Anti-inflammatory consequences of transplanted tumors.

Rats and mice bearing transplanted chemically induced neoplasms have defective macrophage infiltration of inflammatory sites distant to the tumor. The defect limits concurrently accumulation of macrophages within the tumor, raising dramatically the tumor to macrophage cell ratio. The defect may not compromise host surveillance because it requires relatively large numbers of tumor cells. The abnormality does not appear to result from circulating monocyte depletion, defective monocyte chemotaxis, or the traffic of monocytes into the tumor.