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Apoptosis in chronic myeloid leukaemia: normal responses by progenitor cells to growth factor deprivation, X‐irradiation and glucocorticoids
Author(s) -
Amos T. A. S.,
Lewis J. L.,
Grand F. H.,
Gooding R. P.,
Goldman J. M.,
Gordon M. Y.
Publication year - 1995
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 - 10.1111/j.1365-2141.1995.tb05308.x
Subject(s) - progenitor cell , apoptosis , biology , propidium iodide , programmed cell death , cancer research , myeloid , haematopoiesis , immunology , growth factor , microbiology and biotechnology , stem cell , genetics , receptor
Summary. Inhibition of apoptosis (genetically programmed active cell death) by p210 BCR‐ABL expression is a mechanism that might contribute to clonal expansion in chronic myeloid leukaemia (CML). Since cell death following exposure to ionizing radiation and many chemotherapeutic agents can occur by the apoptotic pathway, inhibition of apoptosis would be expected to confer a relative resistance to these treatments. Similarly, cells deprived of growth factors in vitro die by apoptosis, and inhibition of apoptosis would therefore be expected to allow cells to survive better in growth factor‐deprived conditions. We found that the survival of normal and CML myeloid progenitors was the same after in vitro incubation in deprived conditions and after treatment with X‐irradiation or glucocorticoids. We also found that mature cells in colonies produced by CML progenitors (CFU‐GM) did not survive better than those produced by normal progenitor cells. Flow cytometric analysis of propidium iodide‐stained cells provided a direct indication that the degree of apoptosis may correspond to the degree of deprivation. These results suggest that inhibition of apoptosis may not be the primary mechanism whereby BCR‐ABL influences the expansion of the malignant clone in CML.