MOLONEY VIRUS INDUCTION OF T-CELL LYMPHOMAS IN A PLASMACYTOMAGENIC STRAIN OF E-MU-V-ABL TRANSGENIC MICE
Details
Publication Year 1993-10-21,Volume 55,Issue #4,Page 623-629
Journal Title
INTERNATIONAL JOURNAL OF CANCER
Publication Type
Journal Article
Abstract
Although the v-abl gene can provoke several types of lymphoid neoplasm, mice of a transgenic strain (Emu-v-abl 40) in which lymphocytes are targeted for expression of v-abl by a linked immunoglobulin enhancer (Emu) 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, Emu-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 Emu-v-abl 40 expression found in T lymphocytes than in B lymphocytes: Insertion near the c-myc, N-myc or pim-1 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. (C) 1993 Wiley-Liss, Inc.
Publisher
WILEY-LISS
Keywords
MURINE LEUKEMIA-VIRUS; C-MYC; N-MYC; GENE; IDENTIFICATION; TUMORIGENESIS; SEQUENCES; MODELS; EVENTS
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Creation Date: 1993-10-21 12:00:00
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