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Joseph Delaney Ph.D.

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  • Assistant Professor
  • College of Medicine
  • Biochemistry and Molecular Biology
Academic Focus
  • The Delaney lab primarily studies copy-number alterations in cancer.
  • Development of user-friendly bioinformatics
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Education and Training
Duke University
Post-doctoral training
Mentor: Al La Spada, MD, PhD
Grant title: “Copy number alterations in low mutation cancer”


University of California San Diego
Post-doctoral training
Moores Cancer Center
Mentor: Dwayne Stupack, PhD
Grant title: “Copy number alterations in low mutation cancer”


University of Washington
PhD in Molecular and Cellular Biology
Mentor: Matt Kaeberlein, PhD
Thesis: "Elucidation of the molecular pathways of lifespan extension by dietary restriction in yeast"

University of California: Berkeley
BS, Chemical Biology, with Honors




I study the regulation of genome homeostasis mechanisms in the context of cancer and aging. My current focus is on the interaction of autophagy with genome maintenance and bioinformatic analysis of copy number alteration systems in ovarian cancer. The cancer field has exponentially grown in knowledge thanks to national and international sequencing consortiums, and my work translates these findings into meaningful biology and cures. My past PhD work in yeast aging focused on the interaction of genomic instability, longevity, and dietary restriction. I co-first authored the whole genome analysis of genes which can extend lifespan in yeast, a project summarizing a decade of team research. I turned this database information into studies focused on mitochondrial, genetic, and translational homeostasis, which are powerful determinants of both aging and cancer progression. For example, I found a new pathway, Los1 and nuclear tRNA modulation, regulating DNA damage signaling and longevity by RAD proteins. In the Stupack lab, I expanded my molecular and bioinformatic genetics into mammalian studies of ovarian cancer. I discovered allelic losses of autophagy to be important for ovarian cancer oncogenesis via impairment of chromosome homeostasis, and developed drug strategies to target this system. During my the CT2 translational oncology fellowship, I ensured that the chemical agents I used were immediately translatable into the clinic and found a drug combination able to completely eradicate cisplatin/docetaxel resistant cancer in PDX mouse models. We have published these powerful findings and generated much publicity, which we hope encouraged industry to follow up with clinical trials. At MUSC, my research will further investigate how monoallelic changes can alter the biology of cancer cells and how those changes lead to vulnerabilities. Importantly, pathway-based bioinformatic methods I developed were used to identify and prioritize important modulators of autophagy in ovarian cancer. My current research expands this method and the gene-prioritizations the bioinformatics uncovered to elucidate how complex copy number changes begin and can modify homeostatic mechanisms, such as autophagy, and change the underlying biology of cancer cells.