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Dual role of host Par2 in a murine model of spontaneous metastatic B16 melanoma
T. Olejar, D. Vetvicka, M. Zadinova, P. Pouckova, J. Kukal, P. Jezek, R. Matej,
Language English Country Greece
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 2004 to 2 years ago
Open Access Digital Library
from 2004-01-01
PubMed
24982362
Knihovny.cz E-resources
- MeSH
- Immunohistochemistry MeSH
- Melanoma, Experimental genetics metabolism pathology MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Receptor, PAR-2 genetics metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
AIM: We investigated differences of metastatic spread of normal proteinase-activated receptor-2 (Par2+/+) melanoma B16 in Par2-/- (knock-out) animals compared to C57Bl6 mice. MATERIALS AND METHODS: Nine knock-out mice B6.Cg-F2rl1tm1Mslb/J (Par2-/-) and nine C57Bl6/J controls were subcutaneously inoculated with B16 melanoma tissue cells. Twelve days after inoculation, all primary tumors were removed. Survival and metastatic spread was followed for up to 100 days after primary tumor extirpation. RESULTS: Excised primary tumors were on average larger in Par2-/- mice (360 mm3 vs. 221 mm3 in C57Bl6/J). Distant spontaneous metastases developed in only 3 of 9 of Par2-/- mice in comparison to 6 of 9 controls. The average survival time was 84 days in Par2-/- animals compared to 63 days in C57Bl6/J mice. CONCLUSION: Host Par2 melanoma model contributes to the limitation of local cancer progression in one area, while on the other hand is important for enhancing distant metastatic spread.
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- $a Olejar, Tomas $u Department of Pathology and Molecular Medicine, Thomayer Hospital, Prague, Czech Republic Department No. 75, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
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- $a Dual role of host Par2 in a murine model of spontaneous metastatic B16 melanoma / $c T. Olejar, D. Vetvicka, M. Zadinova, P. Pouckova, J. Kukal, P. Jezek, R. Matej,
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- $a AIM: We investigated differences of metastatic spread of normal proteinase-activated receptor-2 (Par2+/+) melanoma B16 in Par2-/- (knock-out) animals compared to C57Bl6 mice. MATERIALS AND METHODS: Nine knock-out mice B6.Cg-F2rl1tm1Mslb/J (Par2-/-) and nine C57Bl6/J controls were subcutaneously inoculated with B16 melanoma tissue cells. Twelve days after inoculation, all primary tumors were removed. Survival and metastatic spread was followed for up to 100 days after primary tumor extirpation. RESULTS: Excised primary tumors were on average larger in Par2-/- mice (360 mm3 vs. 221 mm3 in C57Bl6/J). Distant spontaneous metastases developed in only 3 of 9 of Par2-/- mice in comparison to 6 of 9 controls. The average survival time was 84 days in Par2-/- animals compared to 63 days in C57Bl6/J mice. CONCLUSION: Host Par2 melanoma model contributes to the limitation of local cancer progression in one area, while on the other hand is important for enhancing distant metastatic spread.
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- $a Vetvicka, David $u Institute of Biophysics and Informatics, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic CancerTech s.r.o., Pruhonek, Prague, Czech Republic.
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- $a Zadinova, Marie $u Institute of Biophysics and Informatics, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.
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- $a Pouckova, Pavla $u Institute of Biophysics and Informatics, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.
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- $a Kukal, Jaromir $u Department of Software Engineering, Faculty of Nuclear Science and Physical Engineering, Czech Technical University, Prague, Czech Republic.
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- $a Jezek, Petr $u Department No. 75, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
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- $a Matej, Radoslav $u Department of Pathology and Molecular Medicine, Thomayer Hospital, Prague, Czech Republic Department of Pathology, Third Faculty of Medicine, Charles University in Prague, Prague, Czech Republic radoslav.matej@ftn.cz.
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- $w MED00000478 $t Anticancer research $x 1791-7530 $g Roč. 34, č. 7 (2014), s. 3511-5
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