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Systemic IGF-I administration stimulates the in vivo growth of early, but not advanced, renal cell carcinoma.

Rosendahl, Ann LU ; Holly, Jeff M P; Celander, Mona and Forsberg, Göran (2008) In International Journal of Cancer 123. p.1286-1291
Abstract
Insulin-like growth factor I (IGF-I) is a potent mitogen and antiapoptotic factor. Although elevated serum IGF-I levels have been associated with increased cancer risk, it is not yet clear whether IGF-I sensitivity is sustained throughout tumor progression. To evaluate the biological effects of IGF-I during renal cell carcinoma (RCC) establishment and progression, we administered recombinant human IGF-I to severe combined immuno-deficient mice bearing early or more established Caki-2 human RCC tumors. IGF-I significantly enhanced the tumor growth 2.4-fold when administered early after tumor inoculation. This IGF-I-induced growth was accompanied with enhanced tumor cell proliferation, tumor vascularization, as well as increased intratumoral... (More)
Insulin-like growth factor I (IGF-I) is a potent mitogen and antiapoptotic factor. Although elevated serum IGF-I levels have been associated with increased cancer risk, it is not yet clear whether IGF-I sensitivity is sustained throughout tumor progression. To evaluate the biological effects of IGF-I during renal cell carcinoma (RCC) establishment and progression, we administered recombinant human IGF-I to severe combined immuno-deficient mice bearing early or more established Caki-2 human RCC tumors. IGF-I significantly enhanced the tumor growth 2.4-fold when administered early after tumor inoculation. This IGF-I-induced growth was accompanied with enhanced tumor cell proliferation, tumor vascularization, as well as increased intratumoral insulin-like growth factor binding protein 3 (IGFBP-3) and pSmad2 levels. In contrast, IGF-I administrated to more established RCC tumors showed no effect on tumor growth, with subsequently much lower Ki-67, IGFBP-3 and pSmad2 levels. Taken together, these data suggest that systemic IGF-I has potent actions during early RCC tumor development with a sustained long-term effect on proliferation and neovascularization although with progression, later tumors appear to become desensitized to systemic IGF-I effects. (c) 2008 Wiley-Liss, Inc. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
International Journal of Cancer
volume
123
pages
1286 - 1291
publisher
John Wiley & Sons
external identifiers
  • wos:000258480100008
  • pmid:18561321
  • scopus:49749141155
ISSN
0020-7136
DOI
10.1002/ijc.23642
language
English
LU publication?
yes
id
7280d795-b7ac-4800-a89e-45b50abf1c46 (old id 1168734)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18561321?dopt=Abstract
date added to LUP
2008-07-04 10:52:35
date last changed
2017-07-30 04:52:23
@article{7280d795-b7ac-4800-a89e-45b50abf1c46,
  abstract     = {Insulin-like growth factor I (IGF-I) is a potent mitogen and antiapoptotic factor. Although elevated serum IGF-I levels have been associated with increased cancer risk, it is not yet clear whether IGF-I sensitivity is sustained throughout tumor progression. To evaluate the biological effects of IGF-I during renal cell carcinoma (RCC) establishment and progression, we administered recombinant human IGF-I to severe combined immuno-deficient mice bearing early or more established Caki-2 human RCC tumors. IGF-I significantly enhanced the tumor growth 2.4-fold when administered early after tumor inoculation. This IGF-I-induced growth was accompanied with enhanced tumor cell proliferation, tumor vascularization, as well as increased intratumoral insulin-like growth factor binding protein 3 (IGFBP-3) and pSmad2 levels. In contrast, IGF-I administrated to more established RCC tumors showed no effect on tumor growth, with subsequently much lower Ki-67, IGFBP-3 and pSmad2 levels. Taken together, these data suggest that systemic IGF-I has potent actions during early RCC tumor development with a sustained long-term effect on proliferation and neovascularization although with progression, later tumors appear to become desensitized to systemic IGF-I effects. (c) 2008 Wiley-Liss, Inc.},
  author       = {Rosendahl, Ann and Holly, Jeff M P and Celander, Mona and Forsberg, Göran},
  issn         = {0020-7136},
  language     = {eng},
  pages        = {1286--1291},
  publisher    = {John Wiley & Sons},
  series       = {International Journal of Cancer},
  title        = {Systemic IGF-I administration stimulates the in vivo growth of early, but not advanced, renal cell carcinoma.},
  url          = {http://dx.doi.org/10.1002/ijc.23642},
  volume       = {123},
  year         = {2008},
}