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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 Medical Center Dallas 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.

14

Research Labs

2

Howard Hughes Medical Institute Investigators

2

Members of the National Academy of Sciences

2

Members of the National Academy of Medicine

40%

Trainees who have gone on to tenure-track positions

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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:

  • Make discoveries that change the way we think about important problems.
  • Cure people who would not be cured otherwise.
  • Train the next generation of scientists.
Yafeng Li stands in front of a deep freezer and pulls out a drawer with samples that are labeled in neon orange and green.

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.
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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.
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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.
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Discoveries

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Metabolism
July 2026

New biosensor tracks down missing metabolite from childhood brain disorder

McBrayer Lab: Using their newly developed biosensor to track essential metabolite alpha-ketoglutarate (αKG), researchers found that mitochondrial enzyme GPT2 and transporter protein SLC25A11 work together to control production and transport of αKG from the mitochondria to the nucleus. Since αKG is essential to unwind DNA for gene transcription, this new research suggests αKG supplementation at birth might help diminish disease progression for babies born with a rare inborn error of metabolism, called GPT2 deficiency, who suffer from severe neurological impairment. Science 393, 259-74
Peter Ly, Ph.D., Assistant Professor in Children's Medical Center Research Institute at UT Southwestern and of Cell Biology, Pediatrics, and in the Harold C. Simmons Comprehensive Cancer Center, observes microscope images with Ly Lab researcher Elizabeth Maurais, Ph.D., a recent graduate of the Genetics, Development and Disease Program at UT Southwestern.
Cancer Biology
May 2026

Human cells can exchange genomic DNA that alters cell behavior

Ly Lab: Large pieces of DNA can transfer directly between human cells, and the DNA can persist and change how the recipient cell functions. These Ly Lab findings challenge a long-standing view that the genomes of individual human cells evolve independently from one another. DNA damage and errors in cell division can cause pieces of genomic DNA to escape from the nucleus and move into nearby cells through nanotubes – thin, tubelike structures that briefly form when some cells come into contact. Cell (online first)
From left: Hao Zhu, M.D., Professor in Children’s Medical Center Research Institute at UT Southwestern (CRI) and of Pediatrics and Internal Medicine at UT Southwestern, and Zhu Lab researchers Roger Liang, B.S., UT Southwestern Perot Family Scholar Medical Scientist Training Program graduate student; Zhijie Li, Ph.D., postdoctoral fellow; and Jason Guo, B.S., UT Southwestern medical student.
Cancer Biology, Regenerative Medicine
November 2025

Location matters for liver cancer’s origins

Zhu Lab: Scientists discovered liver cancers arise in specific metabolic zones, where premalignant cells exploit location-specific genes that promote cell survival by chemical detoxification. While hepatocytes in different zones have vastly different gene expression, scientists did not previously know where liver cancers most frequently arise. CRI Researchers discovered cells with Ctnnb1 and Arid2 mutations were preserved in zone 1 but disappeared in zone 3. Unexpectedly, Ctnnb1/Arid2-driven cancers were much more likely to arise in zone 3 than in zone 1 in aged mice. This zonal preference was significant because it also applied to other types of liver cancer caused by different mutations. Science 391:eadv7129
From left: Ralph DeBerardinis, M.D., Ph.D., Professor and Director of the Eugene McDermott Center for Human Growth and Development and Professor in CRI and of Pediatrics, and DeBerardinis Lab postdoctoral fellows Zheng Wu, Ph.D., and Phong Nguyen, Ph.D.
Metabolism
November 2025

Protein regulating balance between purine nucleotide production pathways discovered

DeBerardinis Lab: NUDT5 is a vital regulator of how cells build purine nucleotides, which may determine cancer treatment efficacy. CRI’s new research shows NUDT5 suppresses de novo purine synthesis during purine salvage. Cells containing NUDT5 die when treated with thiopurines, but cells lacking NUDT5 are resistant. NUDT5 binds to phosphoribosyl pyrophosphate amidotransferase (PPAT), a crucial enzyme in de novo purine synthesis. This binding allows thiopurine nucleotides to turn off de novo synthesis, which is part of how these drugs kill cancer cells. Science 390: 1134-42
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CRI researchers sit at desks in a conference room and look at an unseen presenter. There is a back shelf full of magazines.

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.

Training

Inside CRI Newsletter

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

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