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Recent investigations have reported changes in the expression of cell surface adhesion molecules associated with melanoma progression from in situ to invasive to metastatic tumors, including the upregulation of the integrins alpha v beta 3, alpha 3 beta 1, alpha 4 beta 1, and alpha 5 beta 1, downregulation of alpha 6 beta 1, and enhanced expression of intercellular adhesion molecule-1, MUC18, and CD44. Current research is now focused on the function of these adhesion molecules in facilitating melanoma invasion, metastasis and evasion of lysis by effector cells, and the mechanisms involved in controlling the adhesion molecule activation state and signal transduction.
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Michael Edward (1995) studied this question.
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