The c-myc oncogene has been implicated in deregulation of cell growth in neoplastic cells and response to "competence-inducing" growth factors in normal cells. In the latter case, expression of c-myc has been shown to be associated with the transition from the Go to the G1 phase of the cell cycle induced by platelet-derived growth factor (PDGF). In the work reported here, we have introduced the c-myc coding region, in a retroviral vector, into mouse and rat cells. We show that under conditions of anchorage-independent growth, constitutive c-myc expression increases the response of rodent cells to PDGF, as well as to other growth factors of both the competence-inducing and "progression" classes. These effects of the myc product are observed whether or not an exogenous ras gene has also been introduced into the same cells. Possible models for the influence of myc on growth responses are discussed.

Fricke chemical dosimetry is used as an indirect measure of the free radical production of ionizing irradiation. We adapted the Fricke ferrous sulfate radiation dosimeter to examine the chemical effects of high energy shock waves. Significant free radical production was documented. The reaction was dose dependent, predictably increased by acoustic impedance, but curvilinear. A thousand shocks at 18 kilovolts induced the same free radical oxidation as 1100 rad cobalt-60 gamma ionizing irradiation, increasing to 2900 rad in the presence of an air-fluid zone of acoustic impedance. The biological effect of these free radicals was compared to that of cobalt-60 ionizing irradiation by measuring the affect on Chinese hamster cells by clonogenic assay. While cobalt-60 irradiation produced a marked decrease in clonogenic survivors, little effect was noted with high energy shock waves. This suggested that the chemical effects produced by shock waves were either absent or attenuated in the cells, or were inherently less toxic than those of ionizing irradiation.

No abstract

C3H/10T1/2 cells were infected with a retroviral vector expressing a mouse c-myc oncogene and a drug-selection marker. The resulting cells, morphologically indistinguishable from C3H/10T1/2, displayed a greatly enhanced sensitivity to neoplastic transformation by ionizing radiation or by a chemical carcinogen. Constitutive expression of myc therefore appears to synergize with an initial carcinogenic event, providing a function analogous to a subsequent event that apparently is required for the neoplastic transformation of these cells. This cell system should prove useful in exploring early stages in radiation-induced transformation.