Graduate Studies Faculty

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Anupriya Agarwal, Ph.D.

Assistant Professor
Admin Unit: SOM-DOM Hematology & Medical Oncology
Phone: 503-494-7599
Lab Phone: 503-494-3431
Fax: 503-494-3688
Office: BRB517
Mail Code: L592
Programs:
Molecular & Medical Genetics
Program in Molecular & Cellular Biosciences
Cancer Biology
Research Interests:
Hematopoietic Malignancies, AML, ALL, CML, Kinases and nonkinase cytokine receptors, Novel genetic modalities and therapeutic targets, Bone Marrow Microenvironment, Inflammation and Immunity, Hematopoietic and Leukemic Stem Cells » Click here for more about Dr. Agarwal's research » PubMed Listing
Preceptor Rotations
Academic Term Available Fall 2016 Yes Winter 2016 Yes Spring 2016 Yes Summer 2017 Yes Fall 2017 Yes Winter 2017 Yes Spring 2017 Yes
Faculty Mentorship
Dr. Agarwal is available as a mentor for 2016-2017. Dr. Agarwal is available as a mentor for 2017-2018.
Profile

The focus of our laboratory is to identify novel inter- and intracellular signaling pathways that are requisite for disease progression, clonal evolution, and drug resistance in pediatric and adult leukemias. Specifically, my lab is interested in understanding the composite interplay of genetic events and the microenvironment, including cytokine/growth factor signaling pathways, in promoting the growth of leukemia cells and conferring drug resistance. To efficiently characterize these signaling mechanisms and potential drug targets, we have developed several functional screening assays which we employ in tandem with genomic and proteomic approaches. Our group utilizes various state-of-art techniques as well as in vitro and in vivo models to dissect the molecular mechanism, functional role and therapeutic relevance of identified pathways. Our goal is to use this knowledge to improve the understanding of leukemia pathobiology and develop novel, molecularly targeted therapeutic strategies for leukemia patients.
 
Currently we have three main overarching research goals:
 
1) Identify novel intrinsic genetic modalities and therapeutic targets. Mutations and posttranscriptional/posttranslational modifications in kinases, non-kinase receptors, ligands, and phosphatases contribute to leukemogenesis. Our group is implementing cutting-edge methods and technologies to rapidly identify these molecular mechanisms. In addition, we perform functional dissection of identified pathways using primary patient cells and in vivo mouse models to propose novel targeted therapies.
 
2) Identify extrinsic mechanisms that contribute to hematopoiesis of normal and malignant stem cells. We believe that the complex signaling milieu of the bone marrow microenvironment creates a selective pressure to promote clonal growth of leukemia cells. Consistent with this, we and others have identified several proinflammatory cytokines that, while suppressing the growth of normal cells, have a paradoxical effect on clonalgrowth of leukemia cells. We are performing omics-based analyses to determine the effect of microenvironment-driven stimuli on hematopoiesis, growth, differentiation, and methylation of normal and malignant stem cells. This comprehensive approach will allow us to gain insight into the signaling mechanisms that contribute to clonal growth and drug resistance of leukemic stem cells, enabling design of therapeutic strategies to target malignant cells specifically.
 
3) Determine the mechanisms of molecular conduit between the bone marrow/immune microenvironment and leukemic cells in conferring drug resistance. It is likely that not only the bone marrow microenvironment but also leukemia cells reprogram their niche. For instance, treatment with cytotoxic therapy promotes the release of signaling mediators from leukemic cells that recruit immune cell responses from the microenvironment to blunt malignant cell killing. We propose that delineating these mechanisms will establish a novel paradigm for designing therapeutic strategies for targeting aberrant immune responses in leukemia.