Madison, Wisconsin – More than a decade of laboratory research at the University of Wisconsin has proven that a single chemical compound may both detect and treat malignant tumors and certain cancer stem cells.
In three posters presented at the annual meeting of the American Association for Cancer Research (AACR) in Chicago, March 31-April 4, UW-Madison researchers describe exciting advances involving CLR1404, described as a “diapeutic” agent that can both image and destroy a wide range of malignant tumors and the one type of cancer stem cells examined so far.
The presentations are based on basic research in the lab of Dr. Jamey Weichert, associate professor of radiology at the UW School of Medicine and Public Health (SMPH) and a member of the UW Carbone Cancer Center (CCC).
Clinicians at the UW School of Medicine and Public Health and elsewhere are interested in assessing CLR1404′s potential. Several clinical trials evaluating both the cancer imaging and therapeutic capabilities of CLR1404 are under way at the Carbone Cancer Center, with more scheduled to begin soon.
Dr. John Kuo, director of the Comprehensive Brain Tumor Program at UW Hospital and Clinics and a cancer stem-cell scientist at the School of Medicine and Public Health, is studying the possibility of using CLR1404 to treat glioblastoma multiforme (GBM), a deadly form of brain cancer, by targeting GBM stem cells.
In one of the American Association for Cancer Research posters (#3495), Kuo and Weichert describe how CLR1404 decreases glioblastoma stem cell activity, suppresses GBM growth and improves animal survival.
Piece by missing piece, scientists at the Keck School of Medicine of USC are deciphering the powerful gene regulatory circuit that maintains and controls the potential of embryonic stem cells (ESCs) to form any type of cell in the body.
Recent findings by Provost Professor Andrew McMahon, director of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, and Qilong Ying, associate professor of cell and neurobiology, underscore the essential role of basic science in paving the way for future medical breakthroughs.
McMahon and Ying are in pursuit of the ways in which the intricate regulatory circuit balances two qualities of stem cells: pluripotency (the capacity to develop into any type of cell) and differentiation (the process of becoming different types of cells). The scientists are particularly interested in signaling pathways — important routes for intracellular communication.
Howard Hughes Medical Institute (HHMI) scientists have discovered that endothelial cells, the building blocks of the vascular system, keep blood stem cells dividing healthily in a lab dish much longer and more effectively than previous methods of growing the cells. The new advance dramatically improves scientists’ ability to manufacture large quantities of authentic adult blood stem cells, which may help revolutionize the field of bone marrow transplantation.
Shahin Rafii, an HHMI investigator at Weill Cornell Medical College in New York City, and his colleagues report on the development of an endothelial cell platform that supports self-renewal of the blood stem cells, known as long-term hematopoietic stem cells (LT-HSCs), in the March 2010 issue of the journal Cell Stem Cell. Their study also describes a novel mechanism by which endothelial cells support propagation of LT-HSCs in adult mice.
When infections occur in the body, stem cells in the blood often jump into action by multiplying and differentiating into mature immune cells that can fight off illness. But repeated infections and inflammation can deplete these cell populations, potentially leading to the development of serious blood conditions such as cancer.
Now, a team of researchers led by biologists at the California Institute of Technology (Caltech) has found that, in mouse models, the molecule microRNA-146a (miR-146a) acts as a critical regulator and protector of blood-forming stem cells (called hematopoietic stem cells, or HSCs) during chronic inflammation, suggesting that a deficiency of miR-146a may be one important cause of blood cancers and bone marrow failure.
While looking for mechanisms that might be relevant to restoring regenerative potential in older skeletal muscle, HSCI Executive Committee member, Amy Wagers, PhD, and her team, thought about mechanisms that had been studied for a long time evolutionarily as regulating lifespan and longevity. One example of such a mechanism is reduced calorie intake in the absence of malnutrition, also know as calorie restriction, which has been show to extend lifespan in many organisms.
In order to address the question of whether calorie restriction could also affect skeletal muscle regeneration, Wagers and her colleagues placed mice for 12 weeks on a calorie restricted diet. When the animals were challenged with muscle damage, they responded more vigorously and repaired the damage more rapidly and more effectively than the control mice.