ABSTRACT
In 1969, Abelson and Rabstein isolated a new tumor inducing variant of Moloney Murine Leukemia Virus (M-MuLV), a virus known to induce thymomas in mice (Abelson and Rabstein, 1969). In contrast to the parental strain, this new strain is a lymphosarcoma-producing virus that is characterized by a rapid development of solid lymphoid and massive meningeal tumors, without affecting the thymus, in infected mice. While a polymorphonuclear leukemoid reaction is observed in these mice, there is no lymphocytic invasion of their organs (Abelson and Rabstein, 1970). This new virus variant was then named the Abelson Murine Leukemia Virus (A-MuLV). A-MuLV was demonstrated to have transformation ability. It can transform fibroblasts and myeloid cells in vitro (Rabstein et al., 1971; Scher and Siegler, 1975). Later, Witte et al. (1978) identified an A-MuLV encoded protein present in A-MuLV transformed cells. This product contains a viral amino-terminal region derived from the Gag gene of M-MuLV and a carboxyl-terminal region from a normal cellular gene. The cellular gene is referred to as the ABL region. The Gag-Abl fusion protein was later referred to as v-Abl. Comparison of the genome sequences of A-MuLV and M-MuLV revealed a DNA fragment that is present only in A-MuLV. This fragment was used to probe the human cDNA library and to pull out a cellular homolog, which was identified as c-Abl (Witte et al., 1978; Witte et al., 1979; Goff et al., 1980).
