• PhD (Immunopharmacology)1986
• BSc (Hons) Pharmacology 1981

Philip qualified with a BSc (Hons) in Pharmacology from the University of Leeds in 1981. He went on to study for a PhD in Immmunopharmacology in the Department of Clinical Pharmacology, Southampton University under the supervision of Professors Martin Church and Stephen Holgate.

Philip held postdoctoral research positions in Departments of Pharmacology of the School of Pharmacy in London and The University of Cambridge before decamping in 1988 to the Laboratory of Cellular and Molecular Pharmacology of National Institutes of Environmental Health Sciences (Research Triangle Park, North Carolina, USA) as a Fogerty International Visiting Fellow. Philip returned to the UK as a research fellow in the School of Biosciences, University of Birmingham, in 1990. In 2000 Philip Joined the School of Immunity and Infection as a Senior Research Fellow and was eventually appointed to a Senior Lectureship in 2005.

Teaching Programmes

• BMedSci
• MBChb

Personal mentor/tutor to MbCHb and BMedSci students

Philip is interested in supervising doctoral research students in the following areas:

Lineage selection in haematopoietic cells.

The use of retinoid and vitamin D analogues in the treatment of hyperproliferative diseases such as leukaemia and prostate cancer

• Biochemical and molecular biological regulation of steroid sulphatases and sulphotransferases especially their deregulation in hormone dependent cancers
• Translational pharmacology

If you are interesting in studying any of these subject areas please contact Philip on the contact details above, or for any general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings.   

RESEARCH THEMES

Cancer Cell Biology, Stem cell biology

RESEARCH ACTIVITY

Retinoid receptors –translational pharmacology.

All-trans retinoic acid is a natural metabolite of vitamin A and plays an essential in the development and functioning of many tissues and organs. Defects in either the dietary supply of vitamin A or how it works in the body are thought to play an important role in the pathogenesis of diseases such as several types of cancer, diabetes, autoimmunity and male infertility as well as a major cause of severe birth defects. The biological effects of retinoids are brought about when ATRA binds to one its receptors

For the past decade one of the major research effort in the lab has been the development of specific agonists and antagonists of retinoic acid receptors. These small molecules are being used to dissect the function of individual retinoic acid receptor isoforms in a variety of cellular contexts. Current work is centred on the use of selective retinoic acid receptor antagonists as anti-cancer agents and in the prevention of chemotherapy induced neutropenia.

Vitamin D- translational pharmacology.

Vitamin D is an important hormone that is involved in the control of may biological processes in the body. Long term deficiencies in vitamin D supply and action have been implicated in the pathogenesis of many cardiovascular, metabolic and immune diseases. Work in the lab has centred on the mechanism by which vitamin D modifies cellular function. In particular, the lab is interested in how vitamin D changes the signalling landscape in cells by either increasing the level of expression of molecules involved in the control and integration of key intracellular signalling pathways and determining how vitamin D acting by its unique receptor activates some of theses pathways. These studies are aimed at finding ways to improve the sensitivity of cancer cells to the anti-proliferative effects of vitamin D and ultimately identify novel and improved ways of treating diseases such as leukaemia.

Haematopoiesis – lineage selection

Philip has worked closely with Geoffrey Brown (School of Immunity and Infection) to develop a new model of haematopoiesis and in particular we are investigating mechanisms by which hematopoietic cells adopt particular cell fates. As part of the work the group is also trying to dissect how and why this process is disrupted in leukaemia’s with the aim of discovering new therapies for these diseases.

Philip. J. Hughes and G. Brown. 2007 1a,25-dihydroxyvitamin D₃-mediated stimulation of steroid sulphatase activity in myeloid leukaemic cell lines requires VDR_nuc-mediated activation of the RAS/RAF/ERK-MAP kinase signalling pathway. J Cell Biochem 98:590-617.

Brown G, Hughes PJ, Michell RH, Rolink TA and Ceredig R. 2007.Sequential determination models of hematopoiesis. Trends in Immunology. 28:442-448

Philip. J. Hughes,  J. Lee, N.E Reiner and G. Brown. 2008.The vitamin D receptor-mediated activation of phosphatidylinositol 3-kinase (PI3Ka) plays a role in the 1a,25-dihydroxyvitamin D₃–stimulated increase in steroid sulfatase activity in myeloid leukaemic cell lines. J Cell Biochem. 103:1551-1572.

Geoffrey Brown, Philip J. Hughes, Robert H. Michell, Antonius G. Rolink and Rod Ceredig. Ordered development of hematopoietic stem cells [2008]. In: Stem Cell Applications in Disease – pp221-241 (Nova Publishers, New York)

Philip J Hughes and Geoffrey Brown (2009) Complex interplay between c-jun N-terminal kinase (JNK ) isoforms during 1,25a-dihydroxyvitamin D₃ -mediated monocytic differentiation of myeloid cells. Leukemia Research 33:1298-1300.

Philip J Hughes, Ewa Marcinkowska, Elzbieta Gocek, George P Studzinski and Geoffrey Brown. (2010). Vitamin D₃-driven signals for myeloid cell differentiation – Implications for differentiation therapy.    Leukemia Research. 34:553-565

Philip J Hughes and Geoffrey Brown. (2010). 1a,25-dihydroxyvitamin D₃-drives monocytic differentiation by changing the signalling landscape of myeloid leukaemic cell lines. In: Vitamin D: Biochemistry, Nutrition and Side effects. – Chapter 1 pages 1-65 (Nova Publishers, New York)

Geoffrey Brown, Philip J Hughes, Robert H Michell and Rhodri Ceredig. (2010) Molecular plasticity options during Hematopoiesis and implications for leukemia. Critical Reviews in Clinical Laboratory Scences   2010 47:171-80.