Dr Rachel Bayley BSc, PhD

Department of Cancer and Genomic Sciences
Research Fellow

Contact details

Address
Department of Cancer and Genomic Sciences
University of Birmingham
Edgbaston
Birmingham
B15 2TT
UK

Dr Rachel Bayley is a Research Fellow working in the group of Dr Paloma Garcia in the Department of Cancer and Genomic Sciences. Her main area of expertise is studying the DNA damage response in stem cells and how deregulation of this can lead to the development of human diseases including cancer. Her current work focuses on DNA double-strand break repair in breast cancer stem cells and how this influences breast cancer development, persistence, and disease relapse. 

Qualifications

  • PhD in Immunology, University of Birmingham 2014
  • BSc in Biomedical Science (1st Class Hons), University of Birmingham 2010

Biography

Rachel Bayley received her BSc in Biomedical Science from the University of Birmingham in 2010 and continued at this institution to complete her PhD training in the fields of immunology and cell signalling. She went on to carry out post-doctoral training at Loughborough University where she gained an interest in stem cells, haematopoiesis and regenerative medicine. Most recently, Rachel has returned to The University of Birmingham to complete further post-doctoral training in the laboratories of Dr Martin Higgs and Dr Paloma Garcia to continue her work on stem cells through study of the DNA damage response. Her work is now focused on how DNA double-strand break repair in stem cells can be targeted to treat human diseases including cancer. 

Teaching

Undergraduate:

Stem cells and Genetic Inheritance module (Medicine and Surgery, MBChB)

Postgraduate supervision

Dr Rachel Bayley has supervised undergraduate and MRes student projects focused on stem cells and the DNA damage response.

Research

Rachel’s current research focuses on the study of breast cancer stem cells and how they contribute to tumorigenesis, metastatic disease, and therapy resistance. Her work involves characterisation of stem cell properties and the DNA damage response with a view to uncover new therapies to specifically target the cancer stem cell population.     

Her previous work has also identified lysine methylation as a key regulator of DNA double-strand break repair pathway choice.

ResearchGate Profile

Publications

Bayley, R, Sweatman, E & Higgs, M 2023, 'New perspectives on epigenetic modifications and PARP inhibitor resistance in HR-deficient cancers', Cancer drug resistance (Alhambra, Calif.), vol. 6, pp. 35-44.   https://doi.org/10.20517/cdr.2022.73

Bayley, R, Borel, V, Moss, R, Sweatman, E, Ruis, P, Ormrod, A, Goula, A, Mottram, R, Stanage, T, Hewitt, G, Saponaro, M, Stewart, G, Boulton, S & Higgs, M 2022, 'H3K4 methylation by SETD1A/BOD1L facilitates RIF1-dependent NHEJ', Molecular Cell, vol. 82, no. 10, pp. 1924-1939.e10.   https://doi.org/10.1016/j.molcel.2022.03.030

Bayley R*,Ward C, García P, MYBL2 amplification in breast cancer: Molecular mechanisms and therapeutic potential. Biochimica et Biophysica Acta, Reviews on Cancer, 2020, Dec;1874(2):188407  *=co-corresponding author 

Volpe G, Cauchy P, Walton DS, Ward C, Blakemore D, Bayley R, Clarke ML, Schmidt L, Nerlov C, García P, Dumon S, Grebien F, Frampton J. Dependence on Myb expression is attenuated in myeloid leukaemia with N-terminal CEBPA mutations. Life Science Alliance, 2019, Mar 15;2(2) 

Bayley R, Blakemore D, Cancian L, Dumon S, Volpe G, Ward C, Almaghrabi R, Gujar J, Reeve N, Raghavan M, Higgs MR, Stewart GS, Petermann E, García P. MYBL2 supports DNA double strand break repair in haematopoietic stem cells. Cancer Research, 2018, doi: 10.1158/0008-5472.CAN-18-0273. [Epub ahead of print] 

Higgs MR, Sato K, Reynolds JJ, Begum S, Bayley R, Goula A, Vernet A, Paquin KL, Skalnik DG, Kobayashi W, Takata M, Howlett NG, Kurumizaka H, Kimura H, Stewart GS. Histone methylation by SETD1A protects nascent DNA through the nucleosome chaperone activity of FANCD2. Molecular Cell, 2018, 71(1): 25-41

Bayley R, Blakemore D, García P, MYBL2 mRNA expression as a potential biomarker of therapeutic response to genotoxic treatments in myelodysplastic syndrome. Oncotarget, 2018, Vol. 9, (No. 101), pp: 37460-37461 

Begum S, Goula A, Bayley R, Higgs MR, On your marks, get SET(D1A): the race to protect stalled replication forks. Molecular and Cellular Oncology, 2018, doi:10.1080/23723556.2018.1511209 

Bayley R* and García P, DNA repair mechanisms in stem cells and their implications during ageing. Textbook Chapter in DNA Repair and Replication: Mechanisms and Clinical Significance, 2018, Chapter 14 * = co-corresponding author 

Bayley R, Ahmed F, Glen K, McCall M, Stacey A, Thomas R. The productivity limit of manufacturing blood cell therapy in scalable stirred bioreactors. Journal of Tissue Engineering and Regenerative Medicine, 2017, 10.1002/term.2337 

Bayley R, Kite KA, McGettrick HM, Smith JP, Kitas GD, Buckley CD, Young SP. The autoimmune-associated genetic variant PTPN22 R620W enhances neutrophil activation and function in rheumatoid arthritis patients and healthy controls. Annals of the Rheumatic Diseases, 2015, Aug; 74(8):1588-95

Bayley R, Yang P, Buckley CD, Young SP. Measuring the activity of the protein tyrosine phosphatase Lyp. Journal of Immunological Methods, 2013, 388: 1-2, p33-39 

Rider DA, Bayley R, Clay E, Young SP. Does Oxidative Inactivation of CD45 Phosphatase in Rheumatoid Arthritis Underlie Immune Hyporesponsiveness? Antioxidants and Redox Signalling, 2013, 19(18):2280-5 

Richa D, Naylor A, Young SP, Bayley R, Hardie D, Haworth O, Rider DA, Cook A, Buckley CD, Kellie S, Differential Expression of CD148 on leucocyte subsets in inflammatory arthritis. Arthritis Research and Therapy, 2013, 15:R108 

Juarez M, Scheel Toellner D, Karouzakis E, Hardy R, Yeo L, Bayley R, de Paz B, Raza K, Cooper M, Gay S, Buckley CD, Filer A, Early rheumatoid arthritis and resolving fibroblasts segregate according to Dickkopf related protein 1 expression. The Lancet, 2013, p57 

Kapoor S, Fitzpatrick M, Clay E, Bayley R, Wallace GR, Young SP, Metabolomics in the analysis of inflammatory diseases. Textbook chapter in Metabolomics, 2012, Chapter 11; pages 269-288

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