Moloney virus induction of T-cell lymphomas in a plasmacytomagenic strain of Eμ-V-ABL transgenic mice

✍ Scribed by Ygal Haupt; Alan W. Harris; Jerry M. Adams

• Publisher: John Wiley and Sons
• Year: 1993
• Tongue: French
• Weight: 924 KB
• Volume: 55
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910550418

✦ Synopsis

Although the v-abl gene can provoke several types of lymphoid neoplasm, mice of a transgenic strain (Ep-v-a61 40) in which lymphocytes are targeted for expression of v-abl by a linked immunoglobulin enhancer (Ep) spontaneously develop only plasmacytomas. To determine whether other lymphocytes of this strain were susceptible to transformation, and to identify genes that can collaborate with v-abl in tumorigenesis, Ep-v-abl 40 mice were subjected to insertional mutagenesis by neonatal infection with Moloney murine leukemia virus. Tumorigenesis was accelerated moderately, but nearly all the tumors were T lymphomas. The altered tumor type may reflect both the T-cell tropism of Moloney virus and the higher level of Ep-v-abl 40 expression found in T lymphocytes than in B lymphocytes. insertion near the c-myc, N-myc or pim-I gene was observed in 42% of the induced tumors, indicating that each of these genes may collaborate with v-abl in lymphomagenesis. Most of the accelerated tumors had a surprisingly low level of transgene expression. Thus, high expression of v-abl may not be required for Moloney-induced T lymphomagenesis.