Systemic IGF-I administration stimulates the in vivo growth of early, but not advanced, renal cell carcinoma.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1168734
- author
- Rosendahl, Ann LU ; Holly, Jeff M P ; Celander, Mona and Forsberg, Göran
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- International Journal of Cancer
- volume
- 123
- pages
- 1286 - 1291
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000258480100008
- pmid:18561321
- scopus:49749141155
- pmid:18561321
- 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
- 2016-04-04 08:56:45
- date last changed
- 2022-03-15 17:27:07
@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 Inc.}},
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}},
doi = {{10.1002/ijc.23642}},
volume = {{123}},
year = {{2008}},
}