Dr. Jordan has participated in numerous NIH/NCI grant review panels, and has published over 125 peer-reviewed original research articles, review articles and book chapters. His 2018 study, "Subversion of Systemic Glucose Metabolism as a Mechanism to Support the Growth of Leukemia Cells" was named as one of the "Best of Cancer Cell 2018"
I am an instructor conducting basic science research in our laboratory. My research is focused on investigating new ways to target leukemic stem cells in order to improve outcomes in AML. In particular, I am investigating proteins that affect mitochondrial function and oxidative phosphorylation, as leukemic stem cells rely heavily on this for survival.
My research is focused on understanding the biology of leukemia stem cells, the root cause of relapse and chemo-resistance in AML. Previous work in the lab suggests leukemia stem cells have unique metabolic properties that can be exploited in the clinic. I am interested in studying the intersection of canonical signaling pathways such as apoptosis and mitochondrial dynamics with metabolism in AML patient samples. As an MD/PhD student, I hope to leverage my clinical experience in heme/onc to more effectively bridge the gap between the clinic and the laboratory bench.
The main focus of my work is the identification and characterization of molecular pathways that control the survival of human leukemia stem cells. Drawing on many years of experience as a molecular biologist, I have developed methods to target pathways in primary human Leukemia Stem Cell (LSC) populations.
Of particular interest are mechanisms controlling energy metabolism and oxidative states, as these key properties are central to the biology of both normal and malignant hematopoietic stem cells. Recent data indicate that LSCs uniquely regulate energy metabolism and that therapeutic strategies may be evolved to target such properties.
As a trained immunologist, my main research interest is to investigate the interplay between AML progression and its immunological environment. Immune system plays an important role in regulating disease progression, any alteration in a balanced immune response could result in detrimental consequences. Leukemia cells are known to be able to manipulate their immune microenvironment to improve their survivability. Hence, understanding more about the relationship between AML and the host immune system should advance our knowledge of therapy resistance and relapse rate in AML patients, which will shed light on novel therapy development.
I am a Pediatric Oncologist at Children’s Hospital Colorado and am junior faculty in the Jordan lab. My project involves the characterization of chemo-resistant cell populations in acute myeloid leukemias (AML), with the ultimate goal of identifying effective targeted therapies for residual disease. An additional goal of my research is to develop more sensitive and specific assays for the detection of minimal residual disease (MRD) in patients with no clinically apparent disease.
Currently, I am working with adult and pediatric primary AML samples, which I am analyzing with mass cytometry and with targeted sequencing of a panel of AML-associated genes. Mass cytometry allows us to look at >20 cell surface markers and intracellular phosphorylated signaling proteins simultaneously, which in turn allows us to identify individual subpopulations within an AML sample and track their relative abundances during initial chemotherapy. We can then isolate the subpopulations which are most resistant to standard chemotherapies and can study their genetic mutational profiles and sensitivities to targeted drug therapies. We can also use the genotypic information to identify candidate mutations for MRD monitoring via droplet digital PCR, with the goal of detecting molecular evidence of disease at earlier timepoints prior to clinical relapse.
My research focused on the interaction between leukemia cells and their microenvironment, especially the ones created by the adipose tissue.
I am interested in how the microenvironment provided by the adipose tissue affects the metabolism and survival of leukemia cells and how leukemia cells change the biological behavior of the adipose tissue.