In the News
September 22, 2016 – Ralph DeBerardinis, M.D., Ph.D., Director of the Genetic and Metabolic Disease Program at the Children’s Medical Center Research Institute at UT Southwestern (CRI), was among 84 scientists from 43 U.S. institutions chosen as a Howard Hughes Medical Institute Faculty Scholar. The new grant program is a collaboration of HHMI, the Simons Foundation, and the Bill & Melinda Gates Foundation.
Read the article.
May 10, 2016 — Dr. Bo Zhou, a postdoctoral researcher in the Children’s Medical Center Research Institute lab of Dr. Sean Morrison, has been named the winner of the 2016 Award for Excellence in Postdoctoral Research at UT Southwestern Medical Center. The recognition is the highest annual award given to a UT Southwestern postdoctoral scholar participating in the graduate school’s Postdoctoral Certificate Training Program. Read the article.
April 21, 2016 — Dr. Hao Zhu, an Assistant Professor at the Children’s Medical Center Research Institute at UT Southwestern, is one of 10 researchers in the nation to receive a Stand Up To Cancer grant to further his studies of a gene whose absence protects mice against liver cancer and promotes liver tissue regeneration in mammals. Read the news release.
April 7, 2016 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern have identified a novel metabolic pathway that helps cancer cells thrive in conditions that are lethal to normal cells. Read the news release.
March 29, 2016 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern (CRI) report that dietary intake determines the balance between fat formation and bone formation in adult bone marrow. The team led by Dr. Sean Morrison, CRI Director and Professor of Pediatrics, found that leptin, a hormone secreted by fat cells in response to food consumption, acts directly on stem cells in the bone marrow to promote the formation of fat cells at the expense of bone.
“This discovery settles a longstanding controversy in this field over the mechanisms underlying the reciprocal relationship between fat and bone,” Dr. Morrison said.
Dr. Morrison is a Howard Hughes Medical Institute Investigator, the Mary McDermott Cook Chair in Pediatric Genetics at UT Southwestern, the director of the Hamon Laboratory for Stem Cell and Cancer Biology, and a CPRIT Scholar in Cancer Research.
The research was supported by the Damon Runyan Cancer Research Foundation, the Leukemia and Lymphoma Society, the American Heart Association, the Cancer Prevention and Research Institute of Texas, and donors to the Children’s Medical Center Foundation.
The study was published in Cell Stem Cell.
March 25, 2016 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern report that inactivating a certain protein-coding gene promotes liver tissue regeneration in mammals. Read the news release.
Feb. 26, 2016 — Because of the foresight and generosity of several of Dallas’ leading foundations, more than $30 million has recently been committed to Children’s Medical Center Foundation to catapult the Children’s Medical Center Research Institute at UT Southwestern into a leader in pediatric research.
- Read the news release.
- Read the article in the Dallas Morning News.
- Read the article in D Healthcare Daily.
Feb. 4, 2016 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern have pioneered a new method for conducting in-depth research on malignant tumors in patients, in the process discovering new complexities underlying cancer biology and overturning a nearly century-old perception about cancer metabolism.
The findings, published in Cell, may pave the way for exploiting cancer metabolism to predict disease progression and treat cancer. Read the news release.
Jan. 11, 2016 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern (CRI) have teamed with researchers at the Dana-Farber Cancer Institute to pioneer the use of epigenomic profiling and CRISPR-Cas9 gene editing technology in studying how transcription enhancers operate during blood-forming stem cell differentiation and the role enhancers may play in the development of blood cancers.
Transcription enhancers are noncoding sequences of DNA that regulate how, when and where protein-coding genes are expressed, which enables cells to grow and develop into the body’s various, specialized functions.
The study provides new information about the role of transcription enhancers in normal blood-forming stem cell differentiation, and demonstrates how gene editing technology might enable scientists to target the development of blood cancers by modifying certain noncoding regulatory elements that drive those cancers.
“We found that during the course of normal blood-forming stem cell differentiation, transcription enhancers undergo extensive turnover,” said Dr. Jian Xu, an Assistant Professor at CRI, an Assistant Professor of Pediatrics at UT Southwestern, and a CPRIT Scholar in Cancer Research. “We also identified a particular regulatory mechanism that helps explain how genes turn on and off during the differentiation process. Those two discoveries lay the groundwork for using the CRISPR-Cas9 gene editing technology to potentially modify gene expression regulatory elements and target the development of certain blood cancers.”
The findings also provide an opportunity for further study to determine if modification of regulatory genomic elements can advance a personalized method of targeting cancers based on individual genetic mutations.
The study was published in Developmental Cell.
Nov. 16, 2015 — Scientists at the Children’s Medical Center Research Institute at UT Southwestern have determined how the body responds during times of emergency when it needs more blood cells. In a study published in Nature, researchers report that when tissue damage occurs, in times of excessive bleeding, or during pregnancy, a secondary, emergency blood-formation system is activated in the spleen.
Watch the video below identifying blood-forming stem cells inside the spleen, and read the news release.