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Epigenetic deregulation leads to potential novel therapeutic target for retinoblastoma

Research data, published in the journal Nature, has demonstrated that retinoblastoma may develop rapidly, in part due to epigenetic deregulation of key cancer pathways following bi-allelic loss of RB1 (retinoblastoma 1 gene). The research, led by specialists at St. Jude Children’s Research Hospital in Memphis, Tennessee and the Genome Institute, Washington University School of Medicine in St Louis, showed that expression of the spleen tyrosine kinase proto-oncogene (“SYK”) was the only up-regulated kinase gene detected in comparative studies between retinoblastoma tumours and control tissues. As small molecule inhibitors of SYK are currently under-going testing in patients for rheumatoid arthritis (RA) and autoimmune thrombocytopenia, this new target may now advance immediate therapeutic options using a new potential drug with clinical data already established in other indications.