Therapy of chronic myelogenous leukemia.
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.
Talpaz
M
M
Department of Clinical Immunology and Biological Therapy, M. D. Anderson Hospital and Tumor Institute, Houston, Texas 77030, USA.
Kantarjian
H
H
McCredie
K
K
Trujillo
J
J
Keating
M
M
Gutterman
J U
JU
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002999:Clone Cells / Q000187:drug effects; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D010677:Philadelphia Chromosome; D011994:Recombinant Proteins; D012074:Remission Induction
D000970:Antineoplastic Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins