Welcome to the Newsroom
The IDOM Newsroom is your one stop place for announcements, news and events for the:
- Division of Endocrinology, Diabetes and Metabolism
- Institute for Diabetes, Obesity and Metabolism
- Diabetes Research Center
- Penn Rodebaugh Diabetes Center
Current News Features
April 12, 2013
No Need for Genetic Testing for Most Thyroid Cancers
In the majority of patients with papillary thyroid cancer, the most common form of thyroid cancer, there is no need for genetic testing, reports Medscape. However, there might be a role for such testing in the 7% of patients who present with an aggressive form of the disease.
This finding comes from a study published in the April 10 issue of JAMA that explores the association between the BRAF V600E mutation and mortality in patients with papillary thyroid cancer. US News and World Report, via HealthDay says that according to JAMA editorialists, Anne Cappola, MD, ScD, and Susan Mandel, MD, MPH, of the Perelman School of Medicine at the University of Pennsylvania, "Although these findings do not support widespread BRAF V600E testing, they do support the need for additional study of how BRAF testing can be used to improve the already excellent prognosis of patients with papillary thyroid cancer." While the study found an association between the gene mutation and thyroid cancer survival, it did not establish a cause-and-effect relationship.
Mutation Hikes Death Risk in Thyroid Cancer
Medpage Today reports that patients with papillary thyroid cancer (PTC) who are carriers of the BRAF V600E mutation may have worse mortality, researchers reported in the April 10 issue of JAMA. In an accompanying editorial by Penn endocrinologists Anne Cappola, MD, ScD and Susan Mandel, MD, MPH, the findings provide two important insights.
First, they suggest that this mutation "mediates features of the clinically aggressive tumors that account for the vast majority of PTC mortality," and provides a "strong biological rationale for current trials of targeted tyrosine kinase inhibitor therapy" for patients with the mutation who have advanced disease. On the other hand, the results suggest that screening for the mutation "doesn't add predictive value for PTC-related mortality beyond the information collected in the process of PTC tumor staging."
Brown Fat, White Fat, Good Fat, Bad Fat
Fat has been villainized; but all fat was not created equal. Our two main types of fat—brown and white—play different roles. Two teams of NIH-funded researchers have enriched our understanding of adipose tissue. One of those teams is led by Patrick Seale, PhD, assistant professor of Cell and Developmental Biology and a member of the Institute for Diabetes, Obesity, and Metabolism. His work was highlighted in the NIH Director's Blog, describing how the body can recruit white fat and transform it into brown.
Reprogramming Cells to Fight Diabetes
For years researchers have been searching for a way to treat diabetics by reactivating their insulin-producing beta cells, with limited success. The "reprogramming" of related alpha cells into beta cells may one day offer a novel and complementary approach for treating type 2 diabetes. Treating human and mouse cells with compounds that modify cell nuclear material called chromatin induced the expression of beta cell genes in alpha cells, according to a new study that appears online in the Journal of Clinical Investigation.
Reprogramming alpha cells to treat diabetes
In differentiated cells, a stable phenotype is maintained in part by chromatin alterations, referred to as epigenetic marks, which determine the relative transcriptional activity of cell type-specific genes. In this issue, Nuria Bramswig from the Kaestner Lab and colleagues analyzed the epigenetic state of pancreatic cells, and found that in glucagon-producing alpha cells, many genes related to the beta cell program were simultaneously marked by activating and repressing modifications.
Bramswig et al. further found that treating human or mouse islets with chromatin-modifying compounds induced the expression of beta cell genes in alpha cells. These findings suggest that treating islets with chromatin remodelers may be a method to drive transdifferentiation of alpha cells toward a beta cell phenotype, perhaps creating a new source of these cells diabetes therapy.