Dr Ronan Broderick

Supervisor Details

Contact Details

Department of Cancer and Genomic Sciences, University of Birmingham

Scientific Background

Research Interests

I have been interested for many years in understanding how our genomes are duplicated and maintained, and how defects in these processes underpin human disease; particularly cancer. My recent research focuses on the Alternative Lengthening of Telomeres; a telomere maintenance process that is underpinned by DNA replication and DNA repair mechanisms that supports the proliferation of 10-15% of all cancers. By understanding the molecular mechanisms of this process in greater detail, we may be able to treat ALT-reliant cancers such as high-grade glioma, for which no current useful treatments exist.

Research Groups

Alternative Lengthening of Telomeres

Supervision Style

In three words or phrases: detail-oriented, supportive, student-centred.

Provision of Training

I prefer to take responsibility for your initial technical training, with help from my experienced post docs, leading to more independence as you become more experienced.

Progression Monitoring and Management

I like to be kept up to date and to have regular meetings to discuss goals and progress, while allowing you independence to develop your ideas and planning skills.

Communication

I operate an open door policy and am available to chat to discuss any issues to help fulfil your potential and to progress towards your goals.

Meetings

PhD Students can expect scheduled meetings with me at least once fortnight. These meetings will be face-to-face. I am usually contactable for an instant response on every working day.

Work Patterns

Certain tasks in my lab need to occur at set times, and students need to be able to commit to a rota/timetable shared with other members of the team.

Notice Period for Feedback

I need at least 1 week's notice to provide feedback on written work of up to 5,000 words.

MIBTP Project Details

Primary supervisor for:

Understanding the role of RAD52 in the Alternative Lengthening of Telomeres mechanism.

See the PhD Opportunities section to see if this project is currently open for applications via MIBTP.

Please Note: The main page lists projects via BBSRC Research Theme(s) quoted and then relevant Topic(s).

Understanding the role of RAD52 in the Alternative Lengthening of Telomeres mechanism.

Secondary Supervisor(s): Prof Grant Stewart

University of Registration: University of Birmingham

BBSRC Research Themes:

Integrated Understanding of Health (Ageing, Pharmaceuticals)

Project Outline

The project will elucidate the molecular mechanisms of the Alternative Lengthening of Telomeres (ALT); a telomere maintenance mechanism (TMM) used by 10-15% of all cancers1. During healthy aging, telomeres (long arrays of repetitive DNA at the chromosome ends) shorten, thereby limiting cellular proliferation. Cancer, a disease of aging, progresses due to the activation of TMMs allowing replicative immortality2.

ALT is particularly prevalent in high-grade glioma3, for which there are no useful treatments. At the molecular level, ALT operates via DNA double strand break (DSB) repair and replication fork stability mechanisms, whereby collapsed telomeric replication forks undergo homologous-recombination-based telomere lengthening termed Break-Induced Telomere Synthesis (BITS)1.

BITS is predominantly dependent on RAD52, however recent studies have identified a RAD52- and RAD51- independent BITS process operating in cells lacking RAD52 or the EXD2 nuclease4,5. It is currently not well understood how RAD52 is regulated to promote BITS, or how RAD52-independent BITS operates at the molecular level.

Therefore, this work will elucidate the role of RAD52 in BITS further, employing molecular and cell biology techniques and next generation sequencing technologies to carry out the the following aims:

Aim 1: Uncovering the role of RAD52 SUMOylation in BITS.

Aim 2: Examining the processivity of RAD52-independent BITS and identifying genomic “scars” associated with RAD52-deficiency.

Aim 3: Discovering DNA resection/strand-annealing factors mediating RAD52-indepenent BITS.

Collectively, this has the potential to identify new therapeutic targets and biomarkers for the treatment and/or diagnosis of ALT-reliant cancers.

1.O'Sullivan, R. J. & Greenberg, R. (2025). 2.Hanahan, D. & Weinberg, R A. (2011). 3.MacKenzie, D., Jr. et al. Cancers (2021). 4.Zhang, J. M. et al (2019). 5. Broderick, R. et al. (2023).

APPLY HERE