Recombinant interferon alpha‐C for advanced hairy cell leukemia. An Israeli multicenter study

• Published in: Cancer 1988-06, Vol.61 (11), p.2207-2213
• Main Authors: Aderka, Dan, Michalevicz, Rita, Daniel, Yair, Levo, Yoram, Douer, Dan, Ben‐Bassat, Isaac, Ramot, Bracha, Shaklai, Matitiahu, Prokocimer, Miron, Berrebi, Alan, Meytes, Dina, Rosenbaum, Hanna, Wallach, David, Revel, Michel
• Format: Article
• Language: English
• Subjects: Age Factors; Antineoplastic agents; Biological and medical sciences; Chemotherapy; Colony-Forming Units Assay; Female; Hematopoiesis - drug effects; Humans; In Vitro Techniques; Interferon Type I - adverse effects; Interferon Type I - therapeutic use; Leukemia, Hairy Cell - drug therapy; Leukemia, Hairy Cell - pathology; Leukocyte Count; Male; Medical sciences; Pharmacology. Drug treatments; Prospective Studies; Recombinant Proteins - therapeutic use; Spleen - pathology
• ISSN: 0008-543X; 1097-0142
• DOI: 10.1002/1097-0142(19880601)61:11<2207::AID-CNCR2820611114>3.0.CO;2-Q

Thirteen patients with advanced hairy cell leukemia were treated with a new subspecies of interferon (IFN): recombinant IFN (rIFN)‐alpha‐C. The timing of the peripheral hematologic remission of individual blood elements was similar to that reported for other interferons, and 60% of patients attained a complete peripheral hematologic remission at 9 months. Two patients relapsed despite a good initial response to IFN. No anti‐IFN antibodies could be detected in their sera. in vitro studies of colony formation from the peripheral blood of all responding patients showed that rIFN‐alpha‐C did not inhibit the growth of colonies but favorably affected the maturation of their elements towards monocytes, granulocytes, and erythroid elements. The relapsing patient examined initially experienced a similar beneficial in vitro response which paralleled his in vivo improvement. During relapse, rIFN‐alpha‐C inhibited both the colony formation and the myelomonocytic differentiation in the in vitro cultures. These findings may suggest that the acquired resistance to IFN in our patient could be due either to an acquired stem cell maturation arrest in response to IFN or to emergence of a new clone indifferent to IFN‐alpha‐C differentiation effect.