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The University of Southampton
Medicine
Phone:
(023) 8120 5170
Email:
J.P.Blaydes@soton.ac.uk

Dr Jeremy Blaydes BSc Biochemistry, University of Bath. 1990 PhD Cancer Cell Biology, University of Wales, College of Medicine (UWCM), 1994

Associate Professor of Cancer Cell Biology

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Dr Jeremy Blaydes is Reader in Cancer Cell Biology within Medicine at the University of Southampton.

As a cancer cell biologist my aim is to exploit a wide range of molecular and cellular experimental approaches to ultimately identify better way of treating cancer patients.

Dr. Blaydes was appointed as Lecturer at the University of Southampton in 2000, and Reader in Cancer Cell Biology in 2007. His research in based in the Somers Cancer Research Building on the Southampton General Hospital Campus 
 
Dr. Blaydes’ research focuses on transcriptional responses to stress signalling pathways, and their roles in the causes and treatment of cancer. 

Qualifications

Appointments held

Research interests

Transcriptional responses to pathways: roles in the causes and treatment of cancer

Intra-cellular stress-response pathways are activated in response to potentially deleterious conditions in the cell’s environment. In single celled organisms these pathways are generally involved in ensuring the survival and replication of the individual cell. In complex multi-cellular organisms such as man, they are critical in maintaining the normal function of each organ in the body, and the survival of the organism as a whole. Stress-response pathways play a key role in the patho-physiology and treatment of many diseases, including cancer.

At almost every stage of the development of a tumour, cells are exposed to some form of stress. Examples include exposure to toxic compounds or radiation, loss of contact with other cells or the extra-cellular matrix, lack of oxygen (hypoxia), acidic pH, the activation of oncogenes, induction of cellular senescence, oxidative damage or depletion of essential metabolites. In some circumstances, the activation of a stress-response pathway will actually help the tumour cell to survive and proliferate. In other situations the response is cell cycle arrest or programmed cell death (apoptosis), providing a barrier to further tumour development that the tumour may ultimately circumvent through the acquisition of a mutation in one of the genes within the stress-response pathway. The p53 tumour suppressor protein is a key component of one such stress-response pathway, and virtually all cancers loose functionality of the p53-stress response pathway. Many current and prospective treatments for cancer work by either inhibiting, or re-activating stress response pathways.

Our work focuses on the role of regulators of gene transcription in the response of cancer cells to stress. We have a long-standing interest in the p53 protein, a stress-activated transcriptional activator. We have also developed interests in other pathways which regulate gene transcription and cancer cell proliferation in response to stress and changes in cell metabolism. We aim to determine the role of these pathways in the development of cancer, and establish the potential for targeting components of the pathways for cancer therapy.

Our group is based in the purpose-built Somers Cancer Research Building. Modern, well equipped laboratories provide us with an excellent research environment, and the opportunity to interact with researchers working on related areas of cancer biology.

Some Example Projects:
Regulation of HDM2 and HDMX proteins

The HDM2 oncoprotein is the major negative regulator of p53 function in the cell. In the late 1990s work from a number of groups, including Blaydes et al , demonstrated that HDM2 could be targeted in cancer cells to re-activate the p53 stress-response pathway. Subsequently, small molecule inhibitors of HDM2 have been developed that show great promise in pre-clinical trials. We have undertaken a series of projects examining how HDM2, and its paralogue HDMX is regulated in cancer cells (see Phillips et al, 2010, 2008, 2007, 2006a, 2006b and Phelps et al 2005, 2003). A particular interest of our work has been how HDM2 and HDMX protein synthesis is controlled in response to cell-signalling pathways in different cell types, and how this affects p53 function in these cells.

Role of CtBP transcriptional repressors in cancer cell proliferation and survival

In common with p53, CtBP1 and CtBP2 proteins were discovered through their physical association with a viral oncoprotein. We have shown that CtBPs also interact with HDM2 protein, and can consequently regulate p53 function (Mirnezami et al, 2003). The main function of CtBPs is as transcriptional co-repressors. They are involved in a range of cellular processes, depending upon the transcriptional repressor that recruits them to DNA, and they suppress the transcription of genes that cause apoptosis (reviewed in Bergman et al, 2006a). CtBP activity is modified by UV radiation and glycolytic metabolism, suggesting that CtBPs regulate cell survival in response to cellular stress. From 2004 The Breast Cancer Campaign has funded work in our laboratory to study the role of CtBPs in breast cancer. Our studies have progressed from studies of the basic mechanisms whereby CtBPs control breast cancer proliferation and survival (Birts et al 2011 and Bergman et al 2009, 2006a) to their impact on the response to current chemotherapies (Birts et al 2010) to the demonstration that CtBPs are themselves a therapeutically tractable potential molecular target for cancer therapy (Birts et al 2013).

Our group was named Breast Cancer Campaign “Team of the Year 2011” on the basis of this work.

Department(s)

Cancer Sciences

Affiliate Department(s)

Cancer Sciences Research group

Postgraduate Student Supervision

2003 Robert Howell MD 
2004 Alexander Mirnezami PhD 
2006 Timothy Underwood PhD 
2010 Victoria Hammond PhD 
2010 Jariya Romsaiyud PhD (with Chemistry) 
2011 Matthew Wheater PhD  
2012 Sharon Nijjar PhD (with Chemistry) 
2012 Sam Collins PhD (with Biological Sciences) 
2014 Marta Chrzan 
2014 Boris Aillard (with Chemistry 
2015 Charlotte Mardle (with Chemistry) 
2017 Pardis Arvinrad 
2017 Jason Fleming 
2017 Kate Packwood  
2017 Caroline Barker  
2017 Abigail Mead 
2018 Mira Kreuzer

Faculty of Medicine

Research Integrity Champion 
 
Past roles include:

  • Information Strategy for the Cancer Sciences School 
  • Postdoctoral Associate Academic Representative

University of Southampton

Member of Senate (2011-2013)

National and International responsibilities

Scientific Advisory Board: Wessex Medical Research (2019-) 
Scientific Advisory Board: Breast Cancer Now. (2015-2019) 
 
Member of editorial board: Biology Of The Cell (2010-) 
 
Article reviewer for journals including (2007-): Nucleic Acids Research, Oncotarget, Biology of the Cell, Biochemical Journal, Carcinogenesis, Journal of Cell Science, Oncogene, Journal of Molecular Biology, Journal of Cell Science, Journal of Cellular Biochemistry, British Journal of Cancer, BMC Mol Cell Biol, international Journal of Cancer, Bioscience Reports, Human Molecular Genetics, RNA, Current Pharmaceutical Design, Journal of Molecular Endocrinology, Cancer Biology and Therapy, Cancer Letters, Journal of Investigative Dermatology, FEBS letters, PNAS. 
 
Grant & fellowship reviewer (2007-): Association for International Cancer Research, Biotechnology and Biological Sciences Research Council, Medical Research Council, North West Cancer Research, Cancer Research UK, Prostate Cancer Foundation of Australia, Wellcome Trust, Yorkshire Cancer Research, Dutch Cancer Society, A*STAR, Breast Cancer Campaign. Leukaemia Research Fund 
 
External PhD examiner for (2008-):Including Universities of Liverpool, Cardiff, Edinburgh, Dundee & Oxford.

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Articles

Book Chapters

Conferences

Faculty of Medicine 

MMedSc Steering Group 
 
Cancer Sciences 

Co-lead for education 
Graduate School Representative 
iPhD pathway co-coordinator  

Module lead

BIOL 3043 & 6039: Molecular and Cellular Biology 

Lecturer and facilitator on the following courses: 

BIOL 3043 Molecular and Cellular Pathology 
HPRS2016 Pathophysiology of Common Cardiovascular and Respiratory Conditions 
Integrated PhD Cancer Pathway 
BM4 Year 1. Graduate group facilitation  

Research Project Supervisor (students from the following) 

Integrated PhD Cancer Pathway 
MMedSc  
BMedSc 
BIOL3034 

Personal Tutor to undergraduate medical students 

Dr Jeremy Blaydes
Faculty of Medicine University of Southampton Somers Cancer Research Building Southampton General Hospital Mailpoint 824 Tremona Road Southampton SO16 6YD

Room Number: SGH/CSB/MP824

Telephone:(023) 8120 5170
Facsimile:(023) 8120 5152
Email:J.P.Blaydes@soton.ac.uk

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