Cancer cells decide whether to live or die after a short period of intense exposure to targeted therapy, opposing the current requirement for continuous treatment, according to a new study.
The researchers, led by the South Australian Health and Medical Research Institute (SAHMRI) and the University of Adelaide’s Centre for Personalised Cancer Medicine in Adelaide, Australia, say this study presents a new treatment strategy which will translate to a significant reduction in side effects for patients. The results have been published in Leukemia (2014; doi:10.1038/leu.2014.156).
“This discovery is paradigm shifting,” said Professor Deborah White, PhD, FFSc(RCPA), Director, Cancer Research with SAHMRI and University of Adelaide professor. “Our findings are not just applicable to chronic myeloid leukemia (CML) therapy, but to all targeted cancer treatments. In our research, we’re looking for methods that will result in the cancer cell killing itself. This would provide an improved treatment and reduce the risk of cancer relapse.”
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As a consequence of this finding, White and colleagues identified a new target in resistant and persistent disease. They show that by blocking a common protein they can more effectively cause death in leukemia cells.
White and her research team have been investigating the role of a common protein known as STAT5. They found that the activity of STAT5 appears to be a critical determinant of the decision for cancer cells to live or die. When they blocked STAT5 in conjunction with exposure to a regular anti-cancer treatment, the leukemia cells were more effectively targeted.
They also found that timing was important, and that combining STAT5 inhibition with exposure to tyrosine kinase inhibitors for less than one hour was lethal to the progenitors of CML. This was in contrast to inhibiting JAK kinase, which did not cause cell death when it was combined with tyrosine kinase inhibitors. The authors concluded that combining tyrosine kinase inhibitors with inhibiting STAT5 is promising for the treatment of CML.
This article originally appeared on ONA