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Biological Sciences
Phone:
(023) 8059 4423
Email:
C.N.Birts@soton.ac.uk

Dr Charles Birts BSc (Hons), PhD

Lecturer in Antibody Therapeutics, Principle investigator in breast cancer research

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Dr Charles Birts joined the School of Biological Sciences as an Against Breast Cancer funded lecturer in 2018. His research is focused on investigating the effect of metabolic and immunologic targeting on breast cancer development. This work involves developing novel antibody-based therapies for targeting secondary breast cancers.

Career History

2018-present: Lecturer in Antibody Therapeutics. University of Southampton, UK.
2017-2018: European Society for Clinical Nutrition and Metabolism Research Fellow. University of Southampton, UK.
2014-2017: Faculty of Medicine Career Track Fellow. University of Southampton, UK.
2011-2014: Senior Postdoctoral Research Fellow. University of Southampton, UK.
2007-2014: Postdoctoral Research Fellow. University of Southampton, UK.

Academic Qualifications

2003-2007: BBSRC sponsored PhD in Biochemistry. University of Southampton, UK.
2000-2003: BSc (Hons) Biochemistry and Pharmacology. University of Southampton, UK.

 

Understanding the interaction between cancer cells and our own immune cells will allow us to improve the effectiveness of antibody therapies and develop novel therapeutic strategies for treating breast cancer.

The aim of our work is to investigate immune cell function within the tumour microenvironment and determine how we can use antibody-glycan biology and metabolic intervention to fine tune antibody effector functions. This work is generously supported by Against Breast Cancer.

 

 

Against Breast Cancer funds pioneering research into new treatments, tools for earlier diagnosis and advice to reduce the risk of recurrence and secondary spread of breast cancer
Research generously funded by Against Breast Cancer

Designing Bispecific Antibodies against Metastic Breast Cancer

The use of therapeutic antibodies against cancer is a rapidly advancing area of research with many already in use in the clinic. One mechanism by which antibodies work is by targeting specific cell surface markers over-expressed on the surface of tumour cells. These antibodies can then recruit immune effector cells (e.g. macrophages, natural killer cells) through their Fc region to specifically destroy the cancer cells. However the use of therapeutic antibodies is limited by the availability of their specific target and their ability to engage with immune effector cells. The aim of our work is to improve the clinical scope of established therapeutic antibodies through antibody engineering methods to also target known cancer-associated glycan structures on metastic breast cancer cells. These novel antibodies will recognise multiple targets, improving both the specificity to breast cancer cells and also the recruitment of multiple immune effector cells into the tumour.    

In adipose, inflammatory macrophages form crown-like structures, seen in red, at sites of adipocyte death. These macrophages produce further inflammatory cytokines.
Crown-like structures in breast cancer adipose tissue

Obesity and Breast Cancer

Obesity has been shown to increase the risk of breast cancer occurrence and related mortality. Stromal adipocytes in obese adipose secrete chemo-attractants that recruit macrophages into the tissue. Macrophages are phagocytic immune cells and can come in many flavours with a range of functions from pro-inflammatory to anti-inflammatory depending on how they have been activated. In adipose, inflammatory macrophages form crown-like structures at sites of adipocyte death. These macrophages produce further inflammatory cytokines such as IL-6, IL-8 and TGF-B that act to sustain chronic inflammation promoting the onset and growth of tumours. The number of crown-like structures in breast cancer associated adipose is significantly increased in patients with a BMI>25. Fcγ receptors on the macrophage cell surface can bind the Fc region of antibodies. This binding can either be activatory or inhibitory in nature and can thus effect the efficacy of antibody therapies by modulating immune effector cell function within the tumour. By fully understanding these processes we aim to improve clinical outcomes for breast cancer patients.

Past work

Cancer cells show increased glycolysis due to either hypoxia or aerobic glycolysis (Warburg). Previous work has focused on investigating the molecular mechanisms that control changes in cellular metabolism in cancer cells, specifically on a family of proteins called CtBPs. CtBPs are transcriptional co-repressors sensitive to cellular glycolytic metabolites NAD+/NADH, allowing them to sense changes in glycolytic flux. Through this CtBPs have been implicated in the regulation of many pathways that drive the hallmarks of cancer, including cell proliferation, migration and invasion, and cell survival. Our work highlighted novel roles for CtBP in maintaining mitotic fidelity and in p53 homeostasis and has helped identify CtBPs as potential novel therapeutic targets in breast cancer. In collaboration with Jeremy Blaydes and Ali Tavassoli we have designed cyclic peptides to specifically inhibit CtBP dimerisation, demonstrating their potential as lead compounds for novel chemotherapeutics against breast cancer.

Research group

Molecular and Cellular Biosciences

Affiliate research groups

Institute for Life Sciences, Antibody and Vaccine Group, Centre for Cancer Immunology

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Articles

Letter/Editorial

Member of the British Association for Cancer Research and the European Association for Cancer Research.

Breast Cancer Campaign Research Team of the Year award 2011, postdoctoral research fellow.

Young Biochemist of the Year 2005 Award, Bioscience 2005: From molecules to organisms, Glasgow.

 

Dr Charles Birts
School of Biological Sciences
Faculty of Environmental and Life Sciences
Life Sciences Building 85
University of Southampton
Highfield Campus
Southampton
SO17 1BJ

Room Number: 85

Facsimile: (023) 3121

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