Photo of Anupriya Agarwal, Ph.D.

Anupriya Agarwal Ph.D.

  • (503) 494-7599
    • Assistant Professor of Medicine School of Medicine
    • Molecular and Medical Genetics Graduate Program School of Medicine
    • Cancer Biology Graduate Program School of Medicine
    • Program in Molecular and Cellular Biosciences School of Medicine

Our overarching goal is to identify novel drivers of disease initiation, progression, and drug resistance in leukemia and to ultimately translate these discoveries into treatments for leukemia patients. Specifically, our lab is interested in understanding the composite interplay of genetic events and the tumor microenvironment that are requisite for promoting the growth of leukemia cells and conferring drug resistance. To achieve these goals, we have developed various functional assays which we employ in tandem with genomic and proteomic approaches. We take a multidisciplinary approach and utilize various state-of-art techniques to dissect the functional role and therapeutic relevance of identified pathways. Our goal is to use this knowledge to improve the understanding of disease pathobiology and inform the development of novel, molecularly targeted therapies for patients.


  • B.S., C. C. S. University, Meerut India 1996
  • M.S., G.B. Pant University, Pantnagar India 1998
  • Ph.D., Dr. R.M.L. Avadh University, Faizabad India 2003

Memberships and associations

  • American Society of Hematology


  • "Rare but recurrent ROS1 fusions resulting from chromosome 6q22 microdeletions are targetable oncogenes in glioma." Clinical Cancer Research  In: , Vol. 24, No. 24, 15.12.2018, p. 6471-6482.
  • "Functional genomic landscape of acute myeloid leukaemia." Nature  In: , Vol. 562, No. 7728, 25.10.2018, p. 526-531.
  • "Inhibition of interleukin-1 receptor-associated kinase 1 (IRAK1) as a therapeutic strategy." Oncotarget  In: , Vol. 9, No. 70, 01.09.2018, p. 33416-33439.
  • "Targeting of colony-stimulating factor 1 receptor (CSF1R) in the CLL microenvironment yields antineoplastic activity in primary patient samples." Oncotarget  In: , Vol. 9, No. 37, 15.05.2018, p. 24576-24589.
  • "Inhibition of interleukin-1 receptor-associated kinase-1 is a therapeutic strategy for acute myeloid leukemia subtypes." Leukemia  In: , 29.03.2018, p. 1-14.
  • "The tumor suppressor phosphatase PP2A-B56α regulates stemness and promotes the initiation of malignancies in a novel murine model." PLoS One  In: , Vol. 12, No. 11, e0188910, 01.11.2017.
  • "Identification of Interleukin-1 by Functional Screening as a Key Mediator of Cellular Expansion and Disease Progression in Acute Myeloid Leukemia." Cell Reports  In: , Vol. 18, No. 13, 28.03.2017, p. 3204-3218.
  • "Analysis of acquired mutations in transgenes arising in Ba/F3 transformation assays : Findings and recommendations." Oncotarget  In: , Vol. 8, No. 8, 2017, p. 12596-12606.
  • "Novel Method Enabling the Use of Cryopreserved Primary Acute Myeloid Leukemia Cells in Functional Drug Screens." Journal of Pediatric Hematology/Oncology  In: , Vol. 39, No. 7, 2017, p. e359-e366.
  • "FGF2 from marrow microenvironment promotes resistance to FLT3 inhibitors in acute myeloid leukemia." Cancer Research  In: , Vol. 76, No. 22, 15.11.2016, p. 6471-6482.
  • "Discovery and functional characterization of a germline, CSF2RB-activating mutation in leukemia." Leukemia  In: , Vol. 30, No. 9, 01.09.2016, p. 1950-1953.
  • "Ultrasensitive proteomic quantitation of cellular signaling by digitized nanoparticle-protein counting." Scientific Reports  In: , Vol. 6, 28163, 20.06.2016.
  • "Alterations in acute myeloid leukaemia bone marrow stromal cell exosome content coincide with gains in tyrosine kinase inhibitor resistance." British Journal of Haematology  In: , Vol. 172, No. 6, 01.03.2016, p. 983-986.
  • "Cytokine overproduction and crosslinker hypersensitivity are unlinked in Fanconi anemia macrophages." Journal of Leukocyte Biology  In: , Vol. 99, No. 3, 01.03.2016, p. 455-465.
  • "Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism." American Journal of Hematology  In: , Vol. 91, No. 2, 01.02.2016, p. 211-219.
  • "JAK2 results in cytokine hypersensitivity without causing an overt myeloproliferative disorder in a mouse transduction-transplantation model." Experimental Hematology  In: , Vol. 44, No. 1, 01.01.2016, p. 24-29.e1.
  • "RNAi screening of leukemia cells using electroporation."   Methods in Molecular Biology. Vol. 1470 Humana Press Inc., 2016. p. 85-94 (Methods in Molecular Biology; Vol. 1470).
  • "Combined targeting of SET and tyrosine kinases provides an effective therapeutic approach in human T-cell acute lymphoblastic leukemia." Oncotarget  In: , Vol. 7, No. 51, 2016, p. 84214-84227.
  • "Functional RNAi screen targeting cytokine and growth factor receptors reveals oncorequisite role for interleukin-2 gamma receptor in JAK3-mutation-positive leukemia." Oncogene  In: , Vol. 34, No. 23, 04.06.2015, p. 2991-2999.
  • "Molecular biology of chronic leukemias."   Cancer: Principles & Practice of Oncology: Primer of the Molecular Biology of Cancer: Second Edition. Wolters Kluwer Health, 2015.
  • "Molecular biology of chronic leukemias."   DeVita, Hellman, and Rosenberg's Cancer: Principles & Practice of Oncology: Tenth Edition. Wolters Kluwer Health Adis (ESP), 2015.
  • "Acute promyelocytic leukemia with JAK2 V617F and severe differentiation syndrome." Leukemia Research Reports  In: , Vol. 4, No. 1, 01.01.2015, p. 8-11.
  • "BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein." Blood  In: , Vol. 124, No. 22, 20.11.2014, p. 3260-3273.
  • "Muscle atrophy in response to cytotoxic chemotherapy is dependent on intact glucocorticoid signaling in skeletal muscle." PLoS One  In: , Vol. 9, No. 9, e106489, 25.09.2014.
  • "Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia." Clinical Cancer Research  In: , Vol. 20, No. 8, 15.04.2014, p. 2092-2103.
  • "Ponatinib overcomes FGF2-mediated resistance in CML patients without kinase domain mutations." Blood  In: , Vol. 123, No. 10, 06.03.2014, p. 1516-1524.
  • "Foretinib is a potent inhibitor of oncogenic ROS1 fusion proteins." Proceedings of the National Academy of Sciences of the United States of America  In: , Vol. 110, No. 48, 26.11.2013, p. 19519-19524.
  • "The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in Mice that is responsive to therapeutic JAK inhibition." Blood  In: , Vol. 122, No. 22, 21.11.2013, p. 3628-3631.
  • "Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis." Cancer Research  In: , Vol. 73, No. 11, 01.06.2013, p. 3356-3370.
  • "Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML." New England Journal of Medicine  In: , Vol. 368, No. 19, 2013, p. 1781-1790.

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