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Pancreatic Neoplasms: HELP
Articles by Pascal Lorentz
Based on 3 articles published since 2009
(Why 3 articles?)
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Between 2009 and 2019, Pascal Lorentz wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article VEGF receptor-2-specific signaling mediated by VEGF-E induces hemangioma-like lesions in normal and in malignant tissue. 2016

Fagiani, Ernesta / Lorentz, Pascal / Bill, Ruben / Pavotbawan, Kirusigan / Kopfstein, Lucie / Christofori, Gerhard. ·Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland. ernesta.fagiani@unibas.ch. · Department of Biomedicine, University of Basel, Mattenstrasse 28, 4058, Basel, Switzerland. ·Angiogenesis · Pubmed #27038485.

ABSTRACT: VEGF-A: it induces proliferation, migration and sprouting of cultured vascular endothelial cells and proliferative lesions in the skin of sheep, goat and man that are characterized by massive capillary proliferation and dilation. These biological functions are mediated exclusively via its interaction with VEGF receptor-2 (VEGFR-2). Here, we have generated transgenic mice specifically expressing ovVEGF-E in β-cells of the endocrine pancreas (Rip1VEGF-E; RVE). RVE mice show an increase in number and size of the islets of Langerhans and a distorted organization of insulin and glucagon-expressing cells. Islet endothelial cells of RVE mice hyper-proliferate and form increased numbers of functional blood vessels. In addition, the formation of disorganized lymphatic vessels and increased immune cell infiltration is observed. Upon crossing RVE single-transgenic mice with Rip1Tag2 (RT2) transgenic mice, a well-studied model of pancreatic β-cell carcinogenesis, double-transgenic mice (RT2;RVE) display hyper-proliferation of endothelial cells resulting in the formation of hemangioma-like lesions. In addition, RT2;RVE mice exhibit activated lymphangiogenesis at the tumor periphery and increased neutrophil and macrophage tumor infiltration and micro-metastasis to lymph nodes and lungs. These phenotypes markedly differ from the phenotypes observed with the transgenic expression of the other VEGF family members in β-cells of normal mice and of RT2 mice.

2 Article Angiopoietin-1 and -2 exert antagonistic functions in tumor angiogenesis, yet both induce lymphangiogenesis. 2011

Fagiani, Ernesta / Lorentz, Pascal / Kopfstein, Lucie / Christofori, Gerhard. ·Institute of Biochemistry and Genetics, Department of Biomedicine, University of Basel, Basel, Switzerland. ·Cancer Res · Pubmed #21778249.

ABSTRACT: Members of the Angiopoietin family regulate various aspects of physiologic and pathologic angiogenesis. Although Angiopoietin-1 (Ang-1) decreases endothelial cell permeability and increases vascular stabilization via recruitment of pericytes and smooth muscle cells to growing blood vessels, Angiopoietin-2 (Ang-2) mediates angiogenic sprouting and vascular regression. In this study, we used the Rip1Tag2 transgenic mouse model of pancreatic β-cell carcinogenesis to investigate the roles of Ang-1 and Ang-2 in tumor angiogenesis and tumor progression. On their own, transgenic expression of human Ang-1 or Ang-2 in pancreatic β cells caused formation of peri-insular lymphatic vessels in the absence of effects on blood vessel density, islet morphology, or physiology. When crossed to Rip1Tag2 mice, both Ang-1-and Ang-2-expressing β-cell tumors showed increased peritumoral lymphangiogenesis in the absence of metastasis to local lymph nodes or distant organs. There was no alteration in tumor outgrowth, blood vessel density, or vessel maturation in Ang-1-expressing tumors. In contrast, Ang-2-expressing tumors exhibited diminished pericyte recruitment to blood vessels that were dilated, nonfunctional, and highly permeable. These tumors were hemorrhagic, highly infiltrated by leukocytes, and impaired in outgrowth. Together, our findings establish that Ang-2 antagonizes Ang-1 function, leading to excessive vessel sprouting with impaired pericyte recruitment and vessel stabilization. The poor perfusion of immature blood vessels results in retarded tumor growth, defining an important pathophysiologic pathway required for efficient tumorigenesis.

3 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.