Disruption of the CXCR4/CXCL12 chemotactic interaction during hematopoietic stem cell mobilization induced by GCSF or cyclophosphamide.
By J. Lévesque, Jean Hendy, Y. Takamatsu, P. Simmons, L. Bendall. Journal of Clinical Investigation, 2003
830 citations recorded by the source corpus.
Subfields: Hematology, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/3ba4aa46178a24368eb33aed4c4e3f1ea1664477
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In Hematology
In Immunology
- Robert Samstein
- F. Balkwill
- A. Kalinkovich
- J. Joyce
- Lisa M. Coussens
- D. Hanahan
- A. Mantovani
- M. Karin
In Oncology
Citations in the corpus
- Cancer and the chemokine network (2004, background): “Preclinical and clinical studies with stem-cell-mobilizing agents, such as granulocyte colony-stimulating factor and cyclophosphamide, cause a profound decrease in bone-marrow levels of CXCL12, owing to its degradation by neutrophil elastase, cathepsin G and MMP”
- Osteoclasts degrade endosteal components and promote mobilization of hematopoietic progenitor cells (2006, background): “These are followed by degradation of SDF-1, increased expression of CXCR4 and mobilization of maturing leukocytes, progenitors and stem cell”
- HGF, SDF-1, and MMP-9 are involved in stress-induced human CD34+ stem cell recruitment to the liver. (2003, background): “Proteolytic cleavage associated with inactivation of SDF-1 was demonstrated by several degrading enzymes (28, 33, 34) including MMP-2 and MMP-9, which cleave the N-terminus (35).”