Interestingly, combining these two RT regimens with a monoclonal antibody specific for PD-1 (which per se mediates marginal anticancer effects in this tumor model) failed to significantly alter OS extension as provided by RT alone, but considerably changed the relative contribution of primary (irradiated) vs secondary (non-irradiated) disease to cumulative tumor burden at humane endpoint. Here, PDCD1 is linked to neoplasm.