Abstract:An estimated 20-30% of CML patients will become resistant to tyrosine kinase inhibitors (TKIs) including imatinib. Recent reports suggest that CML resistance to TKI's is driven by interactions with protective microenvironment niches that influence their survival and self-renewal capacity. Hyaluronic acid (HA) has emerged as a key contributor in this phenomenon of CML resistance to TKI’s. HA influences cell viability through molecular weight dependent interactions with cell-surface receptors CD44 and RHAMM. Low… Show more
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