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Therapy of chronic myelogenous leukemia
Author(s) -
Talpaz Moshe,
Kantarjian Hagop,
McCredie Kenneth,
Trujillo Jose,
Keating Michael,
Gutterman Jordan U.
Publication year - 1987
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19870201)59:3+<664::aid-cncr2820591316>3.0.co;2-y
Subject(s) - chronic myelogenous leukemia , medicine , philadelphia chromosome , interferon alfa , interferon , alpha interferon , leukemia , immunology , bone marrow , karyotype , immunotherapy , cancer research , chromosome , immune system , biology , chromosomal translocation , genetics , gene
While the demonstrated antiviral, antiproliferative, and immunomodulatory properties of interferons have led to a number of theories regarding their potential use in treating individuals with chronic myelogenous leukemia (CML), their limited availability has prevented thorough clinical investigation. However, in 1980, successful cloning of the mature human alpha–A interferon led to the production of large quantities of bacterially synthesized human alpha–A interferon, now designated interferon alfa–2a (Roferon®–A, Hoffmann‐La Roche, Nutley, NJ). This abundance of alfa–2a made possible clinical studies of alpha interferon's capacity to suppress CML Philadelphia (Ph1) clones as well as restore the cells with normal karyotype. The data resulting from these clinical trials indicate that interferon alfa–2a is effective in inducing hematologic remissions in the majority of minimally treated, benign–phase CML, Ph1‐positive patients. In some of the patients, treatment resulted in Ph1 chromosome suppression in the bone marrow and in the emergence of cells with a normal karyotype.