First Author | Hilbert DM | Year | 1998 |
Journal | Oncogene | Volume | 17 |
Issue | 16 | Pages | 2125-35 |
PubMed ID | 9798684 | Mgi Jnum | J:52752 |
Mgi Id | MGI:1330110 | Doi | 10.1038/sj.onc.1202134 |
Citation | Hilbert DM, et al. (1998) Interaction of abl and raf with IL-7 signaling pathway and transformation of pre-B cells from resistant mice. Oncogene 17(16):2125-35 |
abstractText | After in vivo inoculation with abl/myc- and raf/myc-containing retroviruses, BALB/c mice predominantly develop late stage B cell tumors (plasmacytomas) and less frequently develop earlier B-lineage tumors while DBA/2 mice do not develop B-lineage tumors. We have investigated the in vitro tumorigenic potential of these viruses using cultured normal pre-B cell lymphocytes from both BALB/c and DBA/2 mice. Interestingly, both viruses infect cultured pre-B lymphocytes from both mouse strains. Following infection, IL-7 dependent pre-B cells become independent of normal in vitro growth requirements within 24 h and can rapidly form in vivo pre-B lymphomas in both mouse strains. Mechanisms mediating loss of IL-7 dependence are different depending on whether the raf or abl gene is present in myc-containing viruses. IL-7 JAK-STAT signaling is constitutively active in abl/myc induced pre-B cell tumors. In contrast, IL-7 JAK-STAT signaling is not constitutive in raf/myc induced pre-B cell tumors, demonstrating that subversion of this component of IL-7 signal transduction is not obligatory for pre-B cell transformation or loss of IL-7 dependence. |