Abstract
The effect of macrophage depletion on growth and neovascularization of 7,12-dimethylbenz(a)anthracene (DMBA)-induced hamster buccal pouch carcinomas (HBPC) was evaluated by quantitating tritiated thymidine (3[H]TdR) incorporation by tumor cells and microvascular endothelium in light microscopic autoradiographs. Tumors that were depleted of macrophages with systemic hydrocortisone acetate (HA) and intratumor injections of antimacrophage serum (AMS) were examined 7 days after treatment. In control animals 30% of infiltrating host cells were esterase-positive tumor-associated macrophages (TAM) and 28.14% of tumor cells and 14.45% of endothelial cells were 3[H]TdR labelled. Hamsters treated with HA or HA and control serum showed no significant reduction in either the number of TAM or proportion of [3H]TdR labelled tumor of endothelial cells. AMS administered alone had no effect on either the content of TAM or 3[H]TdR labelling. In contrast hamsters treated with HA and AMS showed a 54% decrease in TAM and a 50% and 63% reduction in tumor and endothelial cell labelling respectively. These results suggest that growth and neovascularization of these tumors is mediated in part by macrophages.
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