Stephen Oh, M.D., Ph.D.

Assistant Professor
Internal Medicine
Hematology

Molecular Cell Biology Program
Molecular Genetics and Genomics Program
Immunology Program

  • (314) 362-8846

  • (314) 362-8819

  • (314) 362-8826

  • 8125

  • CSRB 8836

  • stoh@dom.wustl.edu

  • http://hematology.wustl.edu/people/faculty/Oh/Oh_Bio.html

  • @mpndoc

  • cancer biology, mass cytometry, CyTOF, signal transduction, JAK2, genomics, leukemia, hematopoiesis, stem cells

  • Mechanisms of dysregulated signaling in blood cancers

Research Abstract:

Our laboratory is interested in the basic mechanisms that drive the initiation, development, and progression of hematologic malignancies. Myeloproliferative neoplasms (MPNs) are clonal disorders typified by genetic alterations that activate JAK-STAT signaling. Our research relies on primary patient samples as well as mouse genetic models to study MPN pathogenesis. A major focus of the laboratory is to utilize innovative single cell methods (e.g. mass cytometry) to interrogate dysregulated signaling in MPNs. A second area of interest is the application of next-generation sequencing technologies to delineate genetic complexity and clonal evolution in MPNs. We also utilize functional genomics approaches (iPSCs, CRISPR) to model human MPN pathogenesis. The long-term objective is to integrate these approaches so that phenotype can be connected to underlying genotype. Ultimately, we seek to translate this work into improved therapies for MPN patients.

For more information please go to the: Oh Lab website

Selected Publications:

Bandyopadhyay S, Fisher DA, Malkova O, Oh ST. Analysis of Signaling Networks at the Single Cell Level Using Mass Cytometry. In Methods in Molecular Biology – Kinase Signaling Networks. Edited by Huang P, Tan, A-C. In press.

Zhou AW, Knoche EM, Engle EK, Ban-Hoefen M, Kaiwar C, Oh ST. Clinical Improvement with JAK2 Inhibition in Chuvash Polycythemia. N Engl J Med. 2016 Aug 4;375(5):494-6.

Rashidi A, Heusel JW, Oh ST. Concurrent MPL W515L and Y591D mutations in a patient with myelofibrosis. Blood Cells, Molecules, and Diseases. 2016 Sep (60): 1-2.

Zhou A, Knoche EM, Engle EK, Fisher DA, Oh ST. Concomitant JAK2 V617F-Positive Polycythemia Vera and BCR-ABL-Positive Chronic Myelogenous Leukemia Treated with Ruxolitinib and Dasatinib. Blood Cancer Journal.
2015 Oct 2;5:e351.

Engle EK, Fisher DA, Miller CA, McLellan MD, Fulton RS, Moore DM, Wilson RK, Ley TJ, Oh ST. Clonal evolution revealed by whole genome sequencing in a case of primary myelofibrosis transformed to secondary acute myeloid leukemia. Leukemia 2015 Apr;29(4):869-76.

Prognostication in MF: From CBC to Cytogenetics to Molecular Markers.
Zhou A, Oh ST.
Best Pract Res Clin Haematol. 2014. Epub 2014 Jul 18.

Disseminated tuberculosis associated with ruxolitinib
Hopman RK, Lawrence SJ, Oh ST
Leukemia 2014 Aug;28(8):1750-1

Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML
Maxson JE, Gotlib J, Pollyea DA, Fleischman AG, Agarwal A, Eide CA, Bottomly D, Wilmot B, McWeeney SK,
Tognon CE, Pond JB, Collins RH, Goueli B, Oh ST, Deininger MW, Chang BH, Loriaux MM, Druker BJ, Tyner JW
N Engl J Med 2013 May 9;368(19):1781-90

Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening
Tyner JW, Yang WF, Bankhead A 3rd, Fan G, Fletcher LB, Bryant J, Glover JM, Chang BH, Spurgeon SE, Fleming WH, Kovacsovics T, Gotlib JR, Oh ST, Deininger MW, Zwaan CM, Den Boer ML, van den Heuvel-Eibrink MM, O`Hare T, Druker BJ, Loriaux MM
Cancer Res 2013 Jan 1;73(1):285-296

Pathology consultation on myeloproliferative neoplasms
Schmidt AE, Oh ST
Am J Clin Pathol 2012 Jul;138(1):12-19

A novel splice donor mutation in the thrombopoietin gene leads to exon 2 skipping in a Filipino family with hereditary thrombocythemia
Zhang B, Ng D, Jones C, Oh ST, Nolan GP, Salehi S, Wong W, Zehnder JL, Gotlib J
Blood 2011 Dec 22;118(26):6988-90

When the brakes are lost: LNK dysfunction in mice, men, and myeloproliferative neoplasms
Oh ST
Therapeutic Advances in Hematology 2011;2:11-19

LNK mutation studies in blast-phase myeloproliferative neoplasms, and in chronic-phase disease with TET2, IDH, JAK2 or MPL mutations
Pardanani A, Lasho T, Finke C, Oh ST, Gotlib J, Tefferi A
Leukemia 2010 Oct;24(10):1713-8

Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms
Oh ST, Simonds EF, Jones C, Hale MB, Goltsev Y, Gibbs KD Jr, Merker JD, Zehnder JL, Nolan GP, Gotlib J
Blood 2010 Aug 12;116(6):988-92

JAK2 V617F and beyond: role of genetics and aberrant signaling in the pathogenesis of myeloproliferative neoplasms
Oh ST, Gotlib J
Expert Rev Hematol 2010 Jun;3(3):323-37

Design and evaluation of a real-time PCR assay for quantification of JAK2 V617F and wild-type JAK2 transcript levels in the clinical laboratory
Merker JD, Jones CD, Oh ST, Schrijver I, Gotlib J, Zehnder JL
J Mol Diagn 2010 Jan;12(1):58-64

Last Updated: 9/6/2016 9:33:04 AM

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