Collaboration of PIM-1 and BCL-2 in Lymphomagenesis
作者： D. Acton , J. Domen , H. Jacobs , M. Vlaar , S. Korsmeyer
DOI: 10.1007/978-3-642-77633-5_36
关键词: Oncogene 、 Murine leukemia virus 、 Transgene 、 Genetically modified mouse 、 Carcinogenesis 、 Transplantation 、 Phenotype 、 ABL 、 Cancer research 、 Biology
摘要: Previously, We Have Shown That Pim-1 Transgenic Mice Are Predisposed To Lymphomagenesis. Although The Spontaneous Tumor Incidence In Is Extremely Low, Induction By Carcinogens (Breuer Et Al., 1989; 1991) Or Murine Leukemia Virus Infection (Van Lohuizen 1989) Showed A Dramatic Acceleration Of Disease As Compared Nontransgenic Littermates. Either Proto-Oncogenes C-Myc N-Myc Were Found Be Activated Mulv-Induced T-Cell Lymphomas Mice, Whereas Activation Myc Proviral Insertion Was Only Fraction Induced This Suggested And Efficient Collaborators Lymphomas. Support For Strong Synergistic Interaction Between Came Also From Studies Eμ-Myc Mice. Here Proto-Oncogene Frequently Pre-B Cell 1991). Further Substantiated Crossbreeding Experiments Without Use Any Tumor-Accelerating Agent: Double Carrying Both An Oncogene Died Utero Lymphoblastic (Verbeek Phenotype Crosses L-Myc Somewhat Less Severe, Agreement With Reduced Oncogenicity Oncogenes Order < Observed Culture (MoRoY Transplantation Leukemic Cells Embryos Indicated Additional Events Involved Progression These Tumors Full Malignancy. Mulv Eμ-Pim-1 Has Uncovered Number New Genes Collaborate Transformation. Encompass Bmi-1, Pal-1 Others Which Currently Being Identified (Jonkers & Berns, Unpublished Results). However, Other Can Contribute Types, Such Myb, Abl, Bcl-2 Appeared Not Involved. Particularly Intrigued Lack Involvement Bcl-2, Previously Vitro (Vaux 1988) Vivo. Evidence Collaboration Vivo Presence Rearrangements Immunoblastic Spontaneously Developed Bcl-2-Lg (Mcdonnell support came from crossbreeding of Eμ-myc and Eμ-bcl 2: high incidence primitive lymphoid tumors was found in double transgenic mice (Strasser et al., 1990). we report on the interaction pim-1 bcl-2 crosses between MuLV-induced tumorigenesis these mice.
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