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JNCI Journal of the National Cancer Institute 2001 93(19):1434-1436; doi:10.1093/jnci/93.19.1434
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 19, 1434-1436, October 3, 2001
© 2001 Oxford University Press

EDITORIAL

Cancer, DNA Repair Mechanisms, and Resistance to Chemotherapy

Tito Fojo

Affiliation of author: Center for Cancer Research, National Cancer Institute, Bethesda, MD.

Correspondence to: Tito Fojo, M.D., Ph.D., National Institutes of Health, Bldg. 10, Rm. 12N226, Bethesda, MD 20892 (e-mail: tfojo@helix.nih.gov).

Soon after the introduction of daunomycin and cytosine arabinoside (i.e., cytarabine) in the early 1960's, several reports appeared examining the effects of these agents on bone marrow and peripheral blood cells (1,2). A surprisingly high percentage of normal cells, as many as 92% in some patients treated with daunomycin, had gross chromosomal damage. As we look back on these early studies, it is clear that a cell's capacity to repair DNA damage was overwhelmed by the therapeutic doses of chemotherapy used. Knowing how such damage can lead to DNA rearrangements and, in turn, to secondary leukemias, it is remarkable that the incidence of secondary leukemias in patients treated with chemotherapy has not been higher. Today, it is understood that normal cells damaged beyond repair know when to die. Similar damage was presumably also inflicted on the leukemic cells. Nevertheless, 40 years later, many acute leukemias are . . . [Full Text of this Article]

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