In the human tumor specimens, the majority of both the hepatic and renal specimens investigated stained positive for CD111. To our knowledge, until this study, there have been no reports in the literature addressing the presence of nectin-1 in these tumor types. The expression of nectin-1 in these human specimens provided a basis for proceeding with the cytotoxicity studies and suggests that the humanized version of the M002 virus, M032, may be a beneficial therapeutic option for children with these difficult to treat solid tumors. The number of cell lines available for study of these rare, but deadly, solid tumors is extremely limited. One of the cell lines that we chose to study for rare renal malignancies was the SK-NEP-1 cell line. This cell line was originally thought to be a Wilms tumor cell line, but has since been characterized as a renal Ewing sarcoma cell line. Similar to MRKTs, are clinically much more difficult to treat and carry a significantly worse prognosis than the standard pediatric renal Wilms tumor that has five year survival rates exceeding 90%. In the current study, we have seen that M002 Kinase Inhibitor Library had a significant oncolytic effect upon this cell line both in vitro and in vivo. A novel finding of these studies was the excellent response seen with M002 in SK-NEP-1 xenografts. The Seneca Valley Virus, a replication competent RNA virus, demonstrated only a low to intermediate response against the SK-NEP-1 cell line. Treatment of other sarcoma types including rhabdomyosarcoma, osteosarcoma, Ewing sarcoma and malignant fibrous histiocytoma with oHSVs revealed that these sarcoma cell lines showed viral entry but varied in their sensitivity to viral oncolysis, with the Ewing sarcoma cells being the least susceptible. Previously, investigators have reported that the addition of ionizing radiation to the administration of oHSVs produced a synergistic effect in xenograft models of lung cancer, mesothelioma, and cervical cancer resulting in further decreased xenograft growth. Chung and colleagues studied this concept in Lapatinib hepatocellular carcinoma models. They found that ionizing radiation combined with R7020 recombinant oHSV resulted in a greater reduction in xenograft growth than either radiation or virus alone in one hepatocellular carcinoma cell line. The same results were not seen when they studied a second hepatocellular carcinoma cell line. We had similar findings in our study with HuH6 hepatoblastoma and G401 MRKT xenografts. The addition of ionizing radiation to oHSV therapy did not significantly affect xenograft growth compared to virus alone. We did utilize a lower dose of ionizing radiation than the Chung study, but our choice of radiation exposure was based upon data that demonstrated a dose dependent increase in HSV replication following irradiation with 2 to 5 Gy, without any additional effects seen after 5 Gy. In addition, it was felt that if an effect was seen with the addition of low dose ionizing irradiation, that perhaps dose reduction of both agents might be possible, having significant clinical implications. It is important to note that there are no syngeneic mouse models available to study these tumor types. Therefore, immunodeficient murine xenograft models were chosen for the current studies in order to test the efficacy of M002 on human tumor cells in vivo.