Background. Intensification chemotherapy improves the prognosis for children with acute lymphoblastic leukemia (ALL), but results in considerable morbidity, primarily due to myelosuppression with resultant neutropenia. Recombinant granulocyte colony-stimulating factor (G-CSF) shortens neutropenia fo
Granulocyte colony-stimulating factor and its receptor in acute promyelocytic leukemia
β Scribed by Katayama, Naoyuki; Kita, Kenkichi; Kawakami, Keiki; Mitani, Hidetsugu; Sugawara, Takayuki; Mizuno, Satoroh; Yonezawa, Akihito; Nishii, Kazuhiro; Miwa, Hiroshi; Wada, Hideo; Minami, Nobuyuki; Shiku, Hiroshi
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 64 KB
- Volume
- 58
- Category
- Article
- ISSN
- 0361-8609
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β¦ Synopsis
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.
π SIMILAR VOLUMES
## Background: Our purpose was to increase the dose intensity of chemotherapy and reduce the days with neutropenic fever in childhood high-risk (hr) acute lymphoblastic leukemia (all) by systematic use of granulocyte-macrophage colony-stimulating factor (gm-csf). ## Procedure: All children with h
The use of granulocyte colony-stimulating factor (G-CSF) after chemotherapy for acute myeloblastic leukemia (AML) has been reported. However, there is a drawback in that G-CSF may stimulate the proliferation of AML progenitors. To determine the parameter(s) indicative of responsiveness of AML blasts