Dr Farhat Khanim

Dr Farhat Khanim

School of Biosciences
Research Fellow/Group Leader

Contact details

School of Biosciences
University of Birmingham
B15 2TT

Dr Farhat Khanim is a molecular/cellular biologist working in the field of haemato-oncology. The main goal of her research is to deliver patient benefit from laboratory studies in the form of novel effective therapies.


BSc (Hons) Biological Sciences



Dr Farhat Khanim discovered her desire for research career during the final year of her undergraduate degree in Biological Sciences. After completing a PhD with Prof Lawrence Young on the role of Epstein-Barr Virus in Nasopharyngeal Carcinoma (NPC), she took up a Swedish Cancer Society Fellowship at Microbiology and Tumour biology Centre at the Karolinska Institute in Sweden.  Upon her return to the UK, Dr Khanim completed 3 postdocs before joining the lab of Prof Chris Bunce and Prof Mark Drayson to focus on translational research in haemato-oncology. In 2013, Dr Khanim together with Prof Mark Drayson successfully applied for renewal of a programme grant from the national blood cancer charity Bloodwise (formerly called Leukaemia & Lymphoma Research (LLR)). Dr Khanim and Prof Drayson jointly run a research group in the School of Biosciences at the University of Birmingham.


Dr Khanim lectures on several final year BSc modules and Masters programs. Her main teaching is through research laboratory projects for undergraduate and postgraduate students including intercalating medical students.

Postgraduate supervision

Dr Farhat Khanim currently has 3 PhD students.

 If you are interested in postgraduate projects with Dr Khanim, please contact her directly with your CV and areas of particular interest.


Research group: Translational haemato-oncology research and drug repurposing 

The main aim of Dr Khanim’s research is the identification and delivery of effective, non-toxic therapies for blood cancers to the clinic. To achieve this goal, the group studies the basic biology of haematological malignancies, performs drug redeployment screening and drug mechanism of action studies. Mechanistic studies include analysis of tumour metabolism in response to drugs and tumour niche interactions.

Other activities

Dr Khanim is a member of:

  • the steering committee of the ECMC UK Therapeutic Cancer Prevention Network (UKTCPN) which is a national initiative to develop strategies for cancer prevention.
  • International Society for Experimental Haematology (ISEH)
  • European Association for Cancer Research (EACR)
  • British Association for Cancer Research (BACR)


Doig CL, et al Knockdown of AKR1C3 exposes a potential epigenetic susceptibility in prostate cancer cells. J Steroid Biochem Mol Biol. 2015 Sep 30;155(Pt A):47-55. doi: 10.1016/j.jsbmb.2015.09.037

Koczula KMa, et al. Metabolic plasticity in CLL: Adaptation to the hypoxic niche. Leukemia. 2015 Jul 23. doi: 10.1038/leu.2015.187

Southam AD, et al. Drug Redeployment to Kill Leukemia and Lymphoma Cells by Disrupting SCD1-Mediated Synthesis of Monounsaturated Fatty Acids. Cancer Res. 2015 Jun 15;75(12):2530-40

Lilly AJ, et al. The case for extracellular Nm23-H1 as a driver of acute myeloid leukaemia (AML) progression. Naunyn Schmiedebergs Arch Pharmacol. 2014 Aug 15.

Khanim F, et al. Selective AKR1C3 inhibitors do not recapitulate the anti-leukaemic activities of the pan-AKR1C inhibitor medroxyprogesterone acetate. Br J Cancer. 2014 Mar 18;110(6):1506-16. doi: 10.1038/bjc.2014.83. Epub 2014 Feb 25.

Molyneux E, et al. Bezafibrate and medroxyprogesterone acetate in resistant and relapsed endemic Burkitt lymphoma in Malawi; an open-label, single-arm, phase 2 study (ISRCTN34303497). Br J Haematol. 2014 Mar;164(6):888-90. doi: 10.1111/bjh.12681..

Lodi A, et al. Proton NMR-based metabolite analyses of archived serial paired serum and urine samples from myeloma patients at different stages of disease activity identifies acetylcarnitine as a novel marker of active disease. PLoS One. 2013;8(2):e56422. doi: 10.1371/journal.pone.0056422.

Khanim FL, et al. Redeployment-based drug screening identifies the anti-helminthic niclosamide as anti-myeloma therapy that also reduces free light chain production.. Blood Cancer Journal 2011 Blood Cancer J. 2011 1(10):e39.

Lilly AJ, et al. Nm23-h1 indirectly promotes the survival of acute myeloid leukemia blast cells by binding to more mature components of the leukemic clone. Cancer Res. 2011 Feb 1;71(3):1177-86. doi: 10.1158/0008-5472

Lodi A, et al. Hypoxia triggers major metabolic changes in AML cells without altering indomethacin-induced TCA cycle deregulation. ACS Chem Biol. 2011 Feb 18;6(2):169-75.

Wright KT, et al. Extracellular Nm23H1 stimulates neurite outgrowth from dorsal root ganglia neurons in vitro independently of nerve growth factor supplementation or its nucleoside diphosphate kinase activity. Biochem Biophys Res Commun. 2010 Jul 16;398(1):79-85. doi: 10.1016/j.bbrc.2010.06.039. Epub 2010 Jun 15.

Veliça P, et al. Prostaglandin D2 inhibits C2C12 myogenesis. Mol Cell Endocrinol. 2010 May 5;319(1-2):71-8. PMID: 20109525

Murray JA, et al. Combined bezafibrate and medroxyprogesterone acetate have efficacy without haematological toxicity in elderly and relapsed acute myeloid leukaemia (AML). Br J Haematol. 2010 Apr;149(1):65-9.

Khanim FL, et al. Combined bezafibrate and medroxyprogesterone acetate: potential novel therapy for acute myeloid leukaemia. PLoS One. 2009 Dec 7;4(12):e8147.

Pearce C, et al. Analysis of the role of COP9 Signalosome (CSN) subunits in K562; the first link between CSN and autophagy. BMC Cell Biol. 2009 Apr 28;10:31.

Birtwistle J, et al. The aldo-keto reductase AKR1C3 contributes to 7,12-dimethylbenz(a)anthracene-3,4-dihydrodiol mediated oxidative DNA damage in myeloid cells: implications for leukemogenesis. Mutat Res. 2009 Mar 9;662(1-2):67-74.

Tiziani S, et al. Metabolomic profiling of drug responses in acute myeloid leukaemia cell lines. PLoS One. 2009;4(1):e4251. Epub 2009 Jan 22. Erratum in: PLoS One. 2009;4(4). doi: 10.1371/annotation/39584d38-04f5-4b37-bfd8-eae2318ec6f9.

Khanim FL, et al. Elevated FOSB-expression; a potential marker of valproate sensitivity in AML. Br J Haematol. 2009 Feb;144(3):332-41.

Hayden RE, et al. Treatment of primary CLL cells with bezafibrate and medroxyprogesterone acetate induces apoptosis and represses the pro-proliferative signal of CD40-ligand, in part through increased 15dDelta12,14,PGJ2. Leukemia. 2009 Feb;23(2):292-304.