DNA Damage and Bone Marrow Failure
The Jung Lab studies how endogenous and environmental DNA damage threatens the long-term function of hematopoietic stem cells and contributes to bone marrow failure. We focus on the molecular pathways that protect blood-forming stem cells from aldehydes, oxidative stress, and replication-associated damage, and on how defects in these pathways lead to stem-cell exhaustion, clonal evolution, and cancer predisposition. We combine stem-cell biology, disease models, and genomic approaches to define the sources of genotoxic stress in hematopoiesis and to identify mechanisms that may be therapeutically actionable in Fanconi anemia and related bone marrow failure syndromes.
Alcohol & HSC aging
Alcohol metabolism generates reactive aldehydes that can challenge the long-term integrity of hematopoietic stem cells. We study how alcohol exposure, aldehyde detoxification, and DNA-repair capacity interact to shape stem-cell survival, self-renewal, and aging. By defining dose-dependent effects of alcohol-associated genotoxic stress and identifying the molecular pathways that buffer or fail under this stress, we aim to understand why some individuals may be especially vulnerable to marrow toxicity, cytopenias, or accelerated hematopoietic aging. This work builds on the lab’s broader focus on aldehyde-induced DNA damage and the protective roles of Fanconi anemia pathway components.
Clonal Evolution & Cancer Genetics
Bone marrow failure is not static: under selective pressure, damaged hematopoietic cells can acquire clones that restore fitness, persist, or progress toward malignancy. The Jung Lab studies how inherited defects in DNA repair and stem-cell maintenance shape somatic mosaicism, clonal selection, and cancer evolution. We use genomic and clinical perspectives to investigate both adaptive and harmful outcomes of clonal evolution, including natural genetic reversion, chromosomal alterations, and mutational signatures associated with Fanconi anemia pathway deficiency. By clarifying how clones emerge and compete over time, we seek biomarkers of risk and mechanistic insights that can inform surveillance and intervention.