%0 Journal Article
%T Armed and accurate: engineering cytotoxic T cells for eradication of leukemia
%A Marko Radic
%J BMC Biotechnology
%D 2012
%I BioMed Central
%R 10.1186/1472-6750-12-6
%X Recent advances in cancer immunotherapy have allowed the conversion of T cells from leukemia patients into efficient and specific killers of their own cancer cells. The new technique has been recently tested with remarkable results. The outward signs of the successful therapy were dramatic and clear. The cancer patients shook with fever, chills and pain; their blood pressure precipitously dropped. They drifted in and out of sleep for days following the infusion of their own engineered killer T cells. The internal struggle peaked between two and three weeks after T cell reinfusion. The load of lysed cancer cells stressed and nearly poisoned the patients' kidneys. Their immune systems, reinvigorated by the immunotherapy, had destroyed nearly 1 kg of cancer cells. No other available treatment could have achieved a comparable therapeutic success. The new treatment, administered by Dr. Carl June and his colleagues of the Abrahamson Cancer Center at the University of Pennsylvania, achieved an unprecedented complete eradication of the cancer in two of the three chronic lymphocytic leukemia (CLL) patients in whom it was tried. It had been a dream of many: the harnessing of the immune system's ferocious power to eliminate an advanced metastatic cancer.The stunning results were published in two simultaneous journal articles [1,2], one of the reports presenting data from a single patient [1]. The success was beyond expectation. This, after all, was a Phase I clinical trial, one in which the primary objective was to test different doses of the engineered cytotoxic lymphocytes (CTL). Technically, the success could be traced to the fusion of extracellular and intracellular domains into a new, synthetic receptor for the CD8+ T cells [3]. In immunotherapy jargon, this type of recombinant protein is called a chimeric antigen receptor (CAR). In this case, the extracellular domain was derived from a mouse monoclonal antibody specific for the CD19 surface protein of human B cells. Beca
%U http://www.biomedcentral.com/1472-6750/12/6