The new technique cuts out a cellular middleman. Study senior author Xiaowei “George” Xu, MD, PhD, an associate professor of Pathology and Laboratory Medicine, explains, “Through direct reprogramming, we do not have to go through the pluripotent stem cell stage, but directly convert fibroblasts to melanocytes. …
An investigational drug discovered and being developed by Pfizer Inc., palbociclib targets a key family of proteins (CDK4/6) responsible for cell growth by preventing them from dividing. Results of the multi-year phase 2 study showed a significant increase in PFS for patients with advanced breast cancer that was estrogen receptor positive (ER+), HER2-negative (HER2-), who were given a combination of the standard anti-estrogen treatment, letrozole, and palbociclib compared to letrozole alone. …
But a new University of Michigan study indicates that using those words can have an unintended negative effect. David Hauser, a U-M doctoral student in psychology, and colleague Norbert Schwarz of the University of Southern California, found in three studies that exposure to metaphoric language relating cancer to an enemy significantly lessens the extent to which people consider cancer-prevention behaviors. …
In a study of preclinical models of colorectal cancer, the researchers identified an underlying mechanism for the activation of p53 by FL118. The agent activates the p53 tumor-suppressor protein largely independent of ataxia telangiectasia mutated (ATM)-dependent DNA damage-mediated p53 activation. ATM-dependent activation of p53 is usually induced by many — if not all — types of DNA-damage drugs, including camptothecin compounds such as irinotecan and topotecan, leading the authors to conclude that FL118’s mechanisms of action are distinct among camptothecin analogues. “While FL118 is an analogue of irinotecan and topotecan, two FDA-approved cancer drugs that are also based on the naturally occurring compound camptothecin, our findings add further evidence that FL118 has novel mechanisms of action that may make it especially potent against solid tumors and especially effective as a well-tolerated, targeted therapy,” said Dr. …
The algorithm, called Hotnet2, was used to analyze genetic data from 12 different types of cancer assembled as part of the pan-cancer project of The Cancer Genome Atlas (TCGA). The research looked at somatic mutations — those that occur in cells during one’s lifetime — and not genetic variants inherited from parents. The study identified 16 subnetworks of genes — several of which have not previously received much attention for their potential role in cancer — that are mutated with surprising frequency in the 3,281 samples in the dataset. The researchers hope the new findings, published in Nature Genetics, will provide scientists with new leads in the search for somatic mutations that drive cancer…
Using a new super-resolution microscope they’ve been able to see single molecules of the enzyme at work in a liver cancer cell line. Then they’ve used confocal microscopes to see how disrupting the enzyme slows down living cancer cells. The enzyme is DPP9 (dipeptidyl peptidase 9) which the researchers at the Centenary Institute and the Sydney Medical School were first to discover and clone, in 1999. …
As Rotello and his doctoral graduate student Le Ngoc, one of the lead authors, explain, to discover a new drug for any disease, researchers must screen billions of compounds, which can take months. One of the added keys to bringing a new drug to market, they add, is to identify how it works, its chemical mechanism. “Rapid determination of drug mechanism would greatly streamline the drug discovery process, opening the pipeline of new therapeutics,” Ngoc says. She adds, “Drugs with different mechanisms cause changes in the surface of cells that can be read out using the new sensor system…
“The p53 protein is necessary for tumor suppression,” said Xinbin Chen, professor at the UC Davis Schools of Medicine and Veterinary Medicine. “When Rbm38 suppresses p53, organisms develop tumors. Knocking out Rbm38 increases p53, which we thought might be a good thing. But too much p53 suppresses cell-cycle progression, causing cell death, premature aging and even cancer.” The relationship between p53 and Rbm38 can best be described as a loop: p53 regulates Rbm38 expression, while Rbm38 suppresses p53. …
The researchers investigated patterns of molecules called long noncoding RNAs (lncRNAs), a class of RNA molecules more than 200 nucleotide units long that are involved in regulating genes. The researchers examined the abundance, or expression, of lncRNAs in patients who were 60 years and older and who had cytogenetically normal (CN) AML. The study is published online in the Proceedings of the National Academy of Sciences…
“What we know now about ECP is that it is able to function in more than one way,” said Ratcliffe. “It can immunotolerize in the autoreactive setting, and immunize against, in a situation such as lymphoma. This enigma poses tremendous opportunity for future basic science investigation in immunology where cancer applications in bone marrow transplantation and lymphoma will benefit from novel therapeutics.” Currently, ECP is used to treat cancer patients who have cutaneous T-cell lymphoma or in patients with Graft versus Host disease after transplantation. There are many questions about how the therapy works and the best schedules for treating patients…