used compounds.¹

Regardless of their class, most chemotherapeutic agents appear to exert their major antitumor and toxic effects by inhibiting replication of cells that undergo DNA synthesis sometime during their life cycle. These agents act most effectively against cell populations that have rapid turnovers, and consequently their toxic side effects chiefly influence normal cell populations that also have high turnovers. Thus, the types of clinical toxicity most frequently seen involve bone marrow (producing . . . [Full Text PDF of this Article]

Author Affiliations
From the Mayo Clinic and Mayo Foundation, Rochester, Minn.

Footnotes
Accepted for publication July 8, 1976.

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