Journal article

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

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..

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Grants

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


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).