Dr. Christian Bassi

Profile

I graduated from the Università Statale degli Studi di Milano and obtained my PhD degree from the University of Toronto in 2015, under the supervision of Dr. Vuk Stambolic. During my PhD research, I made a significant discovery regarding the effects of genotoxic stress on cells. Specifically, I found that Ataxia Telangiectasia Mutated (ATM) phosphorylates the tumour suppressor PTEN on threonine 398 (T398) in response to genotoxic stress. This phosphorylation event leads to the export of PTEN from the nucleus and its relocation to the plasma membrane (Bassi et al., Science, 2013).

After completing my PhD, I pursued a postdoctoral fellowship at the Campbell Family Institute for Breast Cancer Research (CFIBCR) in Toronto, under the guidance of Dr. Tak W. Mak. My postdoctoral work, supported by the Cancer Research Institute Irvington Postdoctoral Fellowship Program, focused on investigating the role of PTEN's nuclear localization in the DNA damage response. I demonstrated that cells expressing a mutated form of PTEN (PTEN-398A) have a pronounced propensity to accumulate unrepaired double-strand DNA breaks and promote acceleration of tumour development in HER2-positive breast cancer (Bassi et al., Cell Death and Differentiation, 2021). 

In 2020, I relocated to London, United Kingdom, where I served as a senior postdoctoral fellow in the group of Dr. Jessica Downs at the Institute of Cancer Research. As part of the team for target identification and validation for novel synthetic lethality interactions, I was in charge of the biomarker identification and the development of biochemical and cell-based assay.

I also gained valuable industry experience during his tenure at a top global pharmaceutical CDMO. As an Associate Principal Scientist in the Protein and Process Analytics R&D division, I led the ADCC and real-time cell-based assay program.

In 2023, I assumed my current position as Group Leader and Lecturer at the University of Leeds.

Research interests

My research plan centres around the discovery of novel synthetic lethality interactions through the development of a custom CRISPR library for implementation in a semi-high throughput phenotypic screen. By systematically targeting genes involved in the SUMO pathway, the objective is to unveil potential synthetic lethality interactions within a biologically relevant cell system, thereby holding direct therapeutic implications. 

Moreover, my laboratory has devised an innovative experimental strategy to elucidate the pertinent roles of SUMO in the context of chromatin during neuronal differentiation. Leveraging the cutting-edge opportunities afforded by the new CUT&RUN technology, the research aims to map alterations in SUMO occupancy on chromatin throughout the process of cellular differentiation.