Targeting the Cellular Metabolism and Survival Mechanisms in CLL and Richter’s SyndromePosted: December 14, 2016
The survival of tumor cells is dependent on the tumor cells maintaining a normal interaction with the healthy microenvironment. An increasingly important strategy in the treatment of CLL is to develop new therapies that do not necessarily attack the cancerous cells themselves, but instead attack the molecular processes that allow the cancerous cells to function and thrive in the microenvironment. One potential target for treating CLL is the protein complex NF-kB, which controls important cell functions including the regulation of cell death, cell survival, and cell proliferation. If NF- kB function can be inhibited then CLL can be more easily treated.
The purpose of this recent study presented at the 2016 ASH meeting was to test the efficacy of the newly developed NF-bK inhibitor IT901 in the treatment of CLL and its aggressive transformation Richter’s Syndrome (RS). RS is a transformation that occurs within 5-10% of CLL’s and turns the disease into a fast growing diffuse large B-cell lymphoma, an aggressive non-Hodgkin lymphoma. The treatment of RS currently represents an unmet therapeutic need.
Results from this study were confirmed in a mouse xenograft model for people with CLL and in cell samples obtained from people with RS. In both models the use of IT901 was characterized by decrease in tumor growth and Researchers found that IT901 induced death in cancerous cells within 24 hours of treatment with a minimal impact on normal B-cells.
Researchers concluded that IT901 is effective in rapidly blocking NF-kB activity by decreasing the functions that allow the cell to flourish in the microenvironment. The results from this study are encouraging and point to a potential new treatment option for patients with CLL and RS.