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C-myc required by the immune system
May 12, 2006Infamous proto-oncogene turns up in a new role
Lausanne - C-myc, a gene commonly involved in cancer onset, has been found to have a role in the immune system's normal function according to a study published today in Blood. The surprising finding, by a Swiss research team led by investigators from the Lausanne Branch of the international Ludwig Institute for Cancer Research (LICR), showed that c-myc functions in the immune system's 'memory' of previous infections.
In order to rapidly and efficiently respond to new infections, the immune system evolved such that it stores a 'memory' of previous attack by pathogens. The specialized cells involved in this process are known as 'T memory cells'. The T memory cells are normally maintained at a low level that can be rapidly expanded if the pathogen is detected again. The maintenance of normal, low levels, or 'homeostasis', of T memory cells is dependent on a signalling factor, a so-called cytokine, known as 'IL- 15.
"Very little is known about the signalling pathways that actually control IL-15-dependent homeostasis," explains LICR's Dr. H. Robson MacDonald, the senior author of the study. "By analyzing genetically engineered mouse models with reduced c-myc, reduced IL-15 or absent IL-15, we discovered that it's actually c-myc, which is known primarily as an oncogene, that acts downstream of the IL-15 signaling pathway to regulate T memory cell homeostasis."
According to Dr. MacDonald, the study is basic research that may have implications for therapies of the future. "Understanding how immune memory works might allow us to improve therapeutic vaccines against, say, malaria or cancer. The unexpected finding is that this study is also a cautionary tale. Before we design new therapies that inactivate a gene product, which is an approach being considered for c-myc in cancer, we need to be very sure that we are not going to be also destroying a vital role in a normal process such as the body's immune system."
Ludwig Institute for Cancer Research
"Very little is known about the signalling pathways that actually control IL-15-dependent homeostasis," explains LICR's Dr. H. Robson MacDonald, the senior author of the study. "By analyzing genetically engineered mouse models with reduced c-myc, reduced IL-15 or absent IL-15, we discovered that it's actually c-myc, which is known primarily as an oncogene, that acts downstream of the IL-15 signaling pathway to regulate T memory cell homeostasis."
According to Dr. MacDonald, the study is basic research that may have implications for therapies of the future. "Understanding how immune memory works might allow us to improve therapeutic vaccines against, say, malaria or cancer. The unexpected finding is that this study is also a cautionary tale. Before we design new therapies that inactivate a gene product, which is an approach being considered for c-myc in cancer, we need to be very sure that we are not going to be also destroying a vital role in a normal process such as the body's immune system."
Ludwig Institute for Cancer Research
C-myc Current Events and C-myc News RSSFate Therapeutics announces creation of small molecule platform for commercial-scale reprogramming
Fate Therapeutics, Inc. announced today the generation of human induced-pluripotent stem cells (iPSCs) using a combination of small molecules that significantly improves the speed and efficiency of reprogramming.
A major step in making better stem cells from adult tissue
October 15, 2009 A team led by scientists from The Scripps Research Institute has developed a method that dramatically improves the efficiency of creating stem cells from human adult tissue, without the use of embryonic cells.
Tumor suppressor pulls double shift as reprogramming watchdog
A collaborative study by researchers at the Salk Institute for Biological Studies uncovered that the tumor suppressor p53, which made its name as "guardian of the genome", not only stops cells that could become cancerous in their tracks but also controls somatic cell reprogramming.
UCSF team closer to creating safe embryonic-like stem cells
A team of UCSF researchers has for the first time used tiny molecules called microRNAs to help turn adult mouse cells back to their embryonic state.
SIRT1 takes down tumors
Yuan et al. have identified another anti-cancer effect of the "longevity" protein SIRT1. By speeding the destruction of the tumor promoter c-Myc, SIRT1 curbs cell division.
Stem cell research uncovers mechanism for type 2 diabetes
Taking clues from their stem cell research, investigators at the University of California San Diego (UC San Diego) and Burnham Institute for Medical Research (Burnham) have discovered that a signaling pathway involved in normal pancreatic development is also associated with type 2 diabetes.
Dormant stem cells for emergencies
Many specialized cells, such as in the skin, intestinal mucosa or blood, have a lifespan of only a few days. For these tissues to function, a steady replenishment of specialized cells is indispensable. This is the task of so-called "adult" stem cells also known as tissue stem cells.
Yamanaka eliminates viral vector in stem cell reprogramming
Shinya Yamanaka MD, PhD, of Kyoto University and the Gladstone Institute of Cardiovascular Disease (GICD) has taken another step forward in improving the possibilities for the practical application of induced pluripotent stem (iPS) cell technology.
Recipe for cell reprogramming adds protein
A drug-like molecule called Wnt can be substituted for the cancer gene c-Myc, one of four genes added to adult cells to reprogram them to an embryonic-stem-cell-like state.
UCLA researchers identify leukemia stem cells
Stem cell researchers at UCLA have identified a type of leukemia stem cell and uncovered the molecular and genetic mechanisms that cause a normal blood stem cells to become cancerous.
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