title: Modeling BCR/ABL-driven malignancies in the mouse.
abstract: In this chapter, we describe model systems to study leukemia driven by the Abelson oncogene. In people, the Abelson oncogene results from the chromosomal translocation t(9;22)(q34;q11) that is found in more than 90 % of all human chronic myeloid leukemia (CML) patients and in 20-25 % of patients suffering from acute lymphoid leukemia (ALL). This translocation is also called Philadelphia chromosome and encodes the BCR/ABL oncogene, a constitutive active tyrosine kinase. BCR/ABL renders hematopoietic cells independent from exogenous growth-stimulatory signals by continuously engaging signaling pathways including JAK-STAT signaling and the MAPK pathway. The enforced expression of BCR/ABL suffices to transform hematopoietic cells which made it to one of the best studied model systems in the field. Here we present methods to study BCR/ABL-triggered leukemia and solid lymphoid tumor formation.
authors: University of Veterinary Medicine, Veterinaerplatz 1, A-1210, Vienna, Austria.
authors: Christine
authors: C
authors: Schneckenleithner
authors: Andrea
authors: A
authors: Hoelbl-Kovacic
authors: Veronika
authors: V
authors: Sexl
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D016026:Bone Marrow Transplantation; D045744:Cell Line, Tumor; D018920:Coculture Techniques; D004195:Disease Models, Animal; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D017353:Gene Deletion; D006410:Hematopoiesis; D006801:Humans; D007945:Leukemia, Lymphoid / Q000235:genetics* / Q000473:pathology / Q000601:surgery; D008297:Male; D051379:Mice; D011247:Pregnancy; D012190:Retroviridae / Q000235:genetics; D013045:Species Specificity
chemical_list: D016044:Fusion Proteins, bcr-abl