Athar Aziz

Dr Athar Aziz

Lecturer in Biomedical Science

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I was born in Pakistan and did my undergraduate studies in biomedical sciences at Shaikh Zayed Post Graduate Medical Institute, Lahore, Pakistan. After almost three years of working in diagnostic pathology labs, I decided to study further and did a Masters in Molecular and Cellular Biology at Heidelberg University, Germany. I got a French ministerial (MENRT mobility) fellowship to do a PhD in one of the best immunology institutes in world (CIML), and I worked on macrophages differentiation and transcription factors controlling the macrophages cell fate choice. After that I joined the haematology department at Cambridge University (Addenbrooke’s Hospital, Cambridge) as a Research Associate and developed an in vitro model system to analyse consequences of loss of expression of Del20q imprinted genes cluster. Having worked in different countries I have gathered knowledge of different cultures and languages.


I worked in Shaikh Zayed Post Graduate Medical Institute as a teaching assistant during my tenure as Medical Technologist in Shaikh Zayed Hospital, Lahore, Pakistan. I did bench supervision of PhD students, and research technicians in the haematology department of the University of Cambridge.

Research Interests

Transcription regulation in haematopoietic cells controlling the cell fate choices and leukaemia initiating epigenetic events.

Tumour microenvironment and cross talk between tumour and non-tumour cells in microenvironment.

Qualifications and Memberships

BSc Medical Technology (BioMedical Sciences) 1998

MSc Molecular and Cellular Biology 2004

PhD Immunology 2008


French Society of Haematology 2007

Pakistan Association of Medical Laboratory Technologist 2000


1. “Cooperativity of imprinted genes inactivated by acquired chromosome 20 deletions” Aziz A, Baxter EJ, Edwards C, Ito M, Cheong CY, Bench A, Kelley R, Silber Y, Beer PA, Chng K, Renfree MB, McEwen K, Gray D, Nangalia J, Mufti GJ, Hellstrom-Lindberg E, Kiladjian JJ, McMullin MF, Campbell PJ, Ferguson-Smith AC and Green AR. Journal of Clinical Investigation. 2013 Apr 1. doi:pii: 66113. 10.1172/JCI66113.

2. “Homozygosity for human JAK2V617F causes a phenotypic switch from ET-like to PV-like, and is insufficient to sustain clonal expansion” Li J, Godfrey AL, Kent DG, Aziz A, Chen E, Nangalia J, Sneade R, Hamilton TL, Pask DC, Silber Y, Zhao X, Liu P, Green AR. (In submission)

3. MafB/c-Maf deficiency enables self-renewal of differentiated functional macrophages”. Aziz A, Soucie E, Sarrazin S, Sieweke MH. Science. 2009 Nov 6;326(5954):867-71

4. “MafB restricts M-CSF-dependent myeloid commitment divisions of hematopoietic stem cells”. Sarrazin S, Mossadegh-Keller N, Fukao T, Aziz A, Mourcin F, Vanhille L, Kelley Modis L, Kastner P, Chan S, Duprez E, Otto C, Sieweke MH. Cell. 2009 Jul 23;138(2):300-13.

(Worked the competitive reconstitution analysis of MafB WT/KO bone marrow stem cells)

5. Development of macrophages with altered actin organization in the absence of MafB”. Aziz A, Vanhille L, Mohideen P, Kelly LM, Otto C Bakri Y, Mossadegh N, Sarrazin S, Sieweke MH. Mol Cell Biol. 2006 Sep;26(18):6808-18.