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.

Education

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

Memberships and associations

  • American Society of Hematology

Publications

  • "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.
  • "Effects of plerixafor in combination with BCR-ABL kinase inhibition in a murine model of CML." Blood In: , Vol. 120, No. 13, 27.09.2012, p. 2658-2668.
  • "MDS : Roadblock to differentiation." Blood  In: , Vol. 120, No. 10, 06.09.2012, p. 1968-1969.
  • "Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors." Leukemia In: , Vol. 26, No. 5, 05.2012, p. 1140-1143.
  • "CXCR4 antagonists for the treatment of CML."   Novel Developments in Stem Cell Mobilization: Focus on CXCR4. Springer US, 2012. p. 351-367.
  • "TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms." Blood In: , Vol. 118, No. 24, 08.12.2011, p. 6392-6398.
  • "The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia." Blood In: , Vol. 118, No. 19, 10.11.2011, p. 5250-5254.

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