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Second hit influences the interaction between tumor cells and the immune system in a murine model of Burkitt's lymphoma

BMC Pharmacology
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/1471-2210-8-s1-a21
  • Meeting Abstract
  • Biology
  • Medicine

Abstract BioMed Central Page 1 of 1 (page number not for citation purposes) BMC Pharmacology Open AccessMeeting abstract Second hit influences the interaction between tumor cells and the immune system in a murine model of Burkitt's lymphoma Christian Schuster1, Anna Frenzel2, Andrea Hölbl1, Olivia Simma1, Mathias Müller3, Andreas Villunger2, Veronika Sexl1 and Dagmar Stoiber*1,4 Address: 1Department of Pharmacology, Medical University of Vienna, 1090 Vienna, Austria, 2Division of Developmental Immunology, Medical University of Innsbruck, 6020, Austria, 3Institute of Animal Breeding and Genetics, Veterinary University of Vienna, and Austrian Center for Biomodels and Transgenetics (ÖZBT VUW), 1220 Vienna, Austria and 4Ludwig Boltzmann Institute for Cancer Research, 1090 Vienna, Austria Email: Dagmar Stoiber* - [email protected] * Corresponding author The process of cancerogenesis is driven by the hierarchical accumulation of genetic changes. So, beside the deregu- lated expression of an oncogen, additional genetic defects have to take place in order to transform a normal cell into a tumor cell. In case of Burkitt's lymphoma, a c-myc- driven haematological tumor, two predominant so called 2nd hits have been identified. First, loss-of-function mutations in the p19-Mdm2-p53 tumor suppressor path- way, and second, the over-expression of the anti-apoptotic protein Bcl-2. So far it is not known whether these two dif- ferent 2nd hits translate into cell-autonomous effects or the ability of the immune system of recognizing and destroying the tumor cells. Our studies revealed that nei- ther over-expression of Bcl-2 nor loss-of-function muta- tions in the p19-Mdm2-p53 tumor suppressor pathway alters any analysed cell-autonomous effect significantly. However, we could specify an impact of these additional genetic lesions on the interaction between immune sys- tem and tumor cells. We were able to show that tumor cells over-expressing Bcl-2 can be eliminate

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