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Pancreatic Neoplasms: HELP
Articles by Michael Jeltsch
Based on 1 article published since 2009
(Why 1 article?)
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Between 2009 and 2019, Michael Jeltsch wrote the following article about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. 2010

Albrecht, Imke / Kopfstein, Lucie / Strittmatter, Karin / Schomber, Tibor / Falkevall, Annelie / Hagberg, Carolina E / Lorentz, Pascal / Jeltsch, Michael / Alitalo, Kari / Eriksson, Ulf / Christofori, Gerhard / Pietras, Kristian. ·Department of Biomedicine, Institute of Biochemistry and Genetics, University of Basel, Basel, Switzerland. ·PLoS One · Pubmed #21124841.

ABSTRACT: BACKGROUND: The family of vascular endothelial growth factors (VEGF) contains key regulators of blood and lymph vessel development, including VEGF-A, -B, -C, -D, and placental growth factor. The role of VEGF-B during physiological or pathological angiogenesis has not yet been conclusively delineated. Herein, we investigate the function of VEGF-B by the generation of mouse models of cancer with transgenic expression of VEGF-B or homozygous deletion of Vegfb. METHODOLOGY/PRINCIPAL FINDINGS: Ectopic expression of VEGF-B in the insulin-producing β-cells of the pancreas did not alter the abundance or architecture of the islets of Langerhans. The vasculature from transgenic mice exhibited a dilated morphology, but was of similar density as that of wildtype mice. Unexpectedly, we found that transgenic expression of VEGF-B in the RIP1-Tag2 mouse model of pancreatic neuroendocrine tumorigenesis retarded tumor growth. Conversely, RIP1-Tag2 mice deficient for Vegfb presented with larger tumors. No differences in vascular density, perfusion or immune cell infiltration upon altered Vegfb gene dosage were noted. However, VEGF-B acted to increase blood vessel diameter both in normal pancreatic islets and in RIP1-Tag2 tumors. CONCLUSIONS/SIGNIFICANCE: Taken together, our results illustrate the differences in biological function between members of the VEGF family, and highlight the necessity of in-depth functional studies of VEGF-B to fully understand the effects of VEGFR-1 inhibitors currently used in the clinic.