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Full NameIan Mills
Department:Centre for Cancer Research and Cell Biology
Organisation:Queen's University Belfast
- genetics, genomics and molecular biology
Postgrad Medical Specialties
Other Medical Specialties:
Urology (prostate cancer)
My research group employs genomics and molecular biology approaches to define the adaptive changes occurring in prostate cancer cells in response to therapy. Our primary focus is on the transcriptional reprogramming that takes place and how this is mediated by the androgen receptor and other oncogenic transcription factors. We have previously shown that this in turn leads to a profound alteration in cancer cell metabolism and the unfolded protein response. Targeting key regulators in these biological processes can enhance response to radiotherapy and anti-androgens and our mechanistic work is to further characterise the mechanistic impact of targeting these pathways and to identify additional regulators.
1. Walker, S.M., et al., Molecular Subgroup of Primary Prostate Cancer Presenting with Metastatic Biology. Eur Urol, 2017. 72(4): p. 509-518.
2. Urbanucci, A., et al., Androgen Receptor Deregulation Drives Bromodomain-Mediated Chromatin Alterations in Prostate Cancer. Cell Rep, 2017. 19(10): p. 2045-2059.
3. Itkonen, H.M., et al., Lipid degradation promotes prostate cancer cell survival. Oncotarget, 2017. 8(24): p. 38264-38275.
4. Barfeld, S.J., et al., c-Myc Antagonises the Transcriptional Activity of the Androgen Receptor in Prostate Cancer Affecting Key Gene Networks. EBioMedicine, 2017. 18: p. 83-93.
5. Asim, M., et al., Synthetic lethality between androgen receptor signalling and the PARP pathway in prostate cancer. Nat Commun, 2017. 8(1): p. 374.
6. Asim, M., et al., Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target. J Natl Cancer Inst, 2016. 108(5).
7. Sheng, X., et al., Divergent androgen regulation of unfolded protein response pathways drives prostate cancer. EMBO Mol Med, 2015. 7(6): p. 788-801.
8. Mills, I.G., Maintaining and reprogramming genomic androgen receptor activity in prostate cancer. Nat Rev Cancer, 2014. 14(3): p. 187-98.
Prostate cancer therapy leads to the activation of a number of stress response signalling pathways in tumour cells. We have previously found that the unfolded protein response is dysregulated and in turn this leads to induction of modified Type 1 interferon/innate immune response. To further study this relationship we have generated a number of cell-lines from tumour tissue which we are genetically modifying and using in allograft experiments to determine the interplay between perturbations in the unfolded protein response and the tumour microenvironment. The PhD project will involve the isolation of cell subpopulations from these tumours and downstream genomic profiling of these to create a cell-type specific view of the origin of treatment response signals. It will be complemented by immunohistochemistry and histopathology to assess immune cell and tumour markers. There will be a major focus on radiotherapy response in these models and from this work we hope to identify factors which can modify the immunogenic response to radiotherapy in vivo and help to prime more effective immune therapy responses in prostate cancer models. This project would therefore suit clinical applicants with a pathology, urology or radiation oncology background.