Researchers target the cell’s ‘biological clock’ in promising new therapy to kill cancer cells
Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern, and colleague, Dr. …
Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern, and colleague, Dr. …
SFU molecular biology and biochemistry professor Jack (Nansheng) Chen and three of his lab members collaborated with Chinese researchers to identify how these mutations affect genes and signalling pathways that might drive the formation of tumours in ICC. …
It may soon serve another purpose: zapping tumors. The biomedical advancement, which is under development at the University at Buffalo, could make chemotherapy more efficient, reduce its side effects and improve how doctors treat some of the most deadly forms of cancer. “We are developing a novel endoscopic device that will improve our ability to detect and destroy cancer cells,” says Ulas Sunar, PhD, a research assistant professor in UB’s Department of Biomedical Engineering and the principal investigator of a National Institutes of Health grant that supports the research. Conventional endoscopic imaging has limitations. …
Published in the Journal of Clinical Oncology, the study found that Herceptin, when added to chemotherapy, improved 10-year survival from 75 percent with chemotherapy alone to 84 percent with the addition of trastuzumab. Additionally, results also demonstrated continued improvement of survival without cancer recurrence — the 10-year disease-free survival rate increased from 62 percent to 74 percent with the addition of trastuzumab. Although heart problems are recognized side effects of Herceptin, the incidence rate of such events was found to be about 3 percent and the majority of those patients recovered from the initial effects. “We have found that when Herceptin is used in combination with chemotherapy, a patient’s survival is significantly improved,” said Geyer, who serves as a senior scientific advisor to the NSABP and at Massey is the Harrigan, Haw, Luck Families Chair in Cancer Research, associate director for clinical research and member of the Developmental Therapeutics research program, as well as professor in the Division of Hematology, Oncology and Palliative Care at the VCU School of Medicine. …
“It’s really all about natural selection and survival of the fittest,” says James DeGregori, PhD, investigator at the CU Cancer Center, professor of Biochemistry and Molecular Genetics at the CU School of Medicine, and the paper’s senior author. “When you’re young, healthy cells are optimized to the surrounding tissue — they’re the ‘fittest’,” DeGregori says. …
The scientists say when activated, one protein, called the short form, stops glioblastoma cells from replicating their DNA, and the other, called the long form, prevents cell division if the DNA has already been replicated, explains Rebecca Riggins, PhD, assistant professor of oncology at Georgetown Lombardi. The study was posted online Dec. …
The scientists say when activated, one protein, called the short form, stops glioblastoma cells from replicating their DNA, and the other, called the long form, prevents cell division if the DNA has already been replicated, explains Rebecca Riggins, PhD, assistant professor of oncology at Georgetown Lombardi. The study was posted online Dec…
A better, cheaper, and safer way to look for the telltale signs of breast cancer may be with microwaves, said Neil Epstein, a NSERC CREATE I3T postdoctoral fellow at the University of Calgary in Canada. Epstein and his colleagues–engineering professor Paul Meaney of Dartmouth College’s Thayer School of Engineering and Keith Paulsen, director of the Dartmouth Advanced Imaging Center and the Robert A. Pritzker Professor of Biomedical Engineering and Professor of Radiology at the Geisel School of Medicine at Dartmouth College — describe just such a microwave imaging system in the current issue of the journal Review of Scientific Instruments, from AIP Publishing…
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. …
“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. …