Abstract

Since its discovery in murine thymoma in 1982, the p56lck (lymphocyte cellular kinase) has been shown to be a pivotal enzyme to both maturation of thymocytes and activation and proliferation of peripheral lymphocytes. The p56lck sequence appeared highly homologous to that of the oncogene p60c-src as did its exon-intron organisation. These data have suggested the lck gene originates from the ancestral src gene by the exon-shuffling mechanism. However, and in spite of this relationship with the p60src oncogene which is often implicated in human cancers, p56lck does not appear involved in lymphoproliferative diseases, either by overexpression or activating mutations. Nevertheless, its aberrant expression has been reported in some carcinomas (colon, lung and mammary). This unexpected expression of a lymphoid-specific protein in solid tumors remained enigmatic until recent studies. In this review, we report these data and explain the possible mechanisms which could lead to the p56lck ectopic expression. We also discuss of signalling pathways which could be affected by the abnormal presence of the p56lck in these tumoral epithelial cells. In particular, we indicate that p56lck could favor metastases by facilitating loss of cell adhesion.