As more chronic lymphocytic leukemia CLL treatments are approved, with many more in development, are researchers closer to hitting a “home run” in treating the disease? Patient advocate Dr. Brian Koffman met with CLL expert Dr. Thomas Kipps at ASCO 2014 to explore emerging therapies and the goal for patients to achieve deep remission.
Andrew Schorr from Patient Power in partnership with the CLL Global Research Foundation interview Dr. Thomas Kipps, Director of the Blood Cancer Research Fund and the CLL Research Consortium about the use of rituximab, a monoclonal antibody used to treat patients with chronic lymphocytic leukemia
NCI funding continues work focused on chronic lymphocytic leukemia
An international consortium of scientists studying chronic lymphocytic leukemia (CLL), based at the University of California, San Diego School of Medicine, has been awarded a 5-year, $20 million grant by the National Cancer Institute, part of the National Institutes of Health. The grant is the second renewal of funding for a broad-based effort designed to better understand the pathology of CLL – the most common form of leukemia in the Western world – and develop new drugs and treatments.
Magnified blood smear showing darker CLL cells.
“This funding allows us to continue critical research that has already produced substantial, new insights into how and why CLL develops and progresses differently in patients,” said Thomas J. Kipps, MD, PhD, professor of medicine in the UCSD School of Medicine, deputy director of research at UC San Diego Moores Cancer Center and director of the Chronic Lymphocytic Leukemia Research Consortium (CRC). “Our work has revealed new targets and approaches for both mitigating the disease and perhaps eventually preventing it.”
MiR-125b-1 maps at 11q24, a chromosomal region close to the epicenter of 11q23 deletions in chronic lymphocytic leukemias (CLLs). Our results establish that both aggressive and indolent CLL patients show reduced expression of miR-125b. Overexpression of miR-125b in CLL-derived cell lines resulted in the repression of many transcripts encoding enzymes implicated in cell metabolism.