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Clonal Variation, Autoimmunity, and Neoplasia: An Ecology Lesson from Paroxysmal Nocturnal Hemoglobinuria

Edward J. Benz Jr., MD
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Johns Hopkins University School of Medicine; Baltimore, MD 21205 (Benz)

Requests for Reprints: Edward J. Benz Jr., MD, Johns Hopkins University School of Medicine, Room 926, 1830 East Monument Street, Baltimore, MD 21205.

Ann Intern Med. 1999;131(6):467-468. doi:10.7326/0003-4819-131-6-199909210-00013
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The immune response is regarded as one line of host defense against cancer. Thus, cancer seen in immunodeficient states is attributed to loss of immune surveillance, and immune augmentation strategies for anticancer therapy are strenuously pursued. In this issue, Dunn and colleagues (1) propose that immune attack might actually confer an ecological advantage on some neoplastic cells in their microenvironment. They suggest that the distinctive neoplastic clones encountered in patients with paroxysmal nocturnal hemoglobinuria (PNH) may gain the upper hand only in bone marrow affected by autoimmune destruction of normal clones. Much additional work will be required to test this notion. Nonetheless, this provocative hypothesis merits comment for what it could imply about host-tumor ecology and about potential unintended consequences of immune augmentation therapies.

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