A native of Texas, Jonathan attended the University of North Texas in his hometown of Denton. After obtaining a double major in chemistry and biochemistry, he moved to the west Texas town of El Paso to attend the Paul L. Foster School of Medicine. Here is where he developed a deep interest in neuroendocrine disorders, in particular pituitary adenomas. He is currently an anatomic pathology resident at Stanford University and will begin his neuropathology fellowship starting in July of 2017.

Clinical Focus

  • Neuropathology
  • Pituitary Pathology
  • Head and Neck/Endocrine Pathology
  • Autopsy
  • Fellow

Honors & Awards

  • Department of Pathology’s Trainee Mentored Award in Precision Health, Stanford Medicine ((April 2017))


All Publications

  • Validation and Clinical Use of Whole Slide Digital Imaging at Stanford Neuropathology Lavezo, J., Born, D., Lummus, S., Young, A., Montine, T., Vogel, H. OXFORD UNIV PRESS INC. 2019: 576
  • Neuropathologic Findings in a Patient with CAR T-Cell-Associated Inflammatory Cytokine Release Syndrome Lavezo, J., Mount, C., Monje, M., Miklos, D., Vogel, H. OXFORD UNIV PRESS INC. 2019: 575
  • Macrophage Exclusion after Radiation Therapy (MERT): A First in Human Phase I/II Trial using a CXCR4 Inhibitor in Glioblastoma. Clinical cancer research : an official journal of the American Association for Cancer Research Thomas, R. P., Nagpal, S., Iv, M., Soltys, S. G., Bertrand, S., Pelpola, J. S., Ball, R. L., Yang, J., Sundaram, V., Lavezo, J. L., Born, D. E., Vogel, H., Brown, J. M., Recht, L. 2019


    Preclinical studies have demonstrated that post-irradiation tumor revascularization is dependent on a stromal cell-derived factor-1 (SDF-1)/C-X-C chemokine receptor type 4 (CXCR4)-driven process in which myeloid cells are recruited from bone marrow. Blocking this axis results in survival improvement in preclinical models of solid tumors, including glioblastoma (GBM). We conducted a phase I/II study to determine the safety and efficacy of Macrophage Exclusion after Radiation Therapy (MERT) using the reversible CXCR4 inhibitor plerixafor in newly diagnosed glioblastoma patients.We enrolled 9 patients to the phase I study and an additional 20 patients to phase II using a modified toxicity probability interval (mTPI) design. Plerixafor was continuously infused intravenously via PICC line for four consecutive weeks beginning at day 35 of conventional treatment with concurrent chemo-radiation. Blood serum samples were obtained for pharmacokinetic analysis. Additional studies included relative cerebral blood volume (rCBV) analysis using MRI and histopathology analysis of recurrent tumors.Plerixafor was well tolerated with no drug-attributable grade 3 toxicities observed. At the maximum dose of 400 µg/kg/day, biomarker analysis found suprathreshold plerixafor serum levels and an increase in plasma SDF-1 levels. Median overall survival was 21.3 months (95% Confidence Interval (CI) 15.9, NA) with a progression-free survival of 14.5 months (95% CI 11.8, NA). MRI and histopathology support the mechanism of action to inhibit post-irradiation tumor revascularization.Infusion of the CXCR4 inhibitor plerixafor was well tolerated as an adjunct to standard chemo-irradiation in newly diagnosed GBM patients and improves local control of tumor recurrences.

    View details for DOI 10.1158/1078-0432.CCR-19-1421

    View details for PubMedID 31537527

  • Clinical and Immunohistochemical Analysis of Clinically Non-functional Pituitary Neuroendocrine Tumors Lavezo, J., Frankel, M., Balliu, B., Pan, J., Hoffman, A., Dodd, R., Harsh, G., Katznelson, L., Vogel, H. OXFORD UNIV PRESS INC. 2018: 518
  • Utility of Pit-1 Immunostaining in Distinguishing Pituitary Adenomas of Primitive Differentiation from Null Cell Adenomas ENDOCRINE PATHOLOGY Lee, J. C., Pekmezci, M., Lavezo, J. L., Vogel, H., Katznelson, L., Fraenkel, M., Harsh, G., Dulai, M., Perry, A., Tihan, T. 2017; 28 (4): 287–92


    Pit-1 immunostaining is not routinely used in the characterization of pituitary adenomas, and its utility in distinguishing adenomas dedicated towards the lactotroph, somatotroph, and thyrotroph lineage from null cell adenomas warrants further evaluation. Pituitary adenomas that were negative for expression of a basic panel of hormonal markers (ACTH, prolactin, and growth hormone) were further evaluated for TSH, SF-1, and Pit-1 expression using a tissue microarray. Among the 147 identified pituitary adenomas that were negative for ACTH, prolactin, growth hormone, and TSH, expression of SF-1 was present in 68 cases (46%). Of the remaining 72 cases with sufficient tissue for further analysis, four were Pit-1 positive (6% of the adenomas negative for ACTH, prolactin, growth hormone, TSH, and SF-1); the remaining 68 were potentially null cell adenomas. Two of the Pit-1-positive adenomas displayed a paranuclear CAM 5.2 staining pattern suggestive of a sparsely granulated somatotroph adenoma; however, only one case contained fibrous bodies within a majority of the adenoma cells. Our data suggests that Pit-1 can be utilized as a second tier immunostain in cases of clinically non-functioning adenomas that are immunonegative for ACTH, prolactin, growth hormone, TSH, and SF-1 in order to further segregate rare cases of Pit-1-positive adenomas from null cell adenomas. Pit-1 immunostaining can recognize rare cases of sparsely granulated somatotroph adenomas that appear immunonegative for growth hormone, as well as rare cases of other Pit-1-positive adenomas that are negative for Pit-1 lineage hormones. Overall, pituitary adenomas of the Pit-1 lineage that do not produce prolactin, growth hormone, or TSH are rare, with only four cases identified in the current study.

    View details for PubMedID 28994039

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