Vincent C. Hascall

TL;DR: The roles of HA interactions with CD44 and RHAMM in inflammatory responses and tumor development/progression are described, and how therapeutic strategies that block these key inflammatory/tumorigenic processes may be developed in rodent and human diseases are described.

TL;DR: Evidence is presented which suggests that the hyaluronic acid-proteoglycan interactions described by Hardingham and Muir ((1972) Biochim.

TL;DR: It is shown that hyaluronan binding at the cell surface is a complex interplay of multivalent binding events affected by the size of the multivalent hyaluranan ligand, the quantity and density of cell surface CD44, and the activation state of CD44 as determined by cell-specific factors and/or treatment with CD44-specific monoclonal antibody (mAb).

TL;DR: Experiments with aggregate preparations reconstituted from mixtures with [3H]acetylated or unlabeled proteoglycans showed that the larger protein fraction is derived from a portion of the protein in the proteoglycan monomer molecules while the smaller isderived from one of the small molecular weight "link proteins" that are present in proteogly can aggregate preparations.

TL;DR: The potential involvement of CD44 variants (CD44v4-v7 and CD44v6-v9) in tumor progression has been confirmed for many tumor types in numerous clinical studies as mentioned in this paper.