Reza, a US American Citizen, has joined us in October 2008 as part of his DPhil research which is funded by the NIH-Oxford/Cambridge scholars program.
Reza has previously done a considerable amount of research for NASA and has subsequently trained for two years in a prominent US HNC research lab that is based at the NIH Campus in Bethesda, MD, and headed by Dr. Carter van Waes, the Chief of the Head and Neck Surgery Branch and Clinical Director of NIDCD. Reza is also a medical student on leave from Stanford University, to where he will eventually return to complete his medical studies. With considerable expertise in both, basic research and clinical practice, I expect him to become a crucial link between clinicians and molecular researchers and a key driver of translational research that will help to speed up the process of transforming basic knowledge from the research bench into improved clinical therapies.
After joining our group, Reza soon became interested in the protein ‘survivin’, a multi-functional regulator of cell survival and division.
Survivin is overproduced in a considerable number of tumours and this is believed to aid tumour development through several mechanisms. Accordingly, survivin has been identified as a therapeutic target and the very first clinical trial using a new type of anti-survivin drug known as antisense oligonucleotide (ASO) has been completed in 2009 at the Churchill Hospital in Oxford. From this, it has emerged that the new ASO warrants further clinical evaluation and phase II follow up trials are now being planned.
Screening our panel of HNC cell lines, we found that survivin is also highly expressed in the large majority, but not all of these. Reza is therefore now testing the effects of the ASO in HNC cells with high or low survivin expression. Through these experiments, he has now found striking effects of the ASO on the viability of HNC cells. The drug causes the cells to loose their ability to divide their cell bodies properly and also appears to induce a new kind of self-destruction program that differs greatly from the classical mechanism known as apoptosis. Understanding these mechanistic details allows us to rationally design tests of combinations of novel and established drugs, initially in cell culture models, but eventually also in clinical settings.