Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N Broad Street, Philadelphia, Pennsylvania, PA 19140, USA

Correspondence to: E P Reddy, E-mail: reddy@unix.temple.edu

The Abelson Murine Leukemia Virus (A-MuLV) is the acute transforming retrovirus encoding the v-abl oncogene. Two isolates of the virus encoding proteins of p120 Kd and 160 Kd have been extensively studied. These viral isolates have been found to transform both hematopoietic and fibroblastic cells in vitro, while inducing predominantly pre-B cell leukemias in vivo. Both p120^v-Abl and p160^v-Abl are plasma membrane-associated non-receptor tyrosine kinases and the transforming activity of these proteins requires their tyrosine kinase activity. A-MuLV infection of hematopoietic cells has often been found to result in the abrogation of their cytokine-dependence for growth. In addition, v-Abl expressing hematopoietic cells often lose their ability to differentiate in response to appropriate cytokines. This review discusses some of the early transformation studies of A-MuLV, as well as some of the findings concerning the structure and biochemical activity of the v-Abl protein. Finally, we discuss the mechanisms associated with v-Abl mediated transformation through examination of the various signal transduction pathways activated by this oncogene.

Oncogene (2002) 21, 8568-8576. doi:10.1038/sj.onc.1206084

A-MuLV; tyrosine kinase; transformation; cytokines; apoptosis; signal transduction