Dr Afsar Mian

Assistant Professor

​​​Salma Jahan 265.jpgDr Afsar Ali Mian got his Master of Philosophy (MPhil) in Molecular Biology from Centre of Excellence in Molecular Biology (CEMB), University of the Punjab, Lahore, Pakistan in 2003. After completion of MPhil he was awarded a scholarship under German Exchange Program (DAAD) in the Department of Pharmaceutical Biology, Julius-von-Sachs-Institute for Biosciences, University of Würrzburg, Germany. He completed his PhD from the Department of Hematology and Oncology, School of Medicines, Goethe University Frankfurt am Main, Germany in 2010 under the supervision of PD Dr. Martin Ruthardt. He then continued his research in the same laboratory as a postdoctoral fellow and focused on molecular targeting and resistance mechanisms in Philadelphia chromosome-positive leukemia till 2015. In 2015, Dr Mian joined Professor Dr Oliver Ottmann laboratory in the Department of Hematology, Division of Cancer and Genetics, School of Medicines, Cardiff University as a research fellow.

Dr Mian supervised two PhD, and several MD and bachelor students. He has been scientific journal reviewer of many journals like  BMC Cancer, Biotechnology and Applied Biochemistry, Genetic Vaccines and Therapy, Infection, Genetics and Evolution, and Virology Journal.

Dr Mian has led the development of novel drugs and highly targeted approaches, including peptide therapies and molecularly directed agents against leukemia. His research efforts have been focused on providing therapy for patients suffering from treatment-resistant or refractory leukemia, with a special emphasis on acute lymphoblastic leukemia and on interrogating the mechanisms of resistance to targeted therapy. He has published his work in peer-reviewed journals focused on hematology developmental therapeutics and has particular interests in developing national and international collaborations across the bioscience spectrum and leading pharmaceutical industry.


Mentor at UCSF​

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Dr Neil Shah​


  • Mian AA, Rafiei A, Haberbosch I, Zeifman A, Titov I, Stroylov V, . . . Ruthardt M (2015). PF-114, a potent and selective inhibitor of native and mutated BCR/ABL is active against Philadelphia chromosome-positive (Ph+) leukemias harboring the T315I mutation. Leukemia, 29(5), 1104-1114. doi:10.1038/leu.2014.326. Link

  • Mian AA, Oancea C, Zhao Z, Ottmann OG and Ruthardt M (2009). Oligomerization inhibition, combined with allosteric inhibition, abrogates the transformation potential of T315I-positive BCR/ABL. Leukemia, 23(12), 2242-2247. doi:10.1038/leu.2009.194. Link

  • Mian AA, Schull M, Zhao Z, Oancea C, Hundertmark A, Beissert T, . . . Ruthardt M (2009). The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL. Leukemia, 23(9), 1614-1621. doi:10.1038/leu.2009.69. Link

  • Mian AA, Metodieva A, Najajreh Y, Ottmann OG, Mahajna J, and Ruthardt M (2012). p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia. Haematologica, 97(2), 251-257. doi:10.3324/haematol.2011.047191. Link

Research Team

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Usva Zafar

Research Associate

Usva Zafar completed BSc (Hons.) in Biomedical Sciences from Queen Mary, University of London in 2018. She joined AKU-CRM as a full-time Research Associate on voluntary basis in January, 2019 and formally in November 2019. Since then, she has primarily been working with Dr Afsar Mian, with their research focused on treatment-resistance/relapse mechanisms and molecular therapy in Philadelphia chromosome-positive leukemia, particularly in Chronic Myeloid Leukemia (CML) and Acute Lymphoblastic Leukemia (ALL).  She has previously conducted research on developing novel approaches to improve the efficacy and safety of allogeneic stem cell transplantation and adoptive immunotherapy as treatments for blood cancers, and is interested in stem cell biology, developmental and epigenetics, immunological basis of disease, neuroscience, tissue repair and regeneration.