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About CRI

Children’s Medical Center Research Institute at UT Southwestern (CRI) is a nonprofit research institute built on the clinical expertise of Children’s Health System of Texas and the scientific excellence of UT Southwestern Medical Center. Under the leadership of Sean J. Morrison, Ph.D., CRI has created a world-class research and training environment that is collaborative and inclusive.

We are located in the heart of Dallas, Texas, and are home to an interdisciplinary group of scientists and physicians from all over the world. Our research is focused at the intersection of stem cells, cancer, and metabolism because we believe these areas hold uncommon opportunity for discoveries that are changing the way we think about important scientific questions and yielding new strategies for treating disease.

12

Research Labs

2

Howard Hughes Medical Institute Investigators

2

Members of the National Academy of Medicine

40%

Trainees who have gone on to tenure-track positions

Mission

CRI is improving our understanding of the biological basis of disease by focusing at the interface of stem cells, cancer, and metabolism.

Our ultimate goals are to:

Research Areas

Research requires commitment, vision, and a relentless determination to push the boundaries of knowledge. Our scientists and physicians are working in the fields of stem cells, cancer, and metabolism.

Genetic and Metabolic Disease Program

CRI researchers study the ways in which perturbations in metabolism contribute to diseases such as cancer and to conditions such as inborn errors of metabolism. Inborn errors of metabolism occur when children are born with genetic defects that impair the function of metabolic pathways. CRI established the Genetic and Metabolic Disease Program (GMDP) to integrate patient care and research to advance the diagnosis and treatment of genetically determined metabolic diseases.

Tissue Regeneration Program

Researchers in CRI’s Tissue Regeneration Program are identifying the cellular and genetic basis of tissue healing in a wide range of organs. Elucidation of these mechanisms will advance our ability to repair tissues damaged by age, disease, and trauma.

Cancer Biology

Cancer is a complex group of diseases characterized by rapid and uncontrolled cell proliferation and metastasis to other parts of the body. CRI researchers use a variety of approaches to identify the mechanisms that drive the formation and progression of several cancers in order to find new treatments.
October 2024
Morrison Lab: Scientists discovered retrotransposons are activated during pregnancy and after significant bleeding in blood-forming stem cells to increase blood cell production. This is an important step toward defining the purpose of “junk DNA” in humans. Retrotransposon expression promotes stem cell division by activating the immune sensors, cGAS and STING, which induce an interferon response to stimulate blood cell production. Science [online before print]
August 2024
DeBerardinis lab: Discovered that contrary to how tumors operate while still in the kidney, metastatic kidney cancers rely heavily on mitochondrial metabolism. The mitochondrial electron transport chain is much more active in tumors that have metastasized than in tumors still growing in the kidney. Nature 633, 923-31
July 2024
Hoxhaj lab: Cancer cells salvage purine nucleotides to fuel tumor growth, including purines in foods we eat, an important discovery with implications for cancer therapies. CRI researchers challenged the long-standing belief that tumors primarily acquire purine nucleotides – building blocks for DNA, which is required for cellular growth and function – by constructing them from scratch via de novo synthesis. Research also shows tumors significantly use the more efficient salvage, or recycling, pathway to acquire purines. Cell 187, 3602-18
June 2024
Mishra lab: Researchers identified a type of metabolic inflexibility during liver regeneration that prevents cells with dysfunctional mitochondria from proliferating, which demonstrates one way regenerative cells root out damage. When their mitochondria are damaged, hepatocytes turn on PDK4, a metabolic enzyme that stops the cells from shifting to an alternative source of acetyl-CoA, so they can’t proliferate. Science 384:eadj4301

Training in CRI

CRI has a history of making high-impact discoveries and training students and postdoctoral fellows who have gone on to tenure-track academic faculty positions and leadership positions in biotechnology and pharmaceutical companies. Our trainees benefit from exceptional grant funding, a collaborative environment, and access to state-of-the-art facilities.

Learn more about the training environment in CRI and the impressive careers of our alumni.

Inside CRI Newsletter

Stay up-to-date with our latest discoveries and news by subscribing to our quarterly email newsletter.

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