Abby Green, MD


A GreenI am a physician-scientist and trained in both pediatric oncology and infectious diseases. I grew up wanting to be a pediatric oncologist and, through some lucky connections and fantastic mentors, found that science would be an essential component in my career.

My introduction to science began during college when I worked in a genetics lab at the University of Iowa run by Dr. Jeff Murray. The Murray lab was a huge contributor to the Human Genome Project and my small piece of that entailed mapping a gene suspected to cause a familial craniofacial abnormality syndrome. After doing ~1000 PCR reactions in the Murray Lab, I decided to check out medical school before doing any more lab work.

After medical school in New York City, my clinical training in pediatrics was at the Children’s Hospital of Philadelphia where I became fascinated with the opportunistic pathogens that infect children with cancer and other immunodeficiencies. At Wash U, I am a part of the Immunocompromised Infectious Diseases program at St. Louis Children’s Hospital, which is dedicated to caring for infectious complications that occur in pediatric patients undergoing cancer therapy or organ transplantation.

Following clinical training, I did a post-doctoral fellowship in the lab of Dr. Matt Weitzman who taught me the importance of Western blots, DNA damage responses, and a passion for science. With Matt, I studied the APOBEC3 enzymes which are endogenously encoded DNA mutators that are intended to function as viral restriction factors but sometimes behave badly and act on the host genome causing mutations and DNA damage. I moved to Wash U in 2019 where my lab is now interested in how these DNA mutators contribute to cancer initiation and evolution. Similar to my clinical training, our research sits at the intersection of genome stability, cancer biology, and innate immunity.


Cancer develops through accumulation of DNA mutations and structural aberrations collectively known as genome instability. Genome damage in adult-onset malignancies can be traced to exogenous carcinogens or mutations acquired throughout normal aging. However, pediatric cancers do not arise as a result of aging or exogenous genotoxic agents. We are interested in the etiology of genome instability in pediatric cancers and the resulting genome-protective responses, also called DNA damage responses, that are activated. Our lab uses molecular and cell biology, biochemistry, genome sequencing, proteomics, and animal models to evaluate mechanisms of mutagenesis and the subsequent impact on oncogenesis and tumor evolution. Our long-term goal is to identify predictors of mutagenesis and therapeutic vulnerabilities within DNA damage response pathways in order to develop new treatment options for pediatric patients with cancer.

Mutational Sig Image1
Figure 1. The genome-wide mutational signature of APOBEC3A activity. The mutational spectrum elicited by aberrant APOBEC3A cytidine deamination was determined by whole-genome sequencing of individual cell clones after long-term expression of APOBEC3A in culture. Mutations that occurred in all clones (n=16) are quantified. The APOBEC3A signature consists largely of C>T transitions in a TC dinucleotide context.
Dna Damage
Figure 2. Deamination by APOBEC3A elicits robust DNA damage responses. Immunofluorescent imaging of cells that express APOBEC3A demonstrates phosphorylated H2AX staining consistent with widespread DNA damage.


Lab website:

Recent publications

Green AM and Weitzman MD (2019). The spectrum of APOBEC3 activity: from anti-viral agents to anti-cancer opportunities. DNA Repair, 83:102700.

Green AM, Budagyan K, Hayer KE, Reed MA, Savani MR, Wertheim GB, Weitzman MD (2017). Cytosine Deaminase APOBEC3A sensitizes leukemia cells to inhibition of the DNA replication checkpoint. Cancer Research, 77:4579-4588

Green AM, Landry S, Budagyan K, Avgousti DC, Shalhout S, Bhagwat AS, and Weitzman MD (2016). APOBEC3A damages the cellular genome during DNA replication. Cell Cycle, 15:998-1008