"We have known about some of the molecular signals that mediate this senescence response, but we’ve needed to understand the signaling pathway in much more detail," said Peiqing Sun, associate professor in TSRI’s Department of Cell and Molecular Biology. …
The Side-Out Foundation’s pilot study is part of a cutting-edge approach to personalized medicine that looks beyond genomic analysis alone to combine it with what some say is the next frontier in targeted therapy: proteomics. The pilot study is the first of its kind to utilize novel protein activation mapping technology along with the genomic fingerprint of cancer as a way to find the most effective treatment. The trial was announced at the annual meeting of the American Society of Clinical Oncology and is expected to expand into phase two this month. Standard chemotherapy had failed the 25 women who participated in the 2.5-year pilot study, says study co-author Emanuel "Chip" Petricoin, co-director of George Mason’s Center for Applied Proteomics and Molecular Medicine (CAPMM)…
Under conditions of oxygen starvation often encountered by tumors, the epidermal growth factor receptor (EGFR) gums up the cell’s miRNA-processing machinery, an international team led by scientists at The University of Texas MD Anderson Cancer Center discovered. "So when hypoxia stresses a cell, signaling by EGFR prevents immature miRNAs from growing up to fight cancer," said senior author Mien-Chie Hung, Ph.D., professor and chair of MD Anderson’s Department of Molecular and Cellular Oncology and holder of the Ruth Legett Jones Distinguished Chair…
They say their study, published online May 10 in Human Molecular Genetics, offers a unique and exciting strategy to treat neurodegenerative diseases that feature abnormal buildup of proteins in Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), frontotemporal dementia, Huntington disease and Lewy body dementia, among others. "This drug, in very low doses, turns on the garbage disposal machinery inside neurons to clear toxic proteins from the cell. By clearing intracellular proteins, the drug prevents their accumulation in pathological inclusions called Lewy bodies and/or tangles, and also prevents amyloid secretion into the extracellular space between neurons, so proteins do not form toxic clumps or plaques in the brain," says the study’s senior investigator, neuroscientist Charbel E-H Moussa, MB, PhD. Moussa heads the laboratory of dementia and Parkinsonism at Georgetown. …
More than half of human cancers carry defects in the gene for p53, and almost all other cancers, with a normal p53 gene, carry other defects that somehow impair the function of the p53 protein. Inherited mutations in the p53 gene put people at a very high risk of developing a range of cancers. The p53 protein’s functions are normally stimulated by potentially cancer-causing events, such as DNA damage from ultraviolet radiation (a cause of skin cancer), or the over-activity of cancer-causing genes. Ms Liz Valente, Dr Ana Janic and Professor Andreas Strasser from the Molecular Genetics of Cancer division at the Walter and Eliza Hall Institute have been dissecting the processes that are controlled by p53, to discover how this protein can suppress cancer development…