Journal article
Anti-apoptotic A1 is not essential for lymphoma development in Eμ-Myc mice but helps sustain transplanted Eμ-Myc tumour cells
M Mensink, NS Anstee, M Robati, RL Schenk, MJ Herold, S Cory, CJ Vandenberg
Cell Death and Differentiation | NATURE PUBLISHING GROUP | Published : 2018
Abstract
The transcription factor c-MYC regulates a multiplicity of genes involved in cellular growth, proliferation, metabolism and DNA damage response and its overexpression is a hallmark of many tumours. Since MYC promotes apoptosis under conditions of stress, such as limited availability of nutrients or cytokines, MYC-driven cells are very much dependent on signals that inhibit cell death. Stress signals trigger apoptosis via the pathway regulated by opposing fractions of the BCL-2 protein family and previous genetic studies have shown that the development of B lymphoid tumours in Eμ-Myc mice is critically dependent on expression of pro-survival BCL-2 relatives MCL-1, BCL-W and, to a lesser exten..
View full abstractGrants
Awarded by National Science Foundation
Funding Acknowledgements
We thank K Hughes, C D'Alessandro, G Siciliano, J Corbin, J McManus and T Nikolaou for technical assistance; K Campbell, A Delbridge and S Glaser for tumour samples; and the institute's flow cytometry facility for skilled support. This work was supported by funding from the NHMRC (Australia) program grant 1016701; US Leukaemia and Lymphoma Society Specialized Center for Research Grant 7001-13; and infrastructure support to the institute from the NHMRC Independent Research Institute Infrastructure Support Scheme (IRISS 9000220) and the Victorian State Government Operational Infrastructure Support (OIS).