Dr Andrejs Braun

PhD, FHEA, FIBMS
Reader in Genome Regulation
Group Leader
Research Focus

Our group is interested in epigenetic regulation of somatic mutagenesis in normal and malignant B cells. Specifically, we aim to understand how alterations in the nuclear envelope influence B cell chromatin conformation, and what the epigenetic consequences of these alterations are.

Key Publications

Lamin B1 regulates somatic mutations and progression of B-cell malignancies. Leukemia (2018) 32(2):364-375. PMID: 28804121

Autophagy mediates degradation of nuclear lamina. Nature (2015) 527(7576):105-9. PMID: 26524528

Lysosome-mediated processing of chromatin in senescence. J Cell Biol (2013) 202(1):129-43. PMID: 23816621

Novel type II anti-CD20 monoclonal antibody (GA101) evokes homotypic adhesion and actin-dependent, lysosome-mediated cell death in B-cell malignancies. Blood (2011) 117(17):4519-29. PMID: 21378274

Monoclonal antibodies directed to CD20 and HLA-DR can elicit homotypic adhesion followed by lysosome-mediated cell death in human lymphoma and leukemia cells. J Clin Invest (2009) 119(8):2143-59. PMID: 1962078

Major Funding
  • 2019-2022- Bloodwise, Lamin B1-mediated genomic instability in leukaemia and lymphoma, £229,104
  • Higher Education Funding Council for England (HEFCE)
  • Kay Kendall Leukaemia Fund
Other Activities
  • Director of Postgraduate Taught Programmes, Barts Cancer Institute, Queen Mary University of London
  • Course Director: MSc Cancer and Therapeutics, Barts Cancer Institute, Queen Mary University of London
  • Module lead – Cancer Biology, Cancer MSc Programmes, Barts Cancer Institute, Queen Mary University of London, UK
  • Module lead – Targeted Therapies and Immunotherapy of Haematological Malignancies, Cancer MSc Programmes, Barts Cancer Institute, Queen Mary, University of London, UK
  • Module lead – Human Anatomy, School of Biological and Chemical Sciences, Queen Mary University of London
Research

Our group is interested in epigenetic regulation of somatic mutagenesis in normal and malignant B cells. Specifically, we aim to understand how alterations in the nuclear envelope influence B cell chromatin conformation, and what the epigenetic consequences of these alterations are.

At a systemic level, we are interested in how the lamina-associated chromatin domain (LAD) dynamics influence normal adaptive immunity, and whether dysregulation of this mechanism leads to autoimmunity and cancer.

From a translational perspective, we are aiming to develop novel therapeutic strategies to target nuclear lamina, establishing a new generation of treatment modalities of malignant lymphoma.

Other Activities
  • Director of Postgraduate Taught Programmes, Barts Cancer Institute, Queen Mary University of London
  • Course Director: MSc Cancer and Therapeutics, Barts Cancer Institute, Queen Mary University of London
  • PhD Supervision – Barts Cancer Institute, Queen Mary University of London
  • Module lead – Cancer Biology, Cancer MSc Programmes, Barts Cancer Institute, Queen Mary University of London, UK
  • Module lead – Targeted Therapies and Immunotherapy of Haematological Malignancies. Cancer MSc Programmes, Barts Cancer Institute, Queen Mary, University of London, UK
  • Module lead – Human Anatomy. School of Biological and Chemical Sciences. Queen Mary University of London
  • OSCE2, OSCE 3, OSCE4 and OSCE5 (finals) examiner - Barts and the London School of Medicine and Dentistry
  • A100 and A101 MBBS entry interviewer - Barts and the London School of Medicine and Dentistry
  • Undergraduate Mentor: MBBS Years 4 and 5, Barts and the London School of Medicine and Dentistry
Major Funding
  • 2019-2022- Bloodwise, Lamin B1-mediated genomic instability in leukaemia and lymphoma, £229,104
  • Higher Education Funding Council for England (HEFCE)
  • Kay Kendall Leukaemia Fund
  • Barry Reed Cancer Trust
  • “Bolashak” fellowship programme, Republic of Kazakhstan
Recent Publications

Lamin B1 regulates somatic mutations and progression of B-cell malignancies. Klymenko T, Bloehdorn J, Bahlo J et al. Leukemia 32(1) 364-375
https://www.ncbi.nlm.nih.gov/pubmed/28804121

NUCLEAR LAMINA REGULATES SOMATIC HYPERMUTATION AND PROGRESSION OF B CELL MALIGNANCIES Klymenko T, Bloehdorn J, Bahlo J et al. HAEMATOLOGICA (2017) 102(11) 228-228
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000404127002077&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=612ae0d773dcbdba3046f6df545e9f6a

ONCOGENE-EXPRESSING SENESCENT MELANOCYTES UPREGULATE MHC CLASS II, A CANDIDATE MELANOMA SUPPRESSOR FUNCTION BRAUNS A Journal of Investigative Dermatology (1)

Mammalian autophagy degrades nuclear constituents in response to tumorigenic stress. Dou Z, Ivanov A, Adams PD et al. Autophagy (2016) 12(1) 1416-1417
http://www.ncbi.nlm.nih.gov/pubmed/26654219

EXPLOITING OXIDATIVE PHOSPHORYLATION TO IMPROVE ANTIBODY THERAPY OF LYMPHOMA Vilventhraraja E, Gribben J, Ivanov A HAEMATOLOGICA (2016) 101(11) 574-575
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000379484602177&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=612ae0d773dcbdba3046f6df545e9f6a

Autophagy mediates degradation of nuclear lamina Dou Z, Xu C, Donahue G et al. Nature (2015) 527(7) 105-109

HIRA orchestrates a dynamic chromatin landscape in senescence and is required for suppression of Neoplasia Rai TS, Cole JJ, Nelson DM et al. Genes and Development (2014) 28(7) 2712-2725

Lysosome-mediated processing of chromatin in senescence. Ivanov A, Pawlikowski J, Manoharan I et al. J Cell Biol (2013) 202(2) 129-143
https://www.ncbi.nlm.nih.gov/pubmed/23816621

DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells Jackson TR, Salmina K, Huna A et al. CELL CYCLE (2013) 12(11) 430-441
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000314607100014&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=612ae0d773dcbdba3046f6df545e9f6a

Antibody-induced nonapoptotic cell death in human lymphoma and leukemia cells is mediated through a novel reactive oxygen species-dependent pathway. Honeychurch J, Alduaij W, Azizyan M et al. Blood (2012) 119(2) 3523-3533
https://www.ncbi.nlm.nih.gov/pubmed/22354003

For additional publications, please click here
Team
Postdoctoral Researchers
Dr Marta Crespi-Sallan
 
PhD Students
Gulnara Akylzhanova, Filip Filipsky
Biography
  • Sept 2013 – present Lecturer, Centre for Haemato-Oncology. Barts Cancer Institute. Queen Mary, University of London.
  • Apr 2009 – Sept 2013. Postdoctoral Research Associate. Beatson Institute for Cancer Research. University of Glasgow, Glasgow. UK.
  • Jun 2004 – Sept 2008. Cancer Research UK PhD studentship. Paterson Institute for Cancer Research. University of Manchester.
  • Nov 2002 – Jun 2004. Visiting Research Fellow. Cancer Sciences Division, University of Southampton, Southampton. UK