Athar Aziz

Dr Athar Aziz

Lecturer in Biomedicine

Office Times

Thursdays 11:00am – 1:00pm (in Peel G07a)

Biography

I am passionate father, brother, teacher and learner that makes me a human and a researcher. I studied Biomedical Sciences/Medical Technology at Shaikh Zayed Post Graduate Medical Institute, Lahore, Pakistan and worked as Biomedical Scientist/Medical Technologist in various departments of diagnostic pathology labs for about 3 years. I did Masters in Molecular and Cellular Biology at Heidelberg University, in Germany and after that I got a French ministerial (MENRT mobility) fellowship to do PhD in one of the best immunology institutes in world (CIML) in Marseille France.

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. My passion for life is to be able to help the needy and ill. 

Teaching

I am involved in teaching Haematology, and Clinical Genetics in addition to teaching and leading Clinical Immunology module to undergraduate programmes. At Post-Graduate level I am teaching in Immunology and Medical Biotechnology modules in addition to leading the disorders of blood module in MSc Biomedical Sciences programme. 

Research Interests

My long standing research interest is in transcription regulation in haematopoietic cells controlling the cell fate choices and leukaemia initiating ‘events’. In this context my group is studying tumour microenvironment and cross talk between tumour and non-tumour cells in microenvironment.

One major line of research has taken us to study the role of essential elements in particular ‘calcium ion’ in cell fate choices and cancer development. Since cancer cases are often seen in elderly, we have stared a project on defining age at cellular level using novel systems of ants. 

Qualifications and Memberships

Qualifications:

BSc Medical Technology (BioMedical Sciences) 1998

MSc Molecular and Cellular Biology 2004

PhD Immunology 2008

PGC Higher Education Teaching and Learning 2015

Memberships:

Fellow of Higher Education Academy: 2015

French Society of Haematology 2007

British Society of Cell Biology 2013

Publications

Basal Calcium, an important element in development of CALR mutant MPNs. Mairal, M. M., Papadopoulos, P., Krstic-Demonacos, M., & Aziz, A. (2017, June). In HAEMATOLOGICA (Vol. 102, pp. 536-536)

Dibenzoyl-methane derivatives as a potential and exciting new therapy for the treatment of childhood bone cancer. Almelah, E., Smith, D. P., Mcgown, A., Aziz, A., Potgieter, H. J., & Ragazzon, P. (2016)Anticancer research36(11), 6043-6050.

New insights of mutant calreticulin in myeloproliferative neoplasms. Mairal, M. M., & Aziz, A. (2016). European Journal of Cancer61, S54-S55.

JAK2V617F homozygosity drives a phenotypic switch in myeloproliferative neoplasms, but is insufficient to sustain disease. Li, J., Kent, D. G., Godfrey, A. L., Manning, H., Nangalia, J., Aziz, A & Hamilton, T. L. (2014). Blood123(20), 3139-3151.

Radiation-induced immunogenic modulation of tumor enhances antigen processing and calreticulin exposure, resulting in enhanced T-cell killing. Gameiro, S. R., Jammed, M. L., Wattenberg, M. M., Tsang, K. Y., Ferrone, S., & Hodge, J. W. (2014)Oncotarget5(2), 403.

Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. Nangalia, J., Massie, C. E., Baxter, E. J., Nice, F. L., Gundem, G., Wedge, D. C, & Aziz, A. (2013). New England Journal of Medicine,369(25), 2391-2405.

The genomic landscape of myeloproliferative neoplasms: somatic calr mutations in the majority of JAK2-wildtype patients. Massie, C., Baxter, E. J., Nice, F. L., Gundem, G., Wedge, D., Avezov, & Godfrey, A. L. (2013).

“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.

“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)

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

 “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.

Rôle des facteurs de transcription bZip MafB et c-Maf dans le développement des macrophages: la différenciation macrophagique. Aziz, A. (2008).  Doctoral dissertation, Aix Marseille 2).

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.