Our laboratory is interested in understanding the interplay between genetic drivers and the factors in the tumor microenvironment so new therapeutic approaches can be uncovered for the treatment of leukemia patients.
|2012-2018||NIH/NCI K99/R00 award|
|2016||V Foundation V Scholar Award|
|2017||American Cancer Society Research Scholar Grant|
|2018||OHSU Knight Cancer Institute Pilot Project Award|
|OHSU CEDAR AML working group Research Project grant|
|NIH Build Exito Pilot Project Award|
|The Babich Family Foundation /Alex's Lemonade Stand Foundation|
Identify novel intrinsic genetic modalities and therapeutic targets.
Mutations and posttranscriptional/posttranslational modifications in kinases, non-kinase receptors, ligands, phosphatases, and cell cycle proteins 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.
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 at early leukemic stage to promote clonal growth of leukemia cells. Consistent with this, we and others have identified several proinflammatory cytokines that have a paradoxical effect on clonal growth of leukemia cells while suppressing the growth of healthy nonmalignant cells. Our results indicate that functional and molecular differences in IL-1β-regulated signaling exist between malignant and healthy non-malignant progenitors. We are performing omics-based analyses to identify the molecular signature that leads to microenvironment-driven functional differences in nonmalignant and malignant stem cells. This comprehensive approach will allow us to gain insight into the signaling mechanisms that contribute to clonal growth of leukemic stem cells, enabling design of therapeutic strategies to target malignant cells specifically.
Determine the mechanisms of molecular conduit between the 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 to target aberrant immune responses in leukemia.
Anupriya Agarwal, Ph.D.
Hematology & Medical Oncology
Molecular & Medical Genetics
Knight Cancer Institute
Education: M.S., Microbiology, G.B. Pant Univ., India
Ph.D., Microbiology, Dr. R.M.L. Avadh Univ. and ITRC institute, India
Research Assistant II
Education: B.A., Biology and Anthropology, Colby College
Education: M.S., Bioengineering, University of Missouri
Student Research Intern
Education: B.S., Biology/Chemistry (in progress), Portland State University
Senior Research Assistant
Student Research Intern
Education: B.S. (in progress), Portland State University
- Alyssa Carey, Research Assistant
- Megan Cleary, Sr. Research Assistant
- Swati Garg, Graduate Student, Summer Rotation
- Kristina Halvorson, Research Assistant
- Clayton Hudson, Graduate Student, Summer Rotation
- Bernadette Maertens, Murdock Scholar
- Alka Puri, Visiting Intern
- Rhese Thompson, Murdock Scholar