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Granulocyte colony‐stimulating factor and its receptor in acute promyelocytic leukemia
Author(s) -
Katayama Naoyuki,
Kita Kenkichi,
Kawakami Keiki,
Mitani Hidetsugu,
Sugawara Takayuki,
Mizuno Satoroh,
Yonezawa Akihito,
Nishii Kazuhiro,
Miwa Hiroshi,
Wada Hideo,
Minami Nobuyuki,
Shiku Hiroshi
Publication year - 1998
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199805)58:1<31::aid-ajh6>3.0.co;2-1
Subject(s) - acute promyelocytic leukemia , granulocyte colony stimulating factor , retinoic acid , cancer research , cell cycle , leukemia , granulocyte colony stimulating factor receptor , granulocyte , myeloid leukemia , immunology , colony stimulating factor , myeloid , medicine , granulocyte macrophage colony stimulating factor receptor , in vitro , biology , cell culture , chemotherapy , microbiology and biotechnology , stem cell , haematopoiesis , macrophage colony stimulating factor , biochemistry , cancer , genetics , macrophage
Expression of granulocyte colony‐stimulating factor (G‐CSF) receptor (G‐CSFR) and in vitro proliferative response to G‐CSF were investigated by quantitative immunofluorescence and [ 3 H] thymidine uptake, respectively, in a series of acute myeloid leukemias (AML). The results indicated that G‐CSFR was detected at high levels in acute promyelocytic leukemia (APL) cells, in comparison with other types of AML. Moreover, APL cells were also seen to predominantly proliferate in response to G‐CSF. Based on these observations, we administered recombinant human G‐CSF to a patient with APL in the third relapse that was resistant to both cytotoxic agents and all trans retinoic acid, in an attempt to sensitize the leukemic cells to cell‐cycle‐dependent agents. Complete remission was achieved. The finding that APL cells are exquisitely responsive to G‐CSF supports the view that G‐CSF is useful for augmentation of their vulnerability to cell‐cycle specific agents. Am. J. Hematol. 58:31–35, 1998. © 1998 Wiley‐Liss, Inc.