Moloney virus induction of T-cell lymphomas in a plasmacytomagenic strain of E mu-v-abl transgenic mice.
Although the v-abl gene can provoke several types of lymphoid neoplasm, mice of a transgenic strain (E mu-v-abl 40) in which lymphocytes are targeted for expression of v-abl by a linked immunoglobulin enhancer (E mu) 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, E mu-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 E mu-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.
Haupt
Y
Y
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Harris
A W
AW
Adams
J M
JM
D000818:Animals; D002472:Cell Transformation, Viral; D015870:Gene Expression; D016313:Genes, abl; D016259:Genes, myc; D008214:Lymphocytes / Q000648:ultrastructure; D016399:Lymphoma, T-Cell / Q000235:genetics / Q000382:microbiology*; D051379:Mice; D008822:Mice, Transgenic; D008979:Moloney murine leukemia virus; D016254:Mutagenesis, Insertional; D010954:Plasmacytoma / Q000209:etiology; D014412:Tumor Virus Infections / Q000235:genetics