Anti-apoptotic A1 is not essential for lymphoma development in E mu-Myc mice but helps sustain transplanted E mu-Myc tumour cells
Mark Mensink, Natasha S Anstee, Mikara Robati, Robyn L Schenk, Marco J Herold, Suzanne Cory, Cassandra J Vandenberg
CELL DEATH AND DIFFERENTIATION | NATURE PUBLISHING GROUP | Published : 2018
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 abstract
Awarded by NHMRC (Australia)
Awarded by US Leukaemia and Lymphoma Society Specialized Center for Research Grant
Awarded by NHMRC Independent Research Institute Infrastructure Support Scheme
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).