S Burrow1, I L Andrulis, M Pollak, R S Bell. 1. Samuel Lunenfeld Research Institute, Mount Sinai Hospital and the University of Toronto, Ontario, Canada.
Abstract
BACKGROUND AND OBJECTIVES: We have previously shown that insulin-like growth factor (IGF)-responsive murine sarcomas demonstrate inhibition of local and metastatic disease growth when implanted in an IGF-deficient host animal. In this experiment, we tested whether IGF receptor (IGF-R) and ligands were expressed in human primary and metastatic osteosarcomas. METHODS: Fifty-two specimens of human osteosarcoma tumor from 48 patients were assayed for IGF-R, IGF-1, and IGF-2 using reverse transcriptase polymerase chain reaction. RESULTS: Twenty-one of 46 tumors analyzed had levels of expression of IGF-R greater than or equal to the positive control cell line. Twenty-seven of 44 expressed levels of IGF-1 greater than or equal to the positive control, as did 21 of 38 cases assayed for IGF-2. No differences were found between 40 primary tumor samples and 12 metastatic lesions in mean levels of IGF-R, IGF-1, or IGF-2. There was a moderately strong correlation between expression of IGF-R and IGF-1, suggesting that autocrine stimulation may be an important mechanism for stimulation of osteosarcoma proliferation. CONCLUSIONS: A significant proportion of osteosarcoma tumors express IGF-R and ligands. Higher levels of expression were not correlated with metastatic lesions.
BACKGROUND AND OBJECTIVES: We have previously shown that insulin-like growth factor (IGF)-responsive murinesarcomas demonstrate inhibition of local and metastatic disease growth when implanted in an IGF-deficient host animal. In this experiment, we tested whether IGF receptor (IGF-R) and ligands were expressed in human primary and metastatic osteosarcomas. METHODS: Fifty-two specimens of humanosteosarcoma tumor from 48 patients were assayed for IGF-R, IGF-1, and IGF-2 using reverse transcriptase polymerase chain reaction. RESULTS: Twenty-one of 46 tumors analyzed had levels of expression of IGF-R greater than or equal to the positive control cell line. Twenty-seven of 44 expressed levels of IGF-1 greater than or equal to the positive control, as did 21 of 38 cases assayed for IGF-2. No differences were found between 40 primary tumor samples and 12 metastatic lesions in mean levels of IGF-R, IGF-1, or IGF-2. There was a moderately strong correlation between expression of IGF-R and IGF-1, suggesting that autocrine stimulation may be an important mechanism for stimulation of osteosarcoma proliferation. CONCLUSIONS: A significant proportion of osteosarcoma tumors express IGF-R and ligands. Higher levels of expression were not correlated with metastatic lesions.
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