Bio


Dr. Joshua Menke completed his hematopathology fellowship at Stanford and cytopathology fellowship at University of California San Francisco (UCSF). His clinical and research interests lie at the intersection of hematopathology, cytopathology and advanced single cell and cell free diagnostic techniques. As Associate Director of the Flow Cytometry lab at Stanford, Dr. Menke will be developing new minimal residual disease assays and Dr. Menke is the receipient of the Paul E. Standjord Young Investigator Award from the Academy of Clinical Laboratory Scientists and Laurance J. Marton Award for Excellence in Research from UCSF for his translational work on CALR mutations at the UCSF Molecular Diagnostics Laboroatory. Currently, he is spearheading novel genomic and proteomic analytic techniques to study cytology samples obtained for lymphoma diagnostics, including sequencing cell-free tumor DNA from supernatant samples. Dr. Menke is a founding member of the Cytology-Hematopathology Interinstitution Collaboration (CHIC) that aims to study the performance of cytology samples in diagnosing lymphoma across large datasets from five academic institutions.

Clinical Focus


  • Anatomic and Clinical Pathology

Academic Appointments


  • Clinical Assistant Professor, Pathology

Administrative Appointments


  • Associate Director of Flow Cytometry Laboratory, Stanford (2020 - Present)

Professional Education


  • Board Certification: American Board of Pathology, Hematopathology (2018)
  • Board Certification: American Board of Pathology, Cytopathology (2018)
  • Fellowship: Stanford University Hemapathology Fellowship (2018) CA
  • Fellowship: UCSF Office of Graduate Medical Education (2017) CA
  • Board Certification: American Board of Pathology, Anatomic and Clinical Pathology (2015)
  • Residency: UCSF Pathology Residency Programs (2015) CA
  • Residency: Mayo Clinic Graduate Medical Education (2012) MN
  • Medical Education: Univeristy of Florida College of Medicine (2011) FL
  • Fellowship, Stanford University, Hematopatholoogy (2018)
  • Fellowship, University of California San Francisco, Cytopathology (2017)
  • Clinical Instructor, Johns Hopkins Hospital, Surgical Pathology (2016)
  • Residency, University of California San Francisco, Anatomic and Clinical Pathology (2015)
  • Residency, Mayo Clinic Graduate Medical Education, Anatomic and Clinical Pathology (2012)
  • MD, University of Florida College of Medicine (2011)

All Publications


  • Complexities in the diagnosis of large B-cell lymphomas, classic Hodgkin lymphomas and overlapping peripheral T-cell lymphomas simplified: An evidence-based guide. Annals of diagnostic pathology Wen, K. W., Fakhri, B., Menke, J., Ruiz-Cordero, R., Gill, R. M., Ohgami, R. S. 2020; 46: 151534

    Abstract

    The diagnosis of a large B-cell lymphoma and classic Hodgkin lymphoma (CHL) is often straightforward. However, in select circumstances, these simple diagnoses can be quite complex. In part, diagnostic difficulty may be due to uncertainty in the evaluation of morphologic and immunophenotypic features along a biologic continuum, or alternatively arise from uncertainty in predicting the behavior and outcomes of patients. Here, we systematically discuss and review areas of diagnostic difficulty in the diagnosis of large B-cell lymphomas (LBCL), classic Hodgkin lymphomas (CHL) and peripheral T-cell lymphomas (PTCL). We provide careful data-driven analyses and evidence-based approaches to help guide pathologists and clinicians. We discuss: 1) marginal zone lymphomas with increased large cells versus diffuse large B-cell lymphoma (DLBCL), 2) chronic lymphocytic leukemia with expanded proliferation centers versus diffuse large B-cell lymphoma (DLBCL), 3) chronic lymphocytic leukemia with Hodgkin/Reed-Sternberg-like cells versus CHL arising from chronic lymphocytic leukemia, 4) complex cases of follicular lymphoma versus DLBCL, 5) PTCL with large B-cell proliferations versus PTCL with LBCL, 6) PTCL with Hodgkin/Reed-Sternberg-like cells versus CHL, and finally 7) blastoid/pleomorphic mantle cell lymphoma versus DLBCL. Our evidence and data driven approach may serve as a useful diagnostic guide.

    View details for DOI 10.1016/j.anndiagpath.2020.151534

    View details for PubMedID 32473554

  • CD20-negative nodular lymphocyte-predominant Hodgkin lymphoma is enriched for variant patterns and shows aggressive clinical features Menke, J., Spinner, M., Shrestha, B., Advani, R., Natkunam, Y., Gratzinger, D. NATURE PUBLISHING GROUP. 2019
  • CD20-negative nodular lymphocyte-predominant Hodgkin lymphoma is enriched for variant patterns and shows aggressive clinical features Menke, J., Spinner, M., Shrestha, B., Advani, R., Natkunam, Y., Gratzinger, D. NATURE PUBLISHING GROUP. 2019
  • Histiocytic Sarcoma Associated With Follicular Lymphoma: Evidence for Dramatic Response With Rituximab and Bendamustine Alone and a Review of the Literature CLINICAL LYMPHOMA MYELOMA & LEUKEMIA Farris, M., Hughes, R. T., Lamar, Z., Soike, M. H., Menke, J. R., Ohgami, R. S., Winkfield, K. 2019; 19 (1): E1–E8
  • Histiocytic Sarcoma Associated With Follicular Lymphoma: Evidence for Dramatic Response With Rituximab and Bendamustine Alone and a Review of the Literature. Clinical lymphoma, myeloma & leukemia Farris, M., Hughes, R. T., Lamar, Z., Soike, M. H., Menke, J. R., Ohgami, R. S., Winkfield, K. 2018

    Abstract

    Histiocytic sarcoma (HS) is a rare aggressive malignancy with a dismal prognosis and no agreed-upon standard treatment. Classically, the diagnosis of HS has been difficult to confirm and has relied on inaccurate, crude techniques. Therapy often involves intensive chemotherapeutic regimens, surgery, and/or radiotherapy, which are poorly tolerated with variable response rates. Patients often die of diffusely metastatic disease. Modern diagnostic techniques are helping to slowly uncover more uniquely customized therapeutic approaches in this enigmatic disease. We present a review of the current literature regarding HS diagnosis, treatment, and outcomes. Additionally, we describe the first reported case of HS transdifferentiated from follicular lymphoma that had a dramatic and durable response to rituximab/bendamustine alone as initial treatment. Unlike traditional chemotherapy regimens, this treatment was well tolerated and had a good toxicity profile. The combination of rituximab and bendamustine warrants further investigation in the treatment of HS, especially those originating from prior follicular lymphoma. Modern immunohistochemical and molecular profiling techniques are beginning to reveal heterogeneity among HS tumors and potentially therapeutic targets.

    View details for PubMedID 30396823

  • Comparison of MYC Fluorescent In Situ Hybridization Testing of Diffuse Large B-cell Lymphomas in Fine Needle Aspiration and Surgical Specimens Menke, J., Gupta, S., Bangs, C. D., Kong, C., Natkunam, Y., Long, S., Gratzinger, D. NATURE PUBLISHING GROUP. 2018: 162
  • Comparison of MYC Fluorescent In Situ Hybridization Testing of Diffuse Large B-cell Lymphomas in Fine Needle Aspiration and Surgical Specimens Menke, J., Gupta, S., Bangs, C. D., Kong, C., Natkunam, Y., Long, S., Gratzinger, D. NATURE PUBLISHING GROUP. 2018: 162
  • Mantle cell lymphoma with a novel t(11;12)(q13;p11.2): a proposed alternative mechanism of CCND1 up-regulation. Human pathology Menke, J. R., Vasmatzis, G., Murphy, S., Yang, L., Menke, D. M., Tun, H. W., King, R. L., Smoley, S. A., Ketterling, R. P., Sukov, W. R. 2017; 64: 207–12

    Abstract

    Mantle cell lymphoma (MCL) is typically characterized by t(11;14), which places the IGH@ enhancer elements upstream of CCND1. This fusion results in up-regulation of CCND1 and consequently its protein product cyclin D1. Recent studies have shown that in MCL, mutations or translocations occurring within the 3' untranslated region (UTR) of the CCND1 gene can result in a truncated mRNA transcript that is more stable and associated with more aggressive disease. We identified a case of MCL showing cyclin D1 overexpression by immunohistochemistry and a t(11;12)(q13;p11.2) by conventional cytogenetic studies. Next-generation genomic sequencing indicated a chromosomal break through the CCND1 3'-UTR and fusion with a non-coding region of chromosome 12. We suggest that, in the absence of the typical CCND1/IGH@ fusion, this rearrangement promotes MCL pathogenesis by eliminating miRNA interaction elements within the 3'-UTR of the CCND1 mRNA transcript consequently resulting in CCND1 overexpression.

    View details for DOI 10.1016/j.humpath.2017.01.001

    View details for PubMedID 28132860

  • Prostate-Specific Membrane Antigen-Targeted Imaging With [18F]DCFPyL in High-Grade Gliomas. Clinical nuclear medicine Salas Fragomeni, R. A., Menke, J. R., Holdhoff, M., Ferrigno, C., Laterra, J. J., Solnes, L. B., Javadi, M. S., Szabo, Z., Pomper, M. G., Rowe, S. P. 2017; 42 (10): e433–e435

    Abstract

    High-grade gliomas (World Health Organization grade III-IV) are highly lethal primary brain tumors. Imaging modalities, including MRI and FDG PET, provide a limited ability to differentiate treatment effects (such as radiation necrosis) from recurrent or residual tumor. As the first step in validating the applicability of prostate-specific membrane antigen (PSMA)-targeted imaging in high-grade gliomas, we evaluated the ability of the PSMA-targeted small molecule [F]DCFPyL (2-(3-(1carboxy-5-(6-[F]fluoro-pyridine-3-carbonyl)-amino]-pentyl)-ureido)-pentanedioic acid) to image high-grade gliomas in a series of 3 prospectively recruited patients. We found [F]DCFPyL binds PSMA in the neovasculature of glioblastoma multiforme and tumor cells of anaplastic astrocytoma.

    View details for DOI 10.1097/RLU.0000000000001769

    View details for PubMedID 28737579

    View details for PubMedCentralID PMC5802343

  • Somatostatin receptor 2a is a more sensitive diagnostic marker of meningioma than epithelial membrane antigen. Acta neuropathologica Menke, J. R., Raleigh, D. R., Gown, A. M., Thomas, S., Perry, A., Tihan, T. 2015; 130 (3): 441–43

    View details for DOI 10.1007/s00401-015-1459-3

    View details for PubMedID 26195322

  • Periventricular white matter immunoglobulin lambda light chain deposition disease diagnosed by proteomic analysis. Acta neuropathologica Menke, J. R., Jentoft, M. E., Dogan, A., Avent, J. M., Miller, D. V., Giannini, C. 2012; 124 (2): 293–95

    View details for DOI 10.1007/s00401-012-1008-2

    View details for PubMedID 22760528

  • TMEM106B risk variant is implicated in the pathologic presentation of Alzheimer disease. Neurology Rutherford, N. J., Carrasquillo, M. M., Li, M., Bisceglio, G., Menke, J., Josephs, K. A., Parisi, J. E., Petersen, R. C., Graff-Radford, N. R., Younkin, S. G., Dickson, D. W., Rademakers, R. 2012; 79 (7): 717–18

    View details for DOI 10.1212/WNL.0b013e318264e3ac

    View details for PubMedID 22855871

    View details for PubMedCentralID PMC3467659

  • Intravascular mucinosis: a rare cause of cerebral infarction. Acta neuropathologica Bernardo, M. C., Graff Radford, J., Menke, J., Hallemeier, C., Boes, C. J., Lewis, M., Scheithauer, B., Giannini, C. 2011; 121 (6): 785–88

    View details for DOI 10.1007/s00401-011-0829-8

    View details for PubMedID 21541761

  • Evidence that incidental Lewy body disease is pre-symptomatic Parkinson's disease. Acta neuropathologica Dickson, D. W., Fujishiro, H., DelleDonne, A., Menke, J., Ahmed, Z., Klos, K. J., Josephs, K. A., Frigerio, R., Burnett, M., Parisi, J. E., Ahlskog, J. E. 2008; 115 (4): 437–44

    Abstract

    Lewy bodies, the histologic hallmark of Parkinson's disease (PD), are detected in the brains of about 10% of clinically normal people over the age of 60 years. When Lewy bodies are found in normal individuals, the process is sometimes referred to as incidental Lewy body disease (iLBD). The distribution of Lewy bodies in iLBD is similar to the distribution in PD, but neuronal populations vulnerable to Lewy bodies do not show significant neuronal loss in iLBD. It remains unknown if Lewy bodies in this setting represent pre-symptomatic PD or an age-related change unrelated to PD. To address this question we identified cases of iLBD and used a marker for dopaminergic and noradrenergic neurons, tyrosine hydroxylase (TH), to determine if there were changes similar to those found in PD. TH immunoreactivity in the striatum and the epicardial nerve fibers was decreased in iLBD compared to normal controls, but not to the same extent as in PD. The findings suggest that iLBD is preclinical PD and that the lack of symptoms is due to subthreshold pathology.

    View details for DOI 10.1007/s00401-008-0345-7

    View details for PubMedID 18264713