Open AccessInduction of Differentiation of Mouse Myeloid Leukemia M1 Cells by Serum of Patients with Chronic Myeloid Leukemia
Author(s) -
OkabeKado Junko,
Honma Yoshio,
Hayashi Moriaki,
Hozumi Motoo,
Sampi Kazumi,
Sakurai Masaharu,
Hino Kenichiro,
Tsuruoka Nobuyoshi
Publication year - 1988
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1988.tb01562.x
Subject(s) - promyelocyte , myeloid leukemia , myeloid , leukemia , immunology , cellular differentiation , myelopoiesis , medicine , biology , cancer research , microbiology and biotechnology , stem cell , haematopoiesis , biochemistry , gene
We examined the capacities of sera from patients with myeloid leukemia to induce differentiation in mouse myeloid leukemic M1 cells. Higher differentiation‐inducing activity (D‐activity) was detected in sera of patients with chronic myelomonocytic leukemia or chronic myeloid leukemia (CML) than in sera of patients with acute myeloid leukemia and normal volunteers. The D‐activity in the sera was lost on heating the sera at 56° for 30 min. The major peak of D‐activity on Sephadex G‐200 gel filtration had an apparent molecular weight of 160,000. The origin of the D‐activity in sera of patients with CML was studied by culturing fractions of peripheral blood cells of patients with D‐activity for 3 days and then measuring the ability of the conditioned medium (CM) to induce differentiation of M1 cells. The cells in the myeloblast and promyelocyte fraction differentiated spontaneously into macrophage‐like cells during culture for 3 days and the cells in the late granulopoietic cell fraction differentiated into neutrophil‐like cells. Higher D‐activity was present in CM of cells in the myeloblast and promyelocyte fraction than in CMs of late granulopoietic cell fractions. These results suggest that human leukemic cells produce D‐activity for M1 cells during their differentiation into macrophage‐like cells.