Skip to main content

Prof Paul Murray

Home | Person | Hri Member | Prof Paul Murray

Research in the Murray Group is focussed on the discovery of molecular pathways involved in the development and progression of aggressive cancers derived from blood cells (known as lymphomas) these include the most common form of this disease, called diffuse large B cell lymphoma, a tumour recently defined as one of four haematological cancers with the highest unmet clinical need. Our objective is to better understand the pathogenesis of these malignancies and in doing so develop novel therapeutic approaches. We are particularly interested in the possibility that collagen within the tumour ‘microenvironment’ can cause the cancerous cells to spread around the body and to the central nervous system where they can have devastating consequences. We have already identified novel ways to block collagen and so potentially provide new treatments to cure patients at an earlier stage before the tumour spreads.

Current Research Projects:

  1. Contribution of collagen signalling to chromosome instability
  2. Digital spatial profiling of tumour microenvironments
  3. Novel EBV ‘lytic’ genes in transformation
  4. Role of CamK1D in the pathogenesis of Hodgkin lymphoma
  5. Immunity to EBV in associated cancers and lymphoproliferative diseases

Publications

Lupino L, Perry T, Margielewska S, Hollows R, Ibrahim I, Care M, Allegood J, Tooze R, Sabbadini R, Reynolds G, Bicknell R, Rudski Z, Hock Y-L, Zanetto U, Wei W, Simmons W, Spiegel S, Woodman CB, Rowe M, Vrzalikova K, Murray PG. Sphingosine-1-phosphate signalling drives an angiogenic transcriptional programme in diffuse large B cell lymphoma. Leukemia 2019, in press .

Vockerodt M, Vrzalikova K, Ibrahim M, Nagy E, Margielewska S, Hollows R, Lupino L, Tooze R, Care M, Simmons W, Schrader A, Perry T, Abdullah M, Foster S, Reynolds G, Dowell A, Rudski Z, Krappmann D, Kube D, Woodman CBJ, Wei W, Taylor GM,. Murray PG. Regulation of S1PR2 by the EBV oncogene LMP1 in aggressive ABC-type diffuse large B cell lymphoma. J Pathol 2019, Jan 21. doi: 10.1002/path.5237. https://onlinelibrary.wiley.com/doi/full/10.1002/path.5237

Knoblich K, Migoni SC, Siew SM, Jinks E, Kaul B, Jeffery HC, Baker A, Suliman M, Vrzalikova K, Mehenna H, Murray PG, Barone F, Newsome PN, Hirschfield G, Kelly D, Oo Y, Lee S, Parekkadan B, Turley SJ, Fletcher AL. The human lymph node microenvironment unilaterally regulates T cell activation and differentiation. PLOS Biology 2018, 2018;16:e2005046. doi: 10.1371/journal.pbio.2005046. https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2005046

Vrzalikova K, Ibrahim M, Vockerodt M, Perry T, Margielewska S, Lupino L, Nagy E, Soilleux E, Liebelt D, Hollows R, Last A, Reynolds G, Abdullah M, Curley H, Care M, Krappmann D, Tooze R, Allegood J, Spiegel S, Wei W, Woodman CBJ, Murray PG. S1PR1 drives a feed forward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells. Leukemia 2018; 32:214-223. doi: 10.1038/leu.2017.275. https://www.nature.com/articles/leu2017275

Lee HM, Lo KW, Wei W, Tsao SW, Chung GT, Ibrahim MH, Dawson CW, Murray PG, Paterson IC, Yap LF. Oncogenic S1P signalling in EBV-associated nasopharyngeal carcinoma activates AKT and promotes cell migration through S1P receptor 3. J Pathol 2017: 242: 62-72 doi: 10.1002/path.4879 https://onlinelibrary.wiley.com/doi/full/10.1002/path.4879