Dr Sean Porazinski
Dr Sean Porazinski obtained his PhD in 2014 from the University of Bath, UK. Following this he moved to the European Cancer Stem Cell Research Institute as a Postdoctoral Research Associate funded by a Pancreatic Cancer U.K. Research Innovation Award. Here he elucidated a novel mechanism by which oncogenic Ras cells are eliminated from normal epithelia to maintain tissue homeostasis. In 2016 he took a Senior Research Fellow position at the University of the West of England and University of Exeter, funded by a Prostate Cancer U.K. Research Innovation Award. Here he led a project investigating targeting of the ERG oncogene in prostate cancer with splice-switching oligonucleotides, a first of its kind approach for ERG drugging.
In 2019 he relocated to the Garvan Institute of Medical Research to join the Personalised Cancer Therapeutics Lab as a Senior Research Officer. He leads the Tissue and Tumour Ecosystems Group at Garvan and he is a Cancer Institute NSW Career Development Fellow, with funding from a St Vincent’s Clinic Foundation De Angeli Cancer Research Grant and a PanKind Accelerator Grant. His research interests are in novel personalised approaches for targeting the tumour microenvironment. He has made important advances in understanding the biology of cancer initiation, progression and treatment resistance and his work has been published in international journals including Nature, Oncogene, Current Biology, Nature Chemical Biology, Scientific Reports and the British Journal of Cancer.
- 2023British journal of biomedical science10.3389/bjbs.2023.11041
SPHINX-Based Combination Therapy as a Potential Novel Treatment Strategy for Acute Myeloid Leukaemia.
- 2021Frontiers in oncology10.3389/fonc.2021.750852
Oral Squamous Cell Carcinoma in Young Patients Show Higher Rates of Amplification: Implications for Novel Personalized Therapy.
TLR2 activation promotes tumour growth and associates with patient survival and chemotherapy response in pancreatic ductal adenocarcinoma.
- 2021Nature chemical biology10.1038/s41589-021-00783-w
Substrate-biased activity-based probes identify proteases that cleave receptor CDCP1.