These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effects of colony-stimulating factors on leukemia progenitor cells and oncogene expression.
    Author: Watson JD, Barber KE, Crosier PS.
    Journal: Behring Inst Mitt; 1988 Aug; (83):154-64. PubMed ID: 3071333.
    Abstract:
    Realising the therapeutic potential of colony-stimulating factors (CSFs) depends upon understanding the biological responses elicited by these regulators in target hemopoietic cells, and determining the biochemical nature of signals transduced through their receptors. These signals can lead to growth, differentiation or the activation of an effector function. CSF-dependent cells maintained in culture resemble pre-leukemic cells and releasing cells from a factor-dependent growth state must be a final step in leukemogenesis. The measurement of metabolic changes in cells following ligand-receptor interactions has thus far failed to reveal the biochemical identity of growth signal transducing events. The patterns of growth responses observed in various CSF-dependent cell lines provide some idea of the relationship of these events for different CSF species. A number of IL-3-dependent cell lines can be switched to an IL-2- or a GM-CSF-dependent growth state. This implies the intracellular pathways activated by signal transduction through their different receptors must be related. The expression of the v-src oncogene in IL-3- and GM-CSF-dependent cells leads to CSF-independent growth, whereas in an IL-2-dependent growth state the expression of v-src in these same cells does not lead to a loss of the requirement for IL-2 for growth. It might be argued that signal transduction through IL-3- or GM-CSF-specific receptors involves a protein tyrosine kinase. However, the addition of IL-3 or GM-CSF to cells expressing v-src results in a decrease in tyrosine kinase activity, suggesting that the effect of IL-3- or GM-CSF-specific signal transduction is to inhibit the expression of tyrosine kinase. It is unlikely that G-CSF signal transduction involves a receptor-associated tyrosine kinase. 32Dcl-23 cells respond to G-CSF by cell division and terminal differentiation, but when these cells are transformed to factor-independent growth following v-src infection, they remain responsive to G-CSF but lose the capacity to terminally differentiate. We have investigated the growth and differentiative responses of a range of human myeloid leukemias to G-CSF, IL-3 and GM-CSF. There is heterogeneity in the responses of different leukemic cells to these growth factors.(ABSTRACT TRUNCATED AT 400 WORDS)
    [Abstract] [Full Text] [Related] [New Search]