Clinical Focus

  • Anatomic/Clinical Pathology
  • Hematopathology
  • Diagnostic Flow Cytometry

Academic Appointments

Administrative Appointments

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


2015-16 Courses


All Publications

  • Cell Signaling-Based Classifier Predicts Response to Induction Therapy in Elderly Patients with Acute Myeloid Leukemia PLOS ONE Cesano, A., Willman, C. L., Kopecky, K. J., Gayko, U., Putta, S., Louie, B., Wesdall, M., Purvis, N., Spellmeyer, D. C., Marimpietri, C., Cohen, A. C., Hackett, J., Shi, J., Walker, M. G., Sun, Z., Paietta, E., Tallman, M. S., Cripe, L. D., Atwater, S., Appelbaum, F. R., Radich, J. P. 2015; 10 (4)
  • Indolent T-lymphoblastic Proliferation With Disseminated Multinodal Involvement and Partial CD33 Expression AMERICAN JOURNAL OF SURGICAL PATHOLOGY Ohgami, R. S., Sendamarai, A. K., Atwater, S. K., Liedtke, M., Fleming, M. D., Natkunam, Y., Warnke, R. A. 2014; 38 (9): 1298-1304


    Although indolent T-lymphoblastic proliferations (iT-LBP) are rare, this diagnosis should be excluded in any patient with an extrathymic proliferation of immature TdT+T cells. Unlike T-lymphoblastic leukemia/lymphoma, patients with iT-LBP do not require chemotherapy. We report a case of iT-LBP with disseminated multinodal involvement in an otherwise healthy 49-year-old woman. Multiple lymph node biopsies were performed over the course of several months demonstrating persistent and anatomically diffuse involvement. Over 18 months, and without therapy, she has remained healthy, and her lymphadenopathy significantly improved. No bone marrow or peripheral blood involvement was ever identified. Atypical T cells showed an immunophenotypic spectrum of T-cell antigen expression with partial CD33 on a subset of T cells detected by both flow cytometry and immunohistochemistry. Both T-cell clonality and Human Androgen Receptor Assay (HUMARA) studies, performed on lymph node biopsy specimens, were negative. This case represents the first detailed clinical, morphologic, molecular, and immunophenotypic description of disseminated multinodal involvement by nonclonal iT-LBP with partial CD33 expression on T cells.

    View details for Web of Science ID 000341096800017

    View details for PubMedID 24618611

  • Expression of the Activating Receptor, NKp46 (CD335), in Human Natural Killer and T-Cell Neoplasia. American journal of clinical pathology Freud, A. G., Zhao, S., Wei, S., Gitana, G. M., Molina-Kirsch, H. F., Atwater, S. K., Natkunam, Y. 2013; 140 (6): 853-866


    Objectives To evaluate the expression of CD335 (NKp46), an activation receptor that is selectively expressed on natural killer (NK) cells. Methods We assessed CD335's potential utility as a diagnostic marker in 657 cases by flow cytometry and 410 cases by immunohistochemistry. Results We observed that CD335 was highly specific for NK cells in nonneoplastic tissues. Moreover, 61 (90%) of 68 of NK cell neoplasms demonstrated CD335 expression, whereas B-cell, myelomonocytic, and plasma cell neoplasms lacked expression. Notably, 16 (20%) of 82 mature T-cell neoplasms, particularly T-cell large granular lymphocytic leukemia, mycosis fungoides, and ALK+ anaplastic large cell lymphoma, aberrantly expressed CD335. Conclusions Collectively, these data support the diagnostic utility of CD335 in evaluating hematopoietic malignancies and suggest that CD335 could be a useful target for selective immunotherapy in patients with mature NK and T-cell neoplasms.

    View details for DOI 10.1309/AJCPWGG69MCZOWMM

    View details for PubMedID 24225754

  • 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


    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


    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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