About

Timothy Robinson is a Lector in Greek and Latin at Yale University, where he received his PhD in Classics in 1994 with fellowships from Javits and Mellon. He has taught in several departments at Yale and is currently engaged in studies of Euripidean and Senecan tragedy. His field includes language instruction in Latin and Greek literature, with a specialization in Greek and Latin poetry. Robinson's research focuses on classical literature, particularly poetic works, and he has contributed to the understanding of adaptations of Sapphic strophe, the interpretation of monsters in Seneca's Apocolocyntosis, and the analysis of textiles and pretexts in Catullus' Carmen 64.

Research topics

• Medicine
• Internal medicine
• Oncology
• Biology
• Cancer research

Selected publications

• Stepwise Craniospinal Irradiation: A Practical Approach to Urgent Palliative Focal Radiation Therapy as a “Bridge” to the Definitive Management of Acute Leptomeningeal Disease

  Practical Radiation Oncology · 2026-01-01

  articleSenior author
  PublisherDOI

• A Taxonomy for Assessing Real-World Targeted Cancer Therapy Options in the Context of Broad Genomic Profiling

  Journal of the National Comprehensive Cancer Network · 2026-02-09

  articleOpen access

  BACKGROUND: Broad genomic profiling (BGP) is increasingly used to determine eligibility of molecularly targeted cancer therapies. Understanding the population-level impact of BGP on treatment selection requires a clinically oriented framework guiding interpretation of the guideline-directed actionability of BGP results. METHODS: We developed the Yale Molecular Alteration Taxonomy for Real-World Individualized Treatments (Y-MATRIX) to classify BGP results in relation to contemporaneous FDA approvals and NCCN Guidelines. We then applied our schema to patients with advanced non-small cell lung cancer (aNSCLC) and assessed temporal changes in the distribution of alteration categories using a large, nationwide database of patients with aNSCLC diagnosed from 2017 to 2023. RESULTS: Y-MATRIX classifies molecular testing results as categories A (first-line option), B (later-line option), C (off-label, guideline-concordant option), D (off-label, guideline-discordant option), E (no actionable alterations), or X (no alterations detected). In a sample of 8,717 patients with aNSCLC (median age, 69 years; 49.2% female), the proportion of patients in category A/B increased from 15.8% in 2017 to 33.6% in 2023, driven predominantly by an increase in later-line therapies (category B, 0% to 15.2%). Patients in category C/D increased from 21.2% to 39.3%, whereas patients in category E/X decreased markedly from 63.1% to 27.1%. Nonsmoking status, younger age, and nonsquamous histology were associated with having category A alterations. CONCLUSIONS: Y-MATRIX provided a comprehensive taxonomy of BGP results by clinical actionability and demonstrates the increasing actionability of BGP results as the aNSCLC treatment landscape evolved over time. There was an increase in patients with category C and D findings, representing a diverse set of clinical circumstances of unclear actionability with opportunities for both innovative and potentially inappropriate targeted therapy use. The Y-MATRIX schema can be applied to facilitate research on all cancers, including the study of alterations across strata of targetable potential and the clinical utility of molecular profiling in precision oncology over time.

  PublisherOA PDFDOI

• Abstract 3804: Accumulation of branched chain keto acids promotes immunosuppression and neurodegeneration in leptomeningeal disease

  Cancer Research · 2025-04-21

  article

  Leptomeningeal disease (LMD) occurs when malignant cells seed into the leptomeningeal space and cerebrospinal fluid (CSF), leading to severe neurological symptoms and very short survivals. LMD occurs in 5to15% of cancer patients and is most common in breast, melanoma, lung, and lymphomas. LMD tumors are generally resistant to all standard of care therapies. To better understand LMD biology we used comprehensive multiomic analyses of CSF specimens from LMD patients with different primary tumors to understand its immune and metabolic tumor microenvironment. Single cell RNA sequencing on patient CSF showed a distinct immunosuppressive landscape regardless of the primary histology. We identified significant enrichment of CD4Tregs and exhausted T cells in LMD patients. Lack of active, proliferating T cells and protumorigenic macrophage infiltration were associated with LMD poor survival (<10months, p<0.01). Additionally, proteomic and lipidomic analysis of patients’ CSF showed downregulation in proteins and lipids vital for neuronal development and myelin sheath integrity. Strikingly, the metabolomic analysis demonstrated an accumulation of branched-chain keto acids (BCKA), well known neurotoxins, in CSF of LMD versus controls (p<0.05). Next, we performed correlation analysis between single cell RNA seq data and levels of BCKA in LMD samples (n=8). Results revealed positive correlations between high BCKA concentrations and CD4Tregs (p<0.01), and two exhausted T cell populations (p<0.05), suggesting an immunosuppressive impact of BCKA in LMD patients. Our in-vitro functional data demonstrated that BCKA drastically disrupts the T-lymphocyte viability, proliferation, and effector cytokine secretion. Moreover, BCKA reduced the viability of chimeric antigen receptor CART cells, neurons, and meningeal cells but not tumor cells. These results were validated in immunocompetent LMD animal models. Consistent with BCKA-induced neurotoxicity, we found that LMD mice had a rapid neurological decline (p<0.0001). Furthermore, we found the leptomeningeal layer in LMD mice was compromised and had significantly high levels of BCKA (p<0.01). Highlighting the translatability of this work, we found that phenylbutyrate, a BCKA lowering agent, improved neurological function (p<0.01), survival outcomes (p<0.01), and efficacy of CART therapy in lymphoma LMD model (p<0.05). Phenylbutyrate also improved responses to chemotherapy in breast cancer LMD model. This is the first report describing BCKA accumulation in LMD as a cause of neurotoxicity and immunosuppression and provides a unique strategy to treat these deadly tumors. Repurposing of FDA approved phenylbutyrate improves the quality of life, survival, and efficacy of immune therapies in LMD. Citation Format: Mariam Lotfy Khaled, Ethan Vallebuona, Min Liu, M.Baraa Boozo, Zhihua Chen, Gerald C. Wallace, Yuan Ren, Ronak Kundalia, Hasan Alhaddad, Oscar Ospina, Brittany Evernden, Victoria Izumi, Lancia NF Darville, Ann chen, MacLean Hall, Michael Jain, Shari Pilon-Thomas, Paul Stewart, Fredrick L. Locke, Timothy J. Robinson, John M. Koomen, Peter A. Forsyth, Inna Smalley. Accumulation of branched chain keto acids promotes immunosuppression and neurodegeneration in leptomeningeal disease [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3804.

  PublisherDOI

• Phase 1 trial of hypofractionated stereotactic re-irradiation in combination with nivolumab, ipilimumab, and bevacizumab for recurrent high-grade gliomas

  Neuro-Oncology Advances · 2025-01-01 · 3 citations

  articleOpen access

  Background: Our previous clinical investigation suggested that hypofractionated stereotactic re-irradiation (HFSRT) and PD-1 blockade may act synergistically to enhance the immune response against glioma. This subsequent trial investigated the dual blockade of CTLA4 and PD-1 in combination with HFSRT and bevacizumab. Methods: This phase I study enrolled eligible patients with bevacizumab-naïve recurrent glioblastoma or anaplastic astrocytoma. Participants received nivolumab, ipilimumab, and bevacizumab concurrently with HFSRT (3000 cGy in 5 fractions). Subsequently, nivolumab, ipilimumab, and bevacizumab were administered for a total of 4 cycles followed by nivolumab and bevacizumab until progression. The primary end point of this study was the safety and tolerability of HFSRT in combination with nivolumab, ipilimumab, and bevacizumab in patients with recurrent HGGs. Secondary end points included 6-month survival and 9-month survival. Results: Twenty-six patients were treated. Treatment-related adverse events (TRAEs) of grade 3 or 4 were observed in 12 (48%) evaluable patients with no unexpected TRAEs. Six months and 9 months survival were 92% (95% CI, 82-100%) and 75% (95% CI, 60-95%), respectively. The median progression-free survival and overall survival were 7.1 months (95% CI, 5.2-12.2) and 15.6 months (95% CI, 11.3-27.0), respectively. Conclusions: The combination of HFSRT with ipilimumab, nivolumab, and bevacizumab is safe. Our results underscore the potential synergies between stereotactic re-irradiation and checkpoint immunotherapy in patients with recurrent high-grade gliomas.

  PublisherDOI

• Bridging radiotherapy before chimeric antigen receptor T cells for B-cell lymphomas: an ILROG multicenter study

  Blood Advances · 2025-04-09 · 8 citations

  articleOpen access

  ABSTRACT: Despite the increasing utilization of bridging radiotherapy (Br-RT), its impact on chimeric antigen receptor T-cell therapy (CAR-T) efficacy and toxicity remains poorly characterized. We retrospectively reviewed patients with relapsed/refractory B-cell lymphomas (BCLs) who received Br-RT followed by CAR-T from 2018 to 2020 across 10 institutions. Br-RT toxicities were graded per Common Terminology Criteria for Adverse Events version 5.0, and cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) per American Society for Transplantation and Cellular Therapy Consensus Guidelines. One hundred seventy-two patients (168 large BCL) received Br-RT before axicabtagene ciloleucel (73%), tisagenlecleucel (24%), or brexucabtagene autoleucel (2%). At leukapheresis, most patients (74%) had advanced-stage disease and 39% had bulky disease measuring ≥10cm. Comprehensive Br-RT was administered to 39% and bridging systemic therapy to 35%. Among all patients, grade ≥3 Br-RT toxicity occurred in 2% (1 grade 5 toxicity), grade ≥3 CRS in 9%, and grade ≥3 ICANS in 24%. Median follow-up was 31.3 months. Two-year progression-free survival (PFS) and overall survival (OS) were 38% and 53%, respectively. On multivariable analysis, comprehensive Br-RT was associated with superior PFS (hazard ratio [HR], 0.38; P < .001) and OS (HR, 0.48; P = .011). Patients with lactate dehydrogenase (LDH) normalization after Br-RT (high pre-Br-RT LDH, normal post-Br-RT LDH) had superior PFS and OS compared with those with high post-Br-RT LDH and similar PFS and OS compared with those with normal baseline LDH. In this particularly high-risk cohort, Br-RT before CAR-T demonstrates an acceptable toxicity profile with favorable clinical outcomes compared with historical controls. Comprehensive Br-RT and LDH normalization after Br-RT may be associated with superior PFS and OS.

  PublisherOA PDFDOI

• Beyond the Marrow–Moving Toward a Systemic Perspective of Radiation-Induced Cytopenias

  International Journal of Radiation Oncology*Biology*Physics · 2025-02-21

  editorialSenior author
  PublisherDOI

• Phase <scp>II</scp> Trial of Reduced‐Intensity Fludarabine, Melphalan, and Total Body Irradiation Conditioning With Haploidentical Donor Peripheral Blood Stem Cell Transplant

  American Journal of Hematology · 2025-06-10

  letterOpen access

  Human leukocyte antigen (HLA) haploidentical (haplo) hematopoietic cell transplantation (HCT) with post-transplant cyclophosphamide (PTCy) has expanded access to this curative therapy with rates of graft-versus-host disease (GVHD) that are similar to HLA matched donor HCT [1]. The original Johns Hopkins PTCy platform uses a reduced intensity conditioning (RIC) regimen consisting of Fludarabine (Flu) 150 mg/m2, Cy 14.5 mg/kg on Day-6 and-5, total body irradiation (TBI) 200 cGy on Day-1 (Flu/Cy/TBI) and a bone marrow graft (BMT). Though this regimen yields favorable toxicity including rates of non-relapse mortality (NRM) ~10%–15%, severe acute GVHD ~10%, and chronic GVHD ~10%, outcomes have been marred by high rates of disease relapse > 50% [1]. While myeloablative conditioning (MAC) regimens can reduce the risk of relapse, older and frail patients cannot tolerate MAC regimens. To improve relapse after RIC haplo HCT with PTCy, investigators at the MD Anderson Cancer Center attempted a conditioning regimen consisting of Flu 160 mg/m2, melphalan (Mel) 100–140 mg/m2, and either Thiotepa 5 mg/kg or TBI 200 cGy [2]. While they reported low 1-year relapse rates of 19%, NRM was high at 21%, resulting in 1-year disease-free survival (DFS) of 60%. As haplo HCT with PTCy is increasingly used, strategies to improve outcomes are essential. We hypothesized that reducing the Mel dose to 70 mg/m2 in a Flu/Mel70/TBI regimen followed by haplo peripheral blood stem cell transplant (PBSCT) with PTCy would successfully improve DFS by reducing relapse without a significant increase in NRM compared to Flu/Cy/TBI haplo HCT in patients unfit for MAC. This trial, NCT04191187, is single-institution phase II study of Flu/Mel70/TBI haplo PBSCT with PTCy/sirolimus/mycophenolate mofetil (MMF) in patients with high-risk hematologic malignancies. It was approved by the Advarra Institutional Review Board and is compliant with the Declaration of Helsinki. Eligible patients were required to be ≥ 55 years or < 55 years with significant comorbidities defined as an HCT comorbidity index (HCT-CI) ≥ 3, and receiving an HLA haplo donor HCT for a hematologic malignancy. All patients received conditioning with Flu 30 mg/m2/day from −6 to −2 based on actual body weight, Mel 70 mg/mg2 on day-6 based on actual body weight, and TBI 200 cGy on day-1. On day 0, patients received the PBSCT (Figure 1A). The target CD34+ cell dose was 5 × 106 CD34+ cells/kg, with a maximum allowable dose of 7 × 106 CD34+ cells/kg. GVHD prophylaxis consisted of PTCy/tacrolimus/MMF for the first five subjects. The protocol was subsequently modified to follow the PTCy/sirolimus/MMF platform published separately by our group [3]. The primary endpoint of this study was DFS. Comparing to a historic DFS at 18 months of 40%, we assumed that the DFS in patients treated with Flu/Mel70/TBI would be 60%, corresponding to a hazard ratio (HR) of 0.557 [1, 2]. A total sample size of 34 subjects provided 90% power to detect a HR of 0.557 using the one-sample log-rank test at a one-sided significance level of 0.1. Cumulative incidence was used to estimate the probabilities of GVHD, relapse, infection, and neutrophil and platelet recovery, treating deaths as a competing risk. For GVHD and NRM, relapse also served as a competing risk. The Gray test was used accordingly. Ninety-five percent confidence intervals were estimated from respective standard errors and the complementary log–log transformation. Analyses were performed and plots generated using SAS 9.4 (SAS Institute, Cary, NC) and/or R 3.0.2. Detailed baseline characteristics of the 34 subjects treated are shown in Table 1. Median time to neutrophil engraftment was 18 days (range: 14–42), and the incidence by day 30 was 88%. There were no cases of primary graft failure among evaluable patients who survived past day 30. The median time to platelet engraftment was 29 days (range: 16–67), and engraftment by day 60 was 82%. Donor age in years, median (range) CD34+ cells/kg, median (range) 34 (range: 21–49) 5.72 × 106 (range: 4.45–7.0 × 106) Patient sex Donor relation Karnofsky Performance Scale Race/ethnicity Disease GVHD prophylaxis Of 32 subjects with unsorted marrow chimerism samples, 30 (93.8%) had > 95% donor chimerism (range: 35% to 100%) at day 30. One of the two patients with low donor chimerism reached 100% donor chimerism at day 90, while the other relapsed and ultimately succumbed to his disease. Similarly, 30 of 31 (96.8%) with available peripheral blood chimerism samples reached > 95% donor in both the myeloid (range: 73% to 100%) and lymphoid compartments (range: 4% to 100%) by day 30. A total of four subjects experienced grade II–IV acute GVHD, resulting in a cumulative incidence of 11.8% (95% C.I.: 3.6% to 25.1%) by day 100 (Figure 1B). Of these, one subject developed grade IV acute GVHD and there were no cases of grade III acute GVHD. At 18 months, the cumulative incidence of moderate to severe chronic GVHD was 8.8% (95% C.I.: 2.2% to 21.4%, Figure 1C). With median follow up of 18 months for survivors (range 18–20), the cumulative incidence of relapse at 18 months was 11.8% (95% C.I.: 3.6% to 25.2%, Figure 1D). The diagnoses for the four subjects with disease relapse were MDS (n = 3) and MPN (n = 1). The cumulative incidence of NRM at 18 months was 17.6% (95% C.I.: 7.0% to 32.2%, Figure 1E). Causes of death for these six subjects with NRM events were organ failure (n = 2), sepsis (n = 2), Stevens-Johnson Syndrome (n = 1), and acute kidney injury (n = 1). The observed 18-month DFS was 70.6% (one-sided 90% C.I.: ≥ 59.2%, Figure 1F), thus meeting the primary endpoint of the trial of 18-month DFS of 40% (p = 0.0017). The median DFS was not reached. Kaplan–Meier estimate for OS at 18 months was 73.3% (95% C.I.: 54.9% to 85.1%, Figure 1G). At 18 months, GRFS was 61.8% (95% C.I.: 43.4% to 75.7%). Grade 3–5 adverse events are listed in Table S1. CRS and viral infections are adverse events of interest in haplo HCT. CRS was observed in 28 subjects (82.4%), including 23 subjects (67.6%) with grade 1 CRS and five subjects (14.7%) with grade 2 CRS. Two of these subjects received tocilizumab for treatment of CRS. There were no cases of grade 3–5 CRS. Grade 3 CMV infection was identified in five subjects (14.7%), including one case of CMV pneumonitis. Notably, letermovir for CMV prophylaxis was adopted at our institution during the latter portion of the trial and was administered to 15 subjects, of whom 6 (40%) developed CMV infections. Grade 3 HHV6 reactivation occurred in five cases (14.7%) and resolved with foscarnet, including two cases with confirmed HHV6 in the cerebrospinal fluid. There were no grade 4–5 viral infections. Currently, the role of MMF in the PTCy platform is debated. We collected blood samples on post-transplant day 7 at pre-MMF dose, end of MMF infusion, and 1, 2, 4, and 8 h after the end of MMF infusion to study the pharmacokinetics of MMF and its active metabolite mycophenolic acid (MPA). Concentrations were determined by the Cancer Pharmacokinetics and Pharmacodynamics Core at the Moffitt Cancer Center using LC–MS/MS methods that have been validated according to ICH/FDA guidelines for bioanalytical analysis. MMF and MPA concentrations were evaluated by non-compartmental analysis (NCA) on Day 5 in 33 subjects to determine if steady-state pharmacokinetics of MMF were affected by the coadministration of cyclophosphamide and were consistent with single-agent exposure, highlighting that there does not appear to be a significant MMF drug–drug interaction with Cy exposure (Figure S1, Table S2). A higher volume of distribution of MPA was correlated with a lower risk of grade II-IV acute GVHD (HR = 0.06, 95% CI: 0.01 to 0.54, p = 0.01) suggesting MMF does contribute to acute GVHD prevention in this regimen (Table S3). To date, no studies have evaluated the effects of genetic polymorphisms on patients receiving PTCy. Prior to starting therapy, blood samples were collected from 24 subjects to assess the presence of single nucleotide polymorphisms (SNPs) in genes of interest that influence drug metabolism (Table S4). The association with the incidence of acute and chronic GVHD was explored by the Fine-Gray regression model. Nine genes with differential expression within the cohort were evaluated for associations with clinical outcomes: GSTP1, SLCO2B1, LST3, CYP1A2, SULT1A1, SLC15A2, UGT2B15, UGT2B7, and ABCG2. No significant interactions with GVHD, relapse, or survival were identified (Table S5). However, the sample size in this trial is not adequately powered to evaluate such differences, and future studies are warranted as this may impact outcomes in different ethnicities or inform dosing. The Flu/Mel70/TBI regimen reported here is a promising approach to RIC haplo PBSCT with PTCy, meeting the primary endpoint of improved DFS compared with historical benchmarks in a patient cohort unfit for MAC. While Mel-based conditioning has been successful for matched donor HCT, incorporating Mel with haplo HCT has previously demonstrated high rates of CRS, GVHD, and NRM, even in younger cohorts [4]. We reduced the dose of Mel and moved it earlier in the regimen to day-6 in hopes of decreasing tissue injury and inflammation that drives these complications after transplant [5]. We also hypothesized that the inclusion of TBI after the Flu/Mel may deplete recipient T cells that would contribute to CRS after cell infusion [6]. With these modifications, toxicity and engraftment were similar to prior studies and, encouragingly, relapse rates were low. This regimen offers a favorable approach for patients unfit for MAC regimens and merits further investigation in larger, multicenter prospective trials. H.E. and N.B. were responsible for protocol writing, co-principal investigators of the trial, data analysis, and final manuscript preparation. R.G. and E.D. contributed to protocol writing and pharmacokinetic data analysis. S.S. contributed to protocol writing and pharmacokinetic data acquisition and analysis. J.K. was responsible for statistical design and performing final statistical analysis. All authors contributed to final data analysis and interpretation, critical review of the manuscript, and approval of the final manuscript for publication. We wish to thank the Moffitt research team, clinical staff, patients, and caregivers who participated in this trial. Clinical Trials Registration: NCT04191187. This study was approved by the Moffitt Advarra Institutional Review Board. All subjects completed written informed consent for the participation in the trial and agreement to publish the results. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request. Data S1. Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

  PublisherOA PDFDOI

• Association between transcriptomic metrics of exogenous antigen presentation and adaptive immunity with locoregional recurrence in localized estrogen receptor negative breast cancer: retrospective review of multi-institutional datasets

  Breast Cancer Research · 2025-05-13 · 2 citations

  articleOpen access1st authorCorresponding

  BACKGROUND: Transcriptomic features of breast cancer locoregional recurrence (LRR) remain poorly understood. We therefore sought to investigate transcriptomic features associated with LRR in newly diagnosed invasive breast tumors from our institutional dataset. METHODS: Transcriptomic profiling was performed on 632 tumors from consecutive patients treated within our health system for newly diagnosed non-metastatic breast cancer. Univariable Cox models identified genes whose expression was associated with LRR (q-value < 0.05). Up-regulated (UR) genes were defined as hazard ratio (HR) > 1 and down-regulated (DR) genes were defined as HR < 1. Gene set enrichment analyses were performed for UR and DR gene sets and validated within two external cohorts of ER- tumors. RESULTS: With a median follow-up of 7.6 years, we observed 38 LRRs: 28/481 (5.8%) in ER + and 10/151 (6.6%) in ER-. There were 43 UR and 7 DR genes associated with LRR in ER + tumors, while 417 UR and 1150 DR genes were associated with LRR in ER- tumors. UR genes in ER + tumors were enriched for roles in cell proliferation (q < 0.05). In contrast, LRR in ER- tumors was most strongly associated with DR genes enriched for MHC-II-mediated antigen presentation and T cell activation (q < 0.05). In external cohorts of ER- tumors, 97 significant DR genes (p < 0.05) were enriched for 18 pathways, including 5 pathways involved in MHC-II signaling, antigen presentation and T-cell activation. CONCLUSIONS: Transcriptomic patterns associated with LRR appear distinct between ER + and ER- tumors. In ER + tumors, LRR appears predominantly associated with proliferation, whereas ER- LRR suggests a robust pattern of suppressed antigen presentation via MHC-II.

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• Semaglutide and Tirzepatide Prescribing for Obesity in Patients With Preexisting Comorbid Cancers

  JAMA Oncology · 2025-11-06 · 1 citations

  articleOpen access

  This cohort study compares incident and prevalent prescription rates of glucagon-like peptide-1 receptor agonists among adults with at least 1 obesity-related comorbidity and newly diagnosed cancer.

  PublisherOA PDFDOI

• BPI25-017: A Novel Integrated Classification Schema for Molecular Findings by Potential Clinical Actionability: A Tool for Assessment of Real-World Cancer Care in the Targeted Therapy Era

  Journal of the National Comprehensive Cancer Network · 2025-03-28

  article

  "BPI25-017: A Novel Integrated Classification Schema for Molecular Findings by Potential Clinical Actionability: A Tool for Assessment of Real-World Cancer Care in the Targeted Therapy Era" published on 28 Mar 2025 by National Comprehensive Cancer Network.

  PublisherDOI

Frequent coauthors

• Adam Kirn

  Florida International University

  51 shared

• Indira Chatterjee

  Case Western Reserve University

  51 shared

• Jennifer Amos

  University of Illinois Urbana-Champaign

  51 shared

• Kamran A. Ahmed

  Moffitt Cancer Center

  34 shared

• Arnold B. Etame

  Moffitt Cancer Center

  32 shared

• Mariano A. Garcia‐Blanco

  University of Virginia

  31 shared

• Peter Forsyth

  Moffitt Cancer Center

  31 shared

• Nicholas B. Figura

  Moffitt Cancer Center

  31 shared

Education

• Resident, Radiation Oncology

  Duke University School of Medicine

  2016

Awards & honors

• Javits Fellowship
• Mellon Fellowship