Protein common in cancers jumps anti-tumor mechanisms — ScienceDaily
source : http://www.sciencedaily.com/releases/2014/03/140317155203.htm
source : http://www.sciencedaily.com/releases/2014/03/140317155203.htm
source : http://www.sciencedaily.com/releases/2014/02/140219124734.htm
The research, published in Nature, raises several intriguing possibilities for further investigation that might lead to improved treatments for blood cancers and increased safety and effectiveness of chemotherapy. Before the finding, blood-forming stem cells were thought to be regulated similarly in both males and females, according to the paper’s senior author, Dr. Sean Morrison, Director of CRI, Professor of Pediatrics, and the Mary McDermott Cook Chair in Pediatric Genetics at UT Southwestern Medical Center…
In the study, published online in Cell Reports, scientists found that inhibiting the action of a protein called BRD4 caused cancer cells to die in a mouse model of malignant peripheral nerve sheath tumors (MPNSTs). "This study identifies a potential new therapeutic target to combat MPNST, an incurable type of cancer that is typically fatal," said Dr. …
His work, done in collaboration with Professor of Genetics Jason Moore, PhD, and colleagues at Vanderbilt University, was published in PLOS Genetics journal on November 7, 2013. Genetic mutations can occur in the cells that are passed on from parent to child and may cause birth defects…
The multidisciplinary team discovered that a cholesterol metabolite called 27-hydroxycholesterol, or 27HC, promotes tumor growth in estrogen-receptor positive breast cancers, which are the most common type of breast cancer. Estrogen-receptor positive breast cancer was previously believed to be stimulated primarily by the female sex hormone estrogen and it is commonly treated using endocrine-based medications that starve tumors of estrogen. The discovery of 27HC as another driver of breast cancer may explain why endocrine-based therapy is often unsuccessful, providing a new target for therapy, the researchers say. "This information can be used to develop new therapies that inhibit 27HC action or production, or increase its metabolism, in effect cutting the cancer off from a key growth stimulator," said senior author Dr…
In laboratory studies, researchers found that the pathway, called mammalian target of rapamycin (mTOR), was highly active in pediatric low-grade gliomas, and that mTOR activity could be blocked using an experimental drug, leading to decreased growth of these tumors. "We think mTOR could function as an Achilles heel," says study co-author Eric Raabe, M.D., Ph.D., an assistant professor of pediatrics, oncology and pathology at the Johns Hopkins Kimmel Cancer Center. "It drives cancer growth, but when mTOR is inhibited, the tumor falls apart." The work was described Nov…
"The gold standard of diagnosis is currently colonoscopy," says corresponding author of the study, Dr. Rima Rozen, a geneticist from the Departments of Human Genetics and Pediatrics at The Montreal Children’s Hospital of the MUHC and McGill University. "This is an invasive procedure, where the physician looks for abnormal tissue or growths also known as polyps." Additionally, given surging demand for colonoscopies, this research may ultimately offer an alternative option for early diagnosis, paving the way for the reduction in wait time. According to Dr…
Faculty of Medicine & Dentistry researcher Shairaz Baksh published his team’s discovery in the peer-reviewed journal, PLOS ONE. …
Reuben Kapur, Ph.D., the Frieda and Albrecht Kipp Professor of Pediatrics at the IU School of Medicine and a researcher at the Indiana University Melvin and Bren Simon Cancer Center, and colleagues discovered in pre-clinical and pharmacological models that cancer cells with a mutation in the KIT receptor — an oncogenic/cancerous form of the receptor — in mast cell leukemia and acute myeloid leukemia can be stopped. Their findings were published online Sept…