This hypothesis is supported by a host of preclinical data: (a) osteosarcoma cells express functional IGF-1R on the cell surface, (b) exogenous IGF-1 stimulates osteosarcoma cells to proliferate, (c) IGF-1-dependent growth can be inhibited using monoclonal antibodies or antisense oligonucleotides against IGF-1R [75], (d) the treatment of mice with a humanized anti-IGF-1R antibody resulted in tumor regression in two osteosarcoma xenograft models [76], and (e) the majority of osteosarcoma patient samples express IGF ligands, and 45% express IGF-1R [77]. Here, IGF1R is linked to osteosarcoma.