David A Reardon

Stanford University, Palo Alto, California, United States

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Publications (255)1659.79 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: There are few effective treatments for recurrent glioblastoma multiforme (GBM). We present a patient with recurrent GBM who achieved a prolonged response to treatment with afatinib, an irreversible ErbB family blocker, plus temozolomide. A 58-year-old female patient was diagnosed with multifocal primary GBM. After surgical resection, first-line therapy comprised radiotherapy and temozolomide. Following disease progression after 3 temozolomide cycles, the patient entered a phase I/II clinical trial of afatinib (20-40 mg daily for 28 days) plus temozolomide (50 mg/m2 every 21/28 days). Next-generation sequencing analysis of the brain tumor specimen was performed. At the last assessment, 63 treatment cycles had been completed and the patient had survived for ~5 years since recurrence. Significant disease regression was observed after 5 cycles and was maintained during long-term follow-up. Adverse events were consistent with the known tolerability profile of afatinib and were managed by treatment interruption/dose reduction. The patient had several epidermal growth factor receptor (EGFR) aberrations, including gene amplification and EGFRvIII positivity. Three somatic mutations were identified, including an unprecedented extracellular-domain substitution (D247Y). The patient has survived ~6-fold longer than normally expected in patients with recurrent GBM. The complex EGFR genotype may underlie sustained response to afatinib plus temozolomide.
    Oncotarget 10/2015; · 6.36 Impact Factor
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    ABSTRACT: Background: Atypical teratoid/rhabdoid tumors (AT/RTs) are highly malignant neoplasms that rarely occur in adults. Due to the complex histology of AT/RTs, the differential diagnosis of these tumors is quite challenging and increasingly relies upon demonstration of characteristic SMARCB1/INI1 inactivation in tumor cells. Case description: We present a 51-year-old man who presented with diplopia, lethargy, and memory deficit owing to Parinaud's syndrome and hydrocephalus. MRI revealed a T2-hyperintense and homogeneously enhancing tectal mass that extended to the pineal region. Initial biopsy suggested a WHO grade II myxopapillary astrocytoma. However, subsequent definitive resection revealed an AT/RT, with loss of SMARCB1/INI1 observed through immunohistochemical staining as well as array cytogenetic analysis. Molecular profiling revealed additional mutations in RHPN2(L385I), MDM4(D396G), FLT3(V194M), and NPRL3(D53N). Conclusions: Pathological diagnoses in the modern era increasingly integrate molecular data for confirmation as well as prognostication. We present a rare case of a tectal AT/RT in an adult patient and report several novel mutations previously unrecognized in this tumor subtype, in addition to canonical SMARCB1/INI1 loss. Further investigation of these novel variants may improve understanding of the pathogenesis underlying AT/RTs.
    World Neurosurgery 09/2015; DOI:10.1016/j.wneu.2015.08.076 · 2.88 Impact Factor
  • 09/2015; DOI:10.1093/nop/npv027
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    ABSTRACT: The appropriate use of adjuvant therapy in patients with gross totally resected atypical meningioma requires an accurate assessment of recurrence risk. We sought to determine whether cytogenetic/genetic characterization may facilitate better estimation of the probability of recurrence. We first analyzed our clinical database, including high-resolution DNA copy number data, to identify 11 common copy number aberrations in a pilot cohort of meningiomas of all grades. We summed these aberrations to devise a cytogenetic abnormality score (CAS) and determined the CAS from archived tissue of a separate cohort of 32 patients with gross totally resected atypical meningioma managed with surgery alone. Propensity score adjusted Cox regression was used to determine whether the CAS was predictive of recurrence. An association between higher CAS and higher grade was noted in our pilot cohort with heterogeneity among atypical tumors. Among the 32 patients who underwent gross total resection of an atypical meningioma, the CAS was not significantly associated with age, gender, performance status, or tumor size/location but was associated with the risk of recurrence on univariable analysis (hazard ratio per aberration = 1.52; 95% CI = 1.08-2.14; P = .02). After adjustment, the impact of the dichotomized number of copy aberrations remained significantly associated with recurrence risk (hazard ratio = 4.47; 95% CI = 1.01-19.87; P = .05). The number of copy number aberrations is strongly associated with recurrence risk in patients with atypical meningioma following gross total resection and may inform the appropriate use of adjuvant radiation therapy in these patients or be useful for stratification in clinical trials. © The Author(s) 2015. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    Neuro-Oncology 08/2015; DOI:10.1093/neuonc/nov177 · 5.56 Impact Factor
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    ABSTRACT: The prognosis for patients with atypical and malignant meningioma is guarded; whether the extent of resection is associated with survival-based outcomes in this population remains poorly defined. This study investigated the association between gross total resection (GTR) and all-cause mortality in patients with atypical and malignant meningioma. The Surveillance, Epidemiology, and End Results program was used to identify 575 and 64 patients betweens the ages of 18 and 70 years who were diagnosed with atypical and malignant meningioma, respectively, between 2004 and 2009. Multivariate Cox proportional hazards regression was used to assess the adjusted impact of GTR versus subtotal resection on all-cause mortality. Baseline patient characteristics were similar for patients who did undergo GTR and patients who did not undergo GTR. The 5-year overall survival rates were 91.3% (95% confidence interval [CI], 86.2%-94.5%) and 78.2% (95% CI, 70.0%-84.3%) for patients with atypical meningioma who did and did not undergo GTR, respectively, and 64.5% (95% CI, 45.9%-78.1%) and 41.1% (95% CI, 17.9%-63.1%) for patients with malignant meningioma who did and did not undergo GTR, respectively. After adjustments for available, pertinent confounding variables, GTR was associated with lower all-cause mortality in patients with atypical (hazard ratio, 0.39; 95% CI, 0.23-0.67; P < .001) and malignant meningioma (hazard ratio, 0.35; 95% CI, 0.15-0.81; P = .01). The extent of resection is a powerful predictor of outcome for patients with atypical and malignant meningioma. These data highlight the hazard associated with the presence of gross tumor bulk after surgery and suggest a value for more extensive resections that should be balanced against the additional potential morbidity. Cancer 2015. © 2015 American Cancer Society. © 2015 American Cancer Society.
    Cancer 08/2015; DOI:10.1002/cncr.29639 · 4.89 Impact Factor
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    ABSTRACT: Read whole article: http://rdcu.be/dEIT Glioblastoma is the most common primary brain tumour in adults. Prognosis is poor: even with the current gold-standard first-line treatment-maximal safe resection and combination of radiotherapy with temozolomide chemotherapy-the median overall survival time is only approximately 15-17 months, because the tumour recurs in virtually all patients, and no commonly accepted standard treatment for recurrent disease exists. Several targeted agents have failed to improve patient outcomes in glioblastoma. Immunotherapy with immune checkpoint inhibitors such as ipilimumab, nivolumab, and pembrolizumab has provided relevant clinical improvements in other advanced tumours for which conventional therapies have had limited success, making immunotherapy an appealing strategy in glioblastoma. This Review summarizes current knowledge on immune checkpoint modulators and evaluates their potential role in glioblastoma on the basis of preclinical studies and emerging clinical data. Furthermore, we discuss challenges that need to be considered in the clinical development of drugs that target immune checkpoint pathways in glioblastoma, such as specific properties of the immune system in the CNS, issues with radiological response assessment, and potential interactions with established and emerging treatment strategies.
    Nature Reviews Neurology 08/2015; DOI:10.1038/nrneurol.2015.139 · 15.36 Impact Factor
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    ABSTRACT: Recurrent aggressive falcine meningiomas are uncommon tumors that recur despite receiving extensive surgery and radiation therapy (RT). We have utilized brachytherapy as a salvage treatment in two such patients with a unique implantation technique. Both patients had recurrence of WHO Grade II falcine meningiomas despite multiple prior surgical and RT treatments. Radioactive I-125 seeds were made into strands and sutured into a mesh implant, with 1 cm spacing, in a size appropriate to cover the cavity and region of susceptible falcine dura. Following resection the vicryl mesh was implanted and fixed to the margins of the falx. Implantation in this interhemispheric space provides good dose conformality with targeting of at-risk tissue and minimal radiation exposure to normal neural tissues. The patients are recurrence free 31 and 10 months after brachytherapy treatment. Brachytherapy was an effective salvage treatment for the recurrent aggressive falcine meningiomas in our two patients.
    Journal of Neuro-Oncology 08/2015; DOI:10.1007/s11060-015-1873-3 · 3.07 Impact Factor
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    ABSTRACT: EGFRvIII, a constitutively active EGFR deletion driver mutation, is associated with poor long-term survival in glioblastoma (GB). The investigational vaccine rindopepimut consists of a peptide sequence unique to EGFRvIII conjugated to keyhole limpet hemocyanin (KLH), delivered intradermally with granulocyte macrophage colony-stimulating factor. Three phase II studies in newly diagnosed, resected, EGFRvIII+ GB demonstrated encouraging progression-free survival (PFS), overall survival (OS), and safety profile. Compassionate-use experience suggests that rindopepimut may also provide benefit in relapsed GB, particularly with agents such as bevacizumab (BV). In the Phase II "ReACT" study, BV-naïve patients in 1st or 2nd relapse with EGFRvIII+ GB were randomly assigned 1:1 to BV plus double-blinded injection of rindopepimut or control (KLH). 6-month PFS (PFS6; primary), objective response rate (ORR), PFS, OS, and safety. Accrual is complete (n = 72); study follow-up continues (n = 30). Primary rindopepimut toxicity is grade 1 to 2 injection site reaction. For rindopepimut + BV vs KLH + BV (per investigator; RANO criteria): PFS6 = 27% (9/33) vs 11% (4/35) (P = .048, 1-side χ test); ORR = 24% (7/29) vs 17% (5/30). Central PFS/ORR assessment is underway. Median (95% CI) OS = 12.0 (9.7, -) vs 8.8 (6.8, 11.4) months (HR = 0.47 [0.25, 0.91]; P = .0208), with 8 vs 4 patients progression-free. OS analyses favor rindopepimut including when adjusted for various prognostic factors. Rindopepimut induced robust anti-EGFRvIII titers (1:12800-1:6553600) in 80% of patients. Rapid titer generation was associated with prolonged OS (HR = 0.47 [0.18, 1.27]; P = .128) within the rindopepimut arm, and was most frequent in patients with KPS ≥ 90 (odds ratio = 9.75; P = .007). Evaluation of humoral response quality and HLA typing vs outcome are underway. In an additional cohort of BV-exposed patients (n = 53), four patients experienced objective tumor response. These near-final data show that rindopepimut induces potent EGFRvIII-specific immune response and tumor regression, and appears to significantly prolong survival when administered with BV in patients with relapsed GB.
    Neurosurgery 08/2015; 62 Suppl 1, CLINICAL NEUROSURGERY:198-199. DOI:10.1227/01.neu.0000467069.86811.3f · 3.62 Impact Factor
  • Martha R Neagu · David A Reardon
    Immunotherapy 06/2015; 7(6):1-4. DOI:10.2217/imt.15.39 · 2.07 Impact Factor
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    ABSTRACT: Despite a high symptom burden, little is known about the incidence or predictors of hospitalization among glioblastoma patients, including risks during chemoradiation (CRT). We studied 196 consecutive newly diagnosed glioblastoma patients treated at our institution from 2006-2010. Toxicity data were reviewed during and after the CRT phase, defined as the period between diagnosis and 6 weeks after radiotherapy completion. Logistic regression and proportional hazards modeling identified predictors of hospitalization and overall survival (OS). Median age was 59 years (range, 23-90) and 83 % had Karnofsky performance status (KPS) score ≥ 70. Twenty-six percent of patients underwent gross total resection, 77 % received ≥ 59.4 Gy of radiotherapy, and 89 % received concurrent temozolomide. Median OS was 15.6 months (IQR, 8.5-26.8 months). Forty-three percent of patients were hospitalized during the CRT phase; OS was 10.7 vs. 17.8 months for patients who were vs. were not hospitalized, respectively (P P = .034) and KPS (OR, 0.95; 95 % CI, 0.93-0.97; P Hospitalization during the CRT phase was associated with decreased OS (adjusted hazard ratio, 1.47; 95 % CI, 1.01-2.13; P = .043), after adjustment for known prognostic factors. Hospitalization during the CRT phase is common among glioblastoma patients in the temozolomide era and is associated with shorter overall survival.
    Journal of Neuro-Oncology 06/2015; 124(1). DOI:10.1007/s11060-015-1820-3 · 3.07 Impact Factor
  • David A Reardon · Keith L Ligon · E Antonio Chiocca · Patrick Y Wen
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    ABSTRACT: Over the past few years, understanding the genetic abnormalities associated with glioblastoma, the most common malignant primary tumor of the central nervous system, has increased dramatically. Mutation types and frequencies have been comprehensively assessed, glioblastoma subclasses have been defined based on gene expression and methylation analyses, and novel mutations implicated in gliomagenesis have been identified. Nonetheless, a critical disconnect exists between achieved scientific advances and failure to improve patient outcome. Currently, standard therapy incorporating surgery, cranial irradiation, and temozolomide chemotherapy is uniformly applied for all patients. With this approach, median survival remains unacceptably poor including fewer than 10% of patients surviving 5 years after diagnosis. Salvage therapies are ineffective with PFS-6 rates under 10% for non-bevacizumab regimens and 40% for bevacizumab. Furthermore, all patients ultimately progress on bevacizumab, and then typically die from rapidly progressive tumor. Innovative treatment strategies directed to distinct patient subsets defined by specific genetic and gene expression analyses represent an attractive therapeutic paradigm shift for this highly challenging complex tumor, offering promise to ultimately improve outcome.
    Discovery medicine 06/2015; 19(107):471-7. · 3.63 Impact Factor
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    ABSTRACT: Trials focusing on unresectable multifocal glioblastoma are needed because of the extremely poor prognosis and challenges in receiving standard therapy, such as concurrent radiation and chemotherapy.Developing a strategy to chemically debulk tumors before radiation and/or surgery is warranted. Extent of resection remains a key prognostic factor in glioblastoma (GBM), with gross total resection providing a better prognosis than biopsy or subtotal resection. We conducted a phase II trial of upfront therapy with bevacizumab (BV), irinotecan (CPT-11), and temozolomide (TMZ) prior to chemoradiation in patients with unresectable, subtotally resected, and/or multifocal GBM. Patients received up to 4 cycles of TMZ at 200 mg/m(2) per day on days 1-5 (standard dosing) and BV at 10 mg/kg every 2 weeks on a 28-day cycle. CPT-11 was given every 2 weeks on a 28-day cycle at 125 mg/m(2) or 340 mg/m(2) depending on antiepileptic drugs. Magnetic resonance imaging of the brain was done every 4 weeks, and treatment continued as long as there was no tumor progression or unmanageable toxicity. The primary endpoint was tumor response rate, with a goal of 26% or greater. Forty-one patients were enrolled from December 2009 to November 2010. Radiographic responses were as follows: 9 patients (22.0%) had partial response, 25 (61.0%) had stable disease, and 2 (4.9%) had progression; 5 patients were not assessed. Cumulative response rate was 22%. Median overall survival was 12 months (95% confidence interval: 7.2-13.5 months). Upfront treatment with BV, TMZ, and CPT-11 is tolerable and can lead to radiographic response in unresectable and/or subtotally resected GBM. ©AlphaMed Press; the data published online to support this summary is the property of the authors.
    The Oncologist 05/2015; 20(7). DOI:10.1634/theoncologist.2015-0135 · 4.87 Impact Factor
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    ABSTRACT: Multicentric low-grade gliomas are rare entities that occur in disparate regions of the brain. They can present with distinct pathologic and imaging findings, and may harbor a worse prognosis. We present a case of multicentric low-grade gliomas and highlight their pathogenesis, imaging characteristics, and molecular signatures, with implications for clinical management. A 49-year-old man presented with three months of left-sided headaches. MRI revealed concurrent non-enhancing lesions in the left medial temporal lobe and superior cerebellum. Increased size and development of contrast enhancement in the temporal lesion promoted a left temporal craniotomy, with pathology revealing a grade II ganglioglioma. Three months later, the cerebellar lesion also acquired new contrast enhancement and was found to be a grade II astrocytoma following a supracerebellar infratentorial approach for resection. At two years follow-up, the patient remains clinically stable, receiving adjuvant chemotherapy for new non-enhancing, unresectable pontine lesion. Tumor growth rate, detailed pathologic findings, imaging characteristics and molecular signatures influence the clinical course of multicentric low-grade gliomas. PDGFRA amplifications and IDH1 wildtype status may act in a concerted fashion to produce an accelerated course of radiologic changes and tumor recurrence, as noted in our case. Additional research is needed to stratify the risk of transformation in multicentric low-grade glioma patients and to guide management strategies. Copyright © 2015 Elsevier Inc. All rights reserved.
    World Neurosurgery 05/2015; DOI:10.1016/j.wneu.2015.05.021 · 2.88 Impact Factor
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    ABSTRACT: Conclusive intraoperative pathologic confirmation of diffuse infiltrative glioma guides the decision to pursue definitive neurosurgical resection. Establishing the intraoperative diagnosis by histologic analysis can be difficult in low-cellularity infiltrative gliomas. Therefore, we developed a rapid and sensitive genotyping assay to detect somatic single-nucleotide variants in the telomerase reverse transcriptase (TERT) promoter and isocitrate dehydrogenase 1 (IDH1). This assay was applied to tissue samples from 190 patients with diffuse gliomas, including archived fixed and frozen specimens and tissue obtained intraoperatively. Results demonstrated 96% sensitivity (95% CI, 90%-99%) and 100% specificity (95% CI, 95%-100%) for World Health Organization grades II and III gliomas. In a series of live cases, glioma-defining mutations could be identified within 60 minutes, which could facilitate the diagnosis in an intraoperative timeframe. The genotyping method described herein can establish the diagnosis of low-cellularity tumors like glioma and could be adapted to the point-of-care diagnosis of other lesions that are similarly defined by highly recurrent somatic mutations.
    05/2015; 1(5). DOI:10.1001/jamaoncol.2015.0917
  • Neuro-Oncology 05/2015; 17(8). DOI:10.1093/neuonc/nov071 · 5.56 Impact Factor
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    ABSTRACT: Purpose: ABT-806, a humanized recombinant monoclonal antibody, binds a unique epidermal growth factor receptor (EGFR) epitope exposed in the EGFRde2-7 (EGFRvIII) deletion mutant and other EGFR proteins in the activated state. This phase I study evaluated the safety, pharmacokinetics, and recommended phase two dose (RP2D) of ABT-806 in patients with solid tumors that commonly overexpress activated EGFR or EGFRvlll. Methods: Patients with advanced solid tumors, including glioblastoma, were eligible. Following a dose escalation phase, expanded safety cohorts of patients with solid tumors or EGFR-amplified glioblastoma were enrolled. Adverse events (AEs) were graded by National Cancer Institute Common Terminology Criteria for Adverse Events v4.0; tumor response was assessed by Response Evaluation Criteria in Solid Tumors v1.1. EGFR protein expression was quantified by immunohistochemistry. Results: 49 patients were treated. Frequent AEs (≥10 %) possibly/probably related to ABT-806 were fatigue (18 %), nausea (16 %), dermatitis acneiform (12 %), and vomiting (10 %). Only one dose-limiting toxicity (grade three morbilliform rash) occurred. The RP2D was the pre-specified highest dose (24 mg/kg). Systemic exposures were dose proportional between 2 and 24 mg/kg. Median time to progression was 55 days (95 % confidence interval, 53-57) in all patients and 43 days (22-57) for glioblastoma patients. No objective responses occurred; however, two patients had prolonged stable disease. An EGFR-amplified penile cancer patient has stable disease lasting over 2.5 years. Conclusions: ABT-806 has unique pharmacokinetic and safety profiles. Toxicities were infrequent and typically low grade at the RP2D. Linear ABT-806 pharmacokinetics suggest lack of significant binding to wild-type EGFR in normal tissues.
    Investigational New Drugs 04/2015; 33(3). DOI:10.1007/s10637-015-0234-6 · 2.92 Impact Factor
  • Martha R Neagu · Raymond Y Huang · David A Reardon · Patrick Y Wen
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    ABSTRACT: Opinion statement: Glioblastoma (GBM), the most common malignant primary tumor in adults, carries a dismal prognosis with an average median survival of 14-16 months. The current standard of care for newly diagnosed GBM consists of maximal safe resection followed by fractionated radiotherapy combined with concurrent temozolomide and 6 to 12 cycles of adjuvant temozolomide. The determination of treatment response and clinical decision-making in the treatment of GBM depends on accurate radiographic assessment. Differentiating treatment response from tumor progression is challenging and combines long-term follow-up using standard MRI, with assessing clinical status and corticosteroid dependency. At progression, bevacizumab is the mainstay of treatment. Incorporation of antiangiogenic therapies leads to rapid blood-brain barrier normalization with remarkable radiographic response often not accompanied by the expected survival benefit, further complicating imaging assessment. Improved radiographic interpretation criteria, such as the Response Assessment in Neuro-Oncology (RANO) criteria, incorporate non-enhancing disease but still fall short of definitely distinguishing tumor progression, pseudoresponse, and pseudoprogression. With new evolving treatment modalities for this devastating disease, advanced imaging modalities are increasingly becoming part of routine clinical care in a field where neuroimaging has such essential role in guiding treatment decisions and defining clinical trial eligibility and efficacy.
    Current Treatment Options in Neurology 04/2015; 17(4):343. DOI:10.1007/s11940-015-0343-8 · 1.94 Impact Factor
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    ABSTRACT: Older patients with newly diagnosed glioblastoma have poor outcomes, and optimal treatment is controversial. Hypofractionated radiation therapy (HRT) is frequently used but has not been compared to patients receiving standard fractionated radiation therapy (SRT) and temozolomide (TMZ). We conducted a retrospective analysis of patients ≥65 years of age who received radiation for the treatment of newly diagnosed glioblastoma from 1994 to 2013. The distribution of clinical covariates across various radiation regimens was analyzed for possible selection bias. Survival was calculated using the Kaplan-Meier method. Comparison of hypofractionated radiation (typically, 40 Gy/15 fractions) versus standard fractionation (typically, 60 Gy/30 fractions) in the setting of temozolomide was conducted using Cox regression and propensity score analysis. Patients received SRT + TMZ (n=57), SRT (n=35), HRT + TMZ (n=34), or HRT (n=9). Patients receiving HRT were significantly older (median: 79 vs 69 years of age; P<.001) and had worse baseline performance status (P<.001) than those receiving SRT. On multivariate analysis, older age (adjusted hazard ratio [AHR]: 1.06; 95% confidence interval [CI]: 1.01-1.10, P=.01), lower Karnofsky performance status (AHR: 1.02; 95% CI: 1.01-1.03; P=.01), multifocal disease (AHR: 2.11; 95% CI: 1.23-3.61, P=.007), and radiation alone (vs SRT + TMZ; SRT: AHR: 1.72; 95% CI: 1.06-2.79; P=.03; HRT: AHR: 3.92; 95% CI: 1.44-10.60, P=.007) were associated with decreased overall survival. After propensity score adjustment, patients receiving HRT with TMZ had similar overall survival compared with those receiving SRT with TMZ (AHR: 1.10, 95% CI: 0.50-2.4, P=.82). With no randomized data demonstrating equivalence between HRT and SRT in the setting of TMZ for glioblastoma, significant selection bias exists in the implementation of HRT. Controlling for this bias, we observed similar overall survival for HRT and SRT with concurrent TMZ among elderly patients, suggesting the need for a randomized trial to compare these regimens directly. Copyright © 2015 Elsevier Inc. All rights reserved.
    International journal of radiation oncology, biology, physics 04/2015; 92(2). DOI:10.1016/j.ijrobp.2015.01.017 · 4.26 Impact Factor
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Publication Stats

11k Citations
1,659.79 Total Impact Points


  • 2015
    • Stanford University
      Palo Alto, California, United States
  • 2013–2015
    • Harvard Medical School
      • • Department of Radiation Oncology
      • • Department of Pathology
      Boston, Massachusetts, United States
  • 2011–2015
    • Dana-Farber Cancer Institute
      • Center for Neuro-Oncology
      Boston, Massachusetts, United States
  • 2002–2015
    • Duke University Medical Center
      • • Department of Surgery
      • • Department of Biostatistics and Bioinformatics
      • • Division of Neurosurgery
      Durham, North Carolina, United States
  • 2014
    • Brigham and Women's Hospital
      Boston, Massachusetts, United States
  • 2012–2014
    • Harvard University
      Cambridge, Massachusetts, United States
  • 2002–2014
    • Duke University
      • Department of Surgery
      Durham, North Carolina, United States
  • 2010
    • University of Texas MD Anderson Cancer Center
      Houston, Texas, United States
  • 2006
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 1998–2000
    • St. Jude Children's Research Hospital
      Memphis, Tennessee, United States