¹National Cancer Institute, Division of Basic Science, Basic Research Laboratory, Oncogene Mechanisms Section, Frederick, Maryland, MD 21702-1207, USA

²Intramural Research Support Program, SAIC, Frederick, Maryland, MD 21702-1207, USA

Correspondence to: D G Blair, NCI-Frederick, Bld 469, Room 102, Frederick, Maryland, MD 21702-1207, USA

Studies of retroviral-induced oncogenesis in animal systems led to the initial discovery of viral oncogenes and their cellular homologs, and provided critical insights into their role in the neoplastic process. V-ets, the founding member of the ETS oncogene family, was originally identified as part of the fusion oncogene encoded by the avian acute leukemia virus E26 and subsequent analysis of virus induced leukemias led to the initial isolation of two other members of the ETS gene family. PU.1 was identified as a target of insertional activation in the majority of tumors induced by the murine Spleen Focus Forming virus (SFFV), while fli-1 proved to be the target of Friend murine leukemia virus (F-MuLV) in F-MuLV induced erythroleukemia, as well as that of the 10A1 and Graffi viruses. The common features of the erythroid and myeloid diseases induced by these viruses provided the initial demonstration that these and other members of the ETS family play important roles in hematopoietic development as well as disease. This review provides an overview of the role of ETS genes in retrovirally induced neoplasia, their possible mechanisms of action, and how these viral studies relate to current knowledge of the functions of these genes in hematopoiesis. Oncogene (2000) 19, 6472-6481.

ETS; retrovirus; oncogenesis; E26; F-MuLV; SFFV