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The effects of benzene and other leukaemogenic agents on haematopoietic stem and progenitor cell differentiation
Author(s) -
Irons Richard D.,
Stillman Wayne S.
Publication year - 1996
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1996.tb01657.x
Subject(s) - clonogenic assay , haematopoiesis , progenitor cell , cd34 , stem cell , biology , hydroquinone , cancer research , microbiology and biotechnology , cellular differentiation , chemistry , apoptosis , biochemistry , gene
A characteristic shared by a diverse group of myelotoxic compounds and leukaemogens is the ability to act synergistically with granulocyte–macrophage colony stimulating factor (GM‐CSF) in increasing clonogenic response. Pretreatment of murine or human bone marrow cells with the benzene metabolite, hydroquinone, but not phenol, catechol or trans, trans‐muconaldehyde, results in a selective enhancement of GM‐CSF but not an interleukin‐3 (IL‐3)‐mediated clonogenic response. Clonal enhancement is preserved and magnified in enriched populations of CD34 + cells (> 95% purity), suggesting an intrinsic effect on haematopoietic progenitor cell (HPC) recruitment rather than a secondary effect involving accessory cytokines. Clonogenic enhancement of murine HPCs is not accompanied by alterations in GM‐CSF receptor expression or ligand affinity and appears to be mediated via a p53‐independent mechanism. These observations suggest that hydroquinone treatment alters recruitment and differentiation in a primitive subpopulation of CD34 + cells and are consistent with a role for altered stem cell differentiation in the development of chemically induced myelodysplasias.