| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Samuel Lunenfeld Research Institute [A. S-O., C. O., I. L. A.], Division of Orthopedic Surgery [A. S-O., R. S. B.], and Departments of Molecular and Medical Genetics and Pathology [I. L. A.], University of Toronto [A. S-O., R. S. B., I. L. A.], Mount Sinai Hospital, Toronto, Ontario, Canada, M5G 1X5 [A. S-O., R. S. B., C. O., I. L. A.]; and Lady Davis Research Institute of the Jewish General Hospital, McGill University, Montreal, Quebec, Canada, H3T 1E2 [M. P.]
A variety of bone and soft-tissue sarcoma cell lines have been shown to express receptors for insulin-like growth factor-1 (IGF-1) and to respond mitogenically to IGF-1 in vitro. We have recently demonstrated evidence of IGF dependency in murine MGH-OGS and RIF-1 sarcomas, which express relatively high and intermediate levels of IGF-1 receptors. Overexpression of IGF-1 receptors and/or IGF ligands might, therefore, be a mechanism by which human bone and soft-tissue sarcomas obtain a proliferative advantage over normal adjacent tissues. Therefore, we evaluated 29 human sarcoma specimens for expression of IGF-1 receptor, IGF-1, and IGF-2 by competitive binding and reverse-transcription polymerase chain reaction (RT-PCR) techniques. Twelve of 29 sarcomas examined by RT-PCR and 13 of 25 examined by affinity-binding studies expressed IGF-1 receptor levels equal to or greater than levels determined in the IGF-responsive MCF-7 breast carcinoma cell line. DNA amplification of the IGF-1 receptor gene was not identified in this group of sarcomas that expressed high levels of IGF-1 receptor. Evaluation of IGF ligand expression by RT-PCR revealed that 22 of 28 sarcomas expressed IGF-1 levels comparable to or above those of the RPMI 7666 control line, and 17 of 27 sarcomas expressed significant levels of IGF-2 compared with the NCI H69 control cell line. These results suggest that autocrine/paracrine regulatory mechanisms might be responsible for the growth of some sarcomas.
1 This work was supported by the National Cancer Institute of Canada (Grants 3372 and 3739).
2 To whom requests for reprints should be addressed, at Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Ave., Toronto, Ontario, Canada M5G 1X5.
Received 1/25/94. Accepted 10/31/94.
This article has been cited by other articles:
|
|
 |
|
  A. Prieur, F. Tirode, P. Cohen, and O. Delattre EWS/FLI-1 Silencing and Gene Profiling of Ewing Cells Reveal Downstream Oncogenic Pathways and a Crucial Role for Repression of Insulin-Like Growth Factor Binding Protein 3 Mol. Cell. Biol., August 15, 2004; 24(16): 7275 - 7283. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. de Alava, A. Panizo, C. R. Antonescu, A. G. Huvos, F. J. Pardo-Mindan, F. G. Barr, and M. Ladanyi Association of EWS-FLI1 Type 1 Fusion with Lower Proliferative Rate in Ewing’s Sarcoma Am. J. Pathol., March 1, 2000; 156(3): 849 - 855. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Xie, B. Skytting, G. Nilsson, B. Brodin, and O. Larsson Expression of Insulin-like Growth Factor-1 Receptor in Synovial Sarcoma: Association with an Aggressive Phenotype Cancer Res., August 1, 1999; 59(15): 3588 - 3591. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Lamharzi, A. V. Schally, M. Koppan, and K. Groot Growth hormone-releasing hormone antagonist MZ-5-156 inhibits growth of DU-145 human androgen-independent prostate carcinoma in nude mice and suppresses the levels and mRNA expression of insulin-like growth factor II in tumors PNAS, July 21, 1998; 95(15): 8864 - 8868. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
