Oncogene expression in myelopoiesis

Open Access
Publisher Website
Google Scholar
Abstract
Oncogenes are a class of genes hypothesized to be causally related to neoplasia [1]. To date, specific oncogenes have been recognized chiefly by their ability to transform test cells to a neoplastic phenotype. This has been accomplished largely through mutational analysis of the genotype of retroviruses or through the analysis of tumor cell DNA by in vitro transfection of rodent fibroblasts. Oncogenes are believed to arise by some genetic alteration from normal cellular genes called proto‐oncogenes. Although the normal function of most proto‐oncogenes is unknown, it has been proposed that they may function as tissue‐specific and temporally specific regulators of differentiation [2]. The role of oncogenes in lymphoid malignancies has been extensively analyzed [3]. Less is known about their role in myeloid leukemias and especially in normal myelopoiesis. Space limitations permit discussion of only salient features of a limited number of oncogenes; we have arbitrarily selected myc, myb, fos, fms, fes, sis, and abl.