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Linde A. Miles, PhD

  • Member, Division of Experimental Hematology & Cancer Biology
  • Assistant Professor, UC Department of Pediatrics



I’m an assistant professor, scientist and researcher focused on acute myeloid leukemia, cancer evolution and cancer biology.

I have had a longstanding interest in the mechanisms that dictate cellular transformations and the stepwise progression of tumorigenesis, namely the clonal evolution of cancer. My graduate work focused on developing new therapeutic strategies for the treatment of small cell lung cancer. I then joined the lab of Dr. Ross Levine, which allowed me to expand my skillset to incorporate liquid tumor biology, genetically engineered mouse models of disease, multiparameter flow cytometry, single-cell profiling of primary clinical isolates and gene expression analysis.

Cancer development occurs through sequential genomic, epigenomic and cellular state alterations, which converge to transform normal cells into malignant clones. While these steps can differ based on the cell of origin, tissue identity and specific somatic alterations, the ultimate result is the same — unchecked proliferation/growth, abnormal signaling/response to signals and aberrant cell identity / function.

The investigation of cellular alterations that promote leukemogenesis can now be assessed at single-cell resolution, which was a significant focus of my postdoctoral training. This novel perspective gives us new insight into the unique and sequential steps a cell (or clone) undergoes during transformation. Using single-cell multi-omic patient data and new mouse models we have developed, we can recapitulate the clonal evolution of acute myeloid leukemia. My group aims to answer important questions in cancer biology, such as:

  • How does the precise, stepwise acquisition of somatic mutations alter the cellular traits of the antecedent clone?
  • What cellular traits / alterations imparted by a somatic mutation are absolutely necessary for continued disease maintenance?
  • Are there clone-specific vulnerabilities based on the genotype of the clone and stage of clonal evolution?

My research examines and models clonal evolutionary trajectories during leukemogenesis using single-cell profiling of clinical isolates and deterministic pre-clinical models. The foundation of my research relies on the intersection of single cell multi-omic patient data and the development of mouse models capable of selectively activating individual alleles (or more than one allele) through the use of orthogonal deoxyribonucleic acid (DNA) recombinases. These mouse models will serve as a platform to probe the effects of genetic and chemical perturbation to identify clone-specific vulnerabilities that can be exploited for new therapeutic strategies.

Some of my groundbreaking work includes identifying the cellular receptor, ANTXR1, for an oncolytic virus (Seneca Valley Virus) being investigated for therapeutic use in small cell lung cancer (2017). I was also the lead co-author on one of the first large cohort single-cell DNA sequencing studies interrogating the clonal diversity and architecture of myeloid malignancies in human samples published in Nature (2020).

I’m honored to be the recipient of a National Cancer Institute (NCI) K99/R00 Pathway to Independence Award (2021), a Leukemia and Lymphoma Society (LLS) Career Development Achievement Award (2021), an LLS Fellow Award (2018) and an American Association for Cancer Research (AACR) Women in Cancer Research Scholar award (2016). I have more than 14 years of research experience, and I began my work at Cincinnati Children’s in 2022.

Please note that we are recruiting! Interested graduate students and postdoctoral fellows should apply at