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Granulocyte‐colony stimulating factor‐induced proliferation of primary adult T‐cell leukaemia cells
Author(s) -
MATSUSHITA KAKUSHI,
ARIMA NAOMICHI,
OHTSUBO HIDEO,
FUJIWARA HIROSHI,
HIDAKA SHIROH,
KKITA TOSHIMASA,
SURUGA YUKIO,
FUKUMORI JUNKO,
MATSUMOTO TADASHI,
KANZAKI AKIO,
YAWATA YOSHITO,
TANAKA HIROMITSU
Publication year - 1997
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1997.d01-2102.x
Subject(s) - granulocyte colony stimulating factor , neutropenia , lymphoma , medicine , in vitro , immunology , granulocyte colony stimulating factor receptor , biology , cancer research , chemotherapy , microbiology and biotechnology , biochemistry
Granulocyte‐colony stimulating factor (G‐CSF) is known to induce proliferation and differentiation of granulocyte progenitors, and is widely used to treat neutropenia induced by intensive chemotherapy for malignant lymphoma or adult T‐cell leukaemia/lymphoma (ATL). G‐CSF is thought not to stimulate malignant lymphoid cells. In the present study we examined the ability of G‐CSF to induce in vitro growth of primary ATL cells from 14 patients (nine acute‐type, two chronic‐type and three lymphoma‐type), and we analysed the in vivo counts of ATL cells in patients who received G‐CSF for neutropenia. FACS analysis using phycoerythrin‐labelled recombinant G‐CSF demonstrated that ATL cells from 11/14 patients express some G‐CSF receptor (G‐CSFR), with a range between 5.4% and 87.3%. Cells expressing G‐CSFR also expressed CD4. Reverse polymerase chain reaction (PCR) analysis demonstrated expression of G‐CSFR messenger RNA in G‐CSFR expressing cells. Leukaemic cells derived from seven (four acute‐type, one chronic‐type and two lymphoma‐type) of the 14 patients proliferated in vitro in response to G‐CSF, as measured by [ 3 H]thymidine incorporation; maximum responses were at G‐CSF concentrations of 10–100 ng/ml. Nine of 14 patients receiving rG‐CSF for neutropenia were analysed retrospectively for ATL cell numbers. Four patients whose primary tumour cells proliferated in response to rG‐CSF in vitro showed a significant increase in ATL cell count after administration of rG‐CSF ( P =0.038), whereas five patients whose leukaemic cells did not proliferate in vitro showed no significant increase in ATL cell count. G‐CSF can stimulate proliferation of ATL cells which may complicate therapy for this disease.