Advanced search
1 file | 1.59 MB Add to list

Loss of autocrine endothelial-derived VEGF significantly reduces hemangiosarcoma development in conditional p53-deficient mice

(2014) CELL CYCLE. 13(9). p.1501-1507
Author
Organization
Abstract
Malignant transformation of the endothelium is rare, and hemangiosarcomas comprise only 1% of all sarcomas. For this reason and due to the lack of appropriate mouse models, the genetic mechanisms of malignant endothelial transformation are poorly understood. Here, we describe a hemangiosarcoma mouse model generated by deleting p53 specifically in the endothelial and hematopoietic lineages. This strategy led to a high incidence of hemangiosarcoma, with an average latency of 25 weeks. To study the in vivo roles of autocrine or endothelial cell autonomous VEGF signaling in the initiation and/or progression of hemangiosarcomas, we genetically deleted autocrine endothelial sources of VEGF in this mouse model. We found that loss of even a single conditional VEGF allele results in substantial rescue from endothelial cell transformation. These findings highlight the important role of threshold levels of autocrine VEGF signaling in endothelial malignancies and suggest a new approach for hemangiosarcoma treatment using targeted autocrine VEGF inhibition.
Keywords
CELL-LINE, mouse model, GROWTH-FACTOR, ANGIOSARCOMA, TUMOR, P53, ANGIOGENESIS, ESTABLISHMENT, MODEL, TUMORIGENESIS, METASTASIS, autocrine, p53, VEGF, endothelial cell, hemangiosarcoma

Downloads

  • (...).pdf
    • full text
    • |
    • UGent only
    • |
    • PDF
    • |
    • 1.59 MB

Citation

Please use this url to cite or link to this publication:

MLA
Farhang Ghahremani, Morvarid, Enrico Radaelli, Katharina Haigh, et al. “Loss of Autocrine Endothelial-derived VEGF Significantly Reduces Hemangiosarcoma Development in Conditional P53-deficient Mice.” CELL CYCLE 13.9 (2014): 1501–1507. Print.
APA
Farhang Ghahremani, M., Radaelli, E., Haigh, K., Bartunkova, S., Haenebalcke, L., Marine, J.-C., Goossens, S., et al. (2014). Loss of autocrine endothelial-derived VEGF significantly reduces hemangiosarcoma development in conditional p53-deficient mice. CELL CYCLE, 13(9), 1501–1507.
Chicago author-date
Farhang Ghahremani, Morvarid, Enrico Radaelli, Katharina Haigh, Sona Bartunkova, Lieven Haenebalcke, Jean-Christophe Marine, Steven Goossens, and Jody Haigh. 2014. “Loss of Autocrine Endothelial-derived VEGF Significantly Reduces Hemangiosarcoma Development in Conditional P53-deficient Mice.” Cell Cycle 13 (9): 1501–1507.
Chicago author-date (all authors)
Farhang Ghahremani, Morvarid, Enrico Radaelli, Katharina Haigh, Sona Bartunkova, Lieven Haenebalcke, Jean-Christophe Marine, Steven Goossens, and Jody Haigh. 2014. “Loss of Autocrine Endothelial-derived VEGF Significantly Reduces Hemangiosarcoma Development in Conditional P53-deficient Mice.” Cell Cycle 13 (9): 1501–1507.
Vancouver
1.
Farhang Ghahremani M, Radaelli E, Haigh K, Bartunkova S, Haenebalcke L, Marine J-C, et al. Loss of autocrine endothelial-derived VEGF significantly reduces hemangiosarcoma development in conditional p53-deficient mice. CELL CYCLE. 2014;13(9):1501–7.
IEEE
[1]
M. Farhang Ghahremani et al., “Loss of autocrine endothelial-derived VEGF significantly reduces hemangiosarcoma development in conditional p53-deficient mice,” CELL CYCLE, vol. 13, no. 9, pp. 1501–1507, 2014.
@article{5658593,
  abstract     = {Malignant transformation of the endothelium is rare, and hemangiosarcomas comprise only 1% of all sarcomas. For this reason and due to the lack of appropriate mouse models, the genetic mechanisms of malignant endothelial transformation are poorly understood. Here, we describe a hemangiosarcoma mouse model generated by deleting p53 specifically in the endothelial and hematopoietic lineages. This strategy led to a high incidence of hemangiosarcoma, with an average latency of 25 weeks. To study the in vivo roles of autocrine or endothelial cell autonomous VEGF signaling in the initiation and/or progression of hemangiosarcomas, we genetically deleted autocrine endothelial sources of VEGF in this mouse model. We found that loss of even a single conditional VEGF allele results in substantial rescue from endothelial cell transformation. These findings highlight the important role of threshold levels of autocrine VEGF signaling in endothelial malignancies and suggest a new approach for hemangiosarcoma treatment using targeted autocrine VEGF inhibition.},
  author       = {Farhang Ghahremani, Morvarid and Radaelli, Enrico and Haigh, Katharina and Bartunkova, Sona and Haenebalcke, Lieven and Marine, Jean-Christophe and Goossens, Steven and Haigh, Jody},
  issn         = {1538-4101},
  journal      = {CELL CYCLE},
  keywords     = {CELL-LINE,mouse model,GROWTH-FACTOR,ANGIOSARCOMA,TUMOR,P53,ANGIOGENESIS,ESTABLISHMENT,MODEL,TUMORIGENESIS,METASTASIS,autocrine,p53,VEGF,endothelial cell,hemangiosarcoma},
  language     = {eng},
  number       = {9},
  pages        = {1501--1507},
  title        = {Loss of autocrine endothelial-derived VEGF significantly reduces hemangiosarcoma development in conditional p53-deficient mice},
  url          = {http://dx.doi.org/10.4161/cc.28474},
  volume       = {13},
  year         = {2014},
}

Altmetric
View in Altmetric
Web of Science
Times cited: