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Recombinant interferon alpha‐C for advanced hairy cell leukemia. An Israeli multicenter study
Author(s) -
Aderka Dan,
Michalevicz Rita,
Daniel Yair,
Levo Yoram,
Douer Dan,
BenBassat Isaac,
Ramot Bracha,
Shaklai Matitiahu,
Prokocimer Miron,
Berrebi Alan,
Meytes Dina,
Rosenbaum Hanna,
Wallach David,
Revel Michel
Publication year - 1988
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(19880601)61:11<2207::aid-cncr2820611114>3.0.co;2-q
Subject(s) - medicine , alpha interferon , hairy cell leukemia , recombinant dna , multicenter study , interferon alfa , alpha (finance) , leukemia , cancer research , virology , interferon , oncology , immunology , surgery , randomized controlled trial , genetics , patient satisfaction , construct validity , biology , gene
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.