Bio

Clinical Focus


  • Diagnostic Flow Cytometry
  • Anatomic/Clinical Pathology
  • Hematopathology

Academic Appointments


Administrative Appointments


  • Co-Director, Flow Cytometry, Stanford Hospital Clinical Lab (2005 - Present)
  • Medical Director, Point-of-Care Testing license, Stanford Medical Outpatient Center (2008 - Present)

Honors & Awards


  • Senior CP Faculty Teaching Award, Stanford Pathology residents (2009)

Professional Education


  • Residency:Duke University Medical Center (1990) NC
  • Board Certification: Anatomic/Clinical Pathology, American Board of Pathology (1991)
  • Board Certification: Hematology, American Board of Pathology (1999)
  • Fellowship:University of North Carolina Hospital (1991) NC
  • Internship:Duke University Medical Center (1986) NC
  • Medical Education:Duke University School of Medicine (1985) NC
  • B.S., Duke University, Zoology (1981)
  • M.D., Duke University, School of Medicine (1985)

Research & Scholarship

Current Research and Scholarly Interests


I am interested in optimizing the process of diagnosing leukemias, lymphomas and other hematolymphoid neoplasms, particularly by the use of diagnostic flow cytometry. One goal is to develop flow data analysis processes that function as interactive tools, allowing pathologists to query rich diagnostic data sets in real time.

Teaching

2013-14 Courses


Publications

Journal Articles


  • The PEBP2 beta MYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Kogan, S. C., Lagasse, E., Atwater, S., Bae, S. C., Weissman, I., Ito, Y., BISHOP, J. M. 1998; 95 (20): 11863-11868

    Abstract

    Chromosomal translocations involving the genes encoding the alpha and beta subunits of the Pebp2/Cbf transcription factor have been associated with human acute myeloid leukemia and the preleukemic condition, myelodysplasia. Inv(16)(p13;q22) fuses the gene encoding the beta subunit of Pebp2 to the MYH11 gene encoding a smooth muscle myosin heavy chain (Smmhc). To examine the effect of the inv(16)(p13;q22) on myelopoiesis, we used the hMRP8 promoter element to generate transgenic mice expressing the Pebp2betaSmmhc chimeric fusion protein in myeloid cells. Neutrophil maturation was impaired in PEBP2betaMYH11 transgenic mice. Although the transgenic mice had normal numbers of circulating neutrophils, their bone marrow contained increased numbers of immature neutrophilic cells, which exhibited abnormal characteristics. In addition, PEBP2betaMYH11 inhibited neutrophilic differentiation in colonies derived from hematopoietic progenitors. Coexpression of both PEBP2betaMYH11 and activated NRAS induced a more severe phenotype characterized by abnormal nuclear morphology indicative of granulocytic dysplasia. These results show that PEBP2betaMYH11 can impair neutrophil development and provide evidence that alterations of Pebp2 can contribute to the genesis of myelodysplasia.

    View details for Web of Science ID 000076222200065

    View details for PubMedID 9751756

  • A PMLRAR alpha transgene initiates murine acute promyelocytic leukemia PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Brown, D., Kogan, S., Lagasse, E., Weissman, I., Alcalay, M., Pelicci, P. G., Atwater, S., BISHOP, J. M. 1997; 94 (6): 2551-2556

    Abstract

    The malignant cells of acute promyelocytic leukemia (APL) contain a reciprocal chromosomal translocation that fuses the promyelocytic leukemia gene (PML) with the retinoic acid receptor alpha gene (RAR alpha). To test the hypothesis that the chimera PMLRAR alpha plays a role in leukemogenesis, we expressed a PMLRAR alpha cDNA in myeloid cells of transgenic mice. PMLRAR alpha transgenic mice exhibited impaired neutrophil maturation early in life, which progressed at a low frequency over the course of several months to overt APL. Both the preleukemic state and the leukemia could be transplanted to nontransgenic mice, and the transplanted preleukemia could progress to APL. The APL recapitulated features of the human disease, including a response to retinoic acid. Retinoic acid caused the leukemic cells to differentiate in vitro and in vivo, eliciting remissions of both the preleukemic state and APL in mice. Our results demonstrate that PMLRAR alpha impairs neutrophil differentiation and initiates the development of APL. The transgenic mice described here provide an apparently accurate model for human APL that includes clear evidence of tumor progression. The model should be useful for exploring the molecular pathogenesis of APL and the mechanisms of the therapeutic response to retinoic acid, as well as for preclinical studies of therapeutic regimens.

    View details for Web of Science ID A1997WP33400084

    View details for PubMedID 9122233

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