Suresh S Ramalingam

Emory University, Atlanta, Georgia, United States

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Publications (216)1667.14 Total impact

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    ABSTRACT: In preclinical studies, the efficacy of the combination of antiangiogenic agents with chemotherapy seems to be dependent on the specific cytotoxic agent. We conducted a systematic review of the efficacy of bevacizumab in combination with taxane or non-taxane containing regimens for untreated, nonsquamous non-small-cell lung cancer patients. An extensive search of published clinical trials was conducted from electronic databases (MEDLINE, EMBASE, and Cochrane) and meeting proceedings using relevant search criteria. Phase 2 and randomized trials reporting on the efficacy of bevacizumab combined with taxane or non-taxane regimens were selected. A systematic analysis of extracted data was performed using Comprehensive Meta-Analysis (Version 2.2) software. Clinical outcome in patients treated with taxane versus non-taxane regimen was compared using point estimates for weighted values of median overall survival, progression-free survival, and response rate. Twenty-nine studies reported between 2005 and 2015 were eligible. A total of 5890 patients (2767 and 3123 in the taxane and non-taxane groups, respectively) were included. The taxane and non-taxane groups were comparable in patient characteristics: median age, 62.8 versus 61.2 years; males, 57% versus 58%; adenocarcinomas, 83% versus 83%; stage IV, 87% versus 82%; performance status 0/1- 45/55% versus 41/59%, respectively. The weighted median overall survival was 14.4 versus 13.7 months (p = 0.5); progression-free survival was 6.93 versus 6.99 months (p = 0.61); response rate was 41% versus 39% (p = 0.65) for taxane and non-taxane groups. The outcomes between taxane and non-taxane regimens when given in combination with bevacizumab for patients with nonsquamous non-small-cell lung cancer are comparable.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 08/2015; 10(8):1142-7. DOI:10.1097/JTO.0000000000000572 · 5.80 Impact Factor
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    ABSTRACT: We previously reported that progression-free survival (PFS) may be a candidate surrogate end point for overall survival (OS) in first-line extensive-stage small-cell lung cancer (ES-SCLC) using data from three randomized trials (Foster, Cancer 2011). In this validation study (N0424-Alliance), we assessed the patient-level and trial-level surrogacy of PFS using data from seven new first-line phase II/III ES-SCLC trials and across all 10 trials as well (seven new, three previous). Individual patient data were utilized across the seven new trials (2259 patients) and all 10 trials (2855 patients). Patient-level surrogacy (Kendall's τ) was assessed using the Clayton copula bivariate survival model. Trial-level surrogacy was assessed through association of the log hazard ratios on OS and PFS across trials, including weighted (by trial size) least squares regression (WLS R) of Cox model effects and correlation of the copula effects (copula R). The minimum effect on the surrogate (MES) needed to detect a nonzero treatment effect on OS was also calculated. The median OS and PFS across all 10 trials were 9.8 and 5.9 months, respectively. PFS showed strong surrogacy within the 7 new trials (copula R = 0.90 [standard error = 0.27], WLS R = 0.83 [95% confidence interval: 0.43, 0.95]; MES = 0.67, and Kendall's τ = 0.58) and across all 10 trials (copula R = 0.81 [standard errors = 0.25], WLS R = 0.77 [95% confidence interval: 0.47-0.91], MES = 0.70, and Kendall's τ = 0.57). PFS demonstrated strong surrogacy for OS in first-line ES-SCLC based on this external validation study of individual patient data. PFS is a good alternative end point to OS and should be considered when resource constraints (time or patient) might make it useful or desirable in place of OS. Additional analyses are needed to assess its appropriateness for targeted agents in this disease setting.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 07/2015; 10(7):1099-106. DOI:10.1097/JTO.0000000000000548 · 5.80 Impact Factor
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    ABSTRACT: We describe the landscape of genomic alterations in cutaneous melanomas through DNA, RNA, and protein-based analysis of 333 primary and/or metastatic melanomas from 331 patients. We establish a framework for genomic classification into one of four subtypes based on the pattern of the most prevalent significantly mutated genes: mutant BRAF, mutant RAS, mutant NF1, and Triple-WT (wild-type). Integrative analysis reveals enrichment of KIT mutations and focal amplifications and complex structural rearrangements as a feature of the Triple-WT subtype. We found no significant outcome correlation with genomic classification, but samples assigned a transcriptomic subclass enriched for immune gene expression associated with lymphocyte infiltrate on pathology review and high LCK protein expression, a T cell marker, were associated with improved patient survival. This clinicopathological and multi-dimensional analysis suggests that the prognosis of melanoma patients with regional metastases is influenced by tumor stroma immunobiology, offering insights to further personalize therapeutic decision-making.
    Cell 06/2015; 161(7):1681 - 1696. DOI:10.1016/j.cell.2015.05.044 · 33.12 Impact Factor
  • Conor E. Steuer · Suresh S. Ramalingam
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    ABSTRACT: The development of individualized therapies has become the focus of current oncology research. Precision medicine has demonstrated great potential for bringing safe and effective drugs to those patients stricken with cancer, and is becoming a reality as more oncogenic drivers of malignancy are discovered. The discovery of Epidermal Growth Factor Receptor (EGFR) mutations as a driving mutation in non-small cell lung cancer (NSCLC) and the subsequent success of the tyrosine kinase inhibitors (TKI) have led the way for NSCLC to be at the forefront of biomarker-based drug development. However, this direction was not always so clear, and this article describes the lessons learned in targeted therapy development from EGFR in NSCLC. Copyright © 2015. Published by Elsevier Ltd.
    Molecular Aspects of Medicine 05/2015; DOI:10.1016/j.mam.2015.05.004 · 10.30 Impact Factor
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    ABSTRACT: This trial was designed to evaluate the activity and safety of ganetespib in combination with docetaxel in advanced NSCLC and to identify patient populations most likely to benefit from the combination. Patients with one prior systemic therapy for advanced disease were eligible. Docetaxel (75mg/m(2) on Day 1) was administered alone or with ganetespib (150mg/m(2) on Days 1 and 15) every 3 weeks. The primary endpoints were progression-free survival (PFS) in 2 subgroups of the adenocarcinoma population: patients with elevated lactate dehydrogenase (eLDH) and mutated KRAS (mKRAS). Out of 385 patients enrolled, 381 were treated. Early in the trial increased hemoptysis and lack of efficacy were observed in non-adenocarcinoma patients (n=71), therefore only patients with adenocarcinoma histology were subsequently enrolled. Neutropenia was the most common grade ≥3 adverse event: 41% in the combination arm vs. 42% in docetaxel alone. There was no improvement in PFS for the combination arm in the eLDH (N=114, adjusted HR=0.77, P=0.1134) or mKRAS (N=89, adjusted HR=1.11, P=0.3384) subgroups. In the ITT adenocarcinoma population there was a trend in favor of the combination, with PFS (N=253, adjusted HR=0.82, P=0.0784) and overall survival (OS) (adjusted HR=0.84, P=0.1139). Exploratory analyses showed significant benefit of the ganetespib combination in the prespecified subgroup of adenocarcinoma patients diagnosed with advanced disease >6 months before study entry (N=177): PFS (adjusted HR=0.74, P=0.0417); OS (adjusted HR=0.69, P=0.0191). Advanced lung adenocarcinoma patients treated with ganetespib in combination with docetaxel had an acceptable safety profile. While the study's primary endpoints were not met, significant prolongation of PFS and OS was observed in patients >6 months from diagnosis of advanced disease, a subgroup chosen as the target population for the Phase 3 study. © The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.
    Annals of Oncology 05/2015; DOI:10.1093/annonc/mdv220 · 6.58 Impact Factor
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    ABSTRACT: The BH4 domain of Bcl2 is required for its antiapoptotic function, thus constituting a promising anticancer target. We identified a small-molecule Bcl2-BH4 domain antagonist, BDA-366, that binds BH4 with high affinity and selectivity. BDA-366-Bcl2 binding induces conformational change in Bcl2 that abrogates its antiapoptotic function, converting it from a survival molecule to a cell death inducer. BDA-366 suppresses growth of lung cancer xenografts derived from cell lines and patient without significant normal tissue toxicity at effective doses. mTOR inhibition upregulates Bcl2 in lung cancer cells and tumor tissues from clinical trial patients. Combined BDA-366 and RAD001 treatment exhibits strong synergy against lung cancer in vivo. Development of this Bcl2-BH4 antagonist may provide a strategy to improve lung cancer outcome. Copyright © 2015 Elsevier Inc. All rights reserved.
    Cancer cell 05/2015; 27(6). DOI:10.1016/j.ccell.2015.04.010 · 23.89 Impact Factor
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    ABSTRACT: Veliparib (V) potentiated therapeutic efficacy of cisplatin (C) and etoposide (E) in preclinical models of SCLC. We conducted this phase 1 study to establish the safety of the combination in human subjects. The study employed the 3+3 dose escalation design to establish the safety and recommended phase 2 dose (RP2D) of V when combined with fixed doses of C (75mg/m(2) on day 1) and E (100mg/m(2) on days 1-3) in a 21-day cycle. The starting dose of V was 60mg (bid days 1-7) with plan to escalate to 100mg (days 1-7) or de-escalate to 40mg (days 1-7) depending on the dose limiting toxicity (DLT) experience during cycle 1. Patients with treatment-naïve, extensive stage SCLC were included. The study enrolled 9 patients: M/F (4/5); median age (60); White/African American (8/1). V was tolerated at the 60mg (DLT in 0 of 3 patients) and 100mg dose (DLT in 1 of 6 patients; grade 5 cardiac failure). Veliparib at 100mg in combination with standard doses of C and E was established as the RP2D. Grades 3-5 adverse events irrespective of attribution during cycle 1 included: dehydration (1), diarrhea (1), fatigue (1), febrile neutropenia (1), heart failure (1), leukopenia (6), lymphopenia (1), nausea (2), neutropenia (8), respiratory failure (1), and thrombocytopenia (2). Investigator-assessed efficacy outcome in 7 evaluable patients were stable disease in 2/7 (28.6%), partial response in 4/7 (57.1%), and complete response in 1/7 (14.3%) patients. This study demonstrated the safety of combining veliparib with cisplatin and etoposide in previously untreated SCLC patients. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Lung cancer (Amsterdam, Netherlands) 05/2015; 89(1). DOI:10.1016/j.lungcan.2015.04.015 · 3.74 Impact Factor
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    ABSTRACT: The EGFR T790M mutation is the most common mechanism of drug resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in patients who have lung cancer with an EGFR mutation (EGFR-mutated lung cancer). In preclinical models, the EGFR inhibitor AZD9291 has been shown to be effective against both EGFR tyrosine kinase inhibitor-sensitizing and T790M resistance mutations. We administered AZD9291 at doses of 20 to 240 mg once daily in patients with advanced lung cancer who had radiologically documented disease progression after previous treatment with EGFR tyrosine kinase inhibitors. The study included dose-escalation cohorts and dose-expansion cohorts. In the expansion cohorts, prestudy tumor biopsies were required for central determination of EGFR T790M status. Patients were assessed for safety, pharmacokinetics, and efficacy. A total of 253 patients were treated. Among 31 patients enrolled in the dose-escalation cohorts, no dose-limiting toxic effects occurred at the doses evaluated. An additional 222 patients were treated in five expansion cohorts. The most common all-cause adverse events were diarrhea, rash, nausea, and decreased appetite. The overall objective tumor response rate was 51% (95% confidence interval [CI], 45 to 58). Among 127 patients with centrally confirmed EGFR T790M who could be evaluated for response, the response rate was 61% (95% CI, 52 to 70). In contrast, among 61 patients without centrally detectable EGFR T790M who could be evaluated for response, the response rate was 21% (95% CI, 12 to 34). The median progression-free survival was 9.6 months (95% CI, 8.3 to not reached) in EGFR T790M-positive patients and 2.8 months (95% CI, 2.1 to 4.3) in EGFR T790M-negative patients. AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors. (Funded by AstraZeneca; ClinicalTrials.gov number, NCT01802632.).
    New England Journal of Medicine 04/2015; 372(18):1689-99. DOI:10.1056/NEJMoa1411817 · 54.42 Impact Factor
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    ABSTRACT: The incidence of oral tongue cancer (OTC) in the US is increasing in women. To understand this phenomenon, we examined factors influencing OTC incidence and survival. We identified women diagnosed with OTC that were reported to the Surveillance, Epidemiology and End Results (SEER) program from 1973 to 2010. Incidence and survival rates were compared across metropolitan, urban and rural residential settings and several other demographic categories by calculating rate ratios (RRs) with the corresponding 95% confidence intervals (CIs). We examined changes in incidence of OTC across racial groups using joinpoint analyses since 1973, and assessed factors associated with survival. Patients diagnosed prior to 1988 were excluded from the survival analysis due to lack of data on treatment. OTC incidence in white females demonstrated a significant upward trend with 0.53 annual percentage change (APC) between 1973 and 2010. The change seems to be limited to white women under the age of 50years and appears to have become pronounced in the 1990s. For African Americans (AA) on the other hand, the incidence has decreased. Incidence estimates did not differ in metropolitan, small urban and rural setting. The 1-, 5- and 10-year relative survival estimates were 86%, 63% and 54% for white women, and 76%, 46% and 33% for AA women. On multivariable analyses factors significantly associated with better survival included lower stage, younger age, married status, and receipt of surgical treatment, but not race. The racial disparity in OTC survival is evident, but may be attributable to the differences in stage at diagnosis as well as access to and receipt of care. As the incidence of OTC is increasing in young white women, identifying the risk factors in this group may lead to a better understanding of OTC causes. Copyright © 2015 Elsevier Ltd. All rights reserved.
    04/2015; 51(6). DOI:10.1016/j.oraloncology.2015.03.010
  • Annals of Oncology 04/2015; 26(suppl 1):i30-i30. DOI:10.1093/annonc/mdv050.02 · 6.58 Impact Factor
  • Annals of Oncology 04/2015; 26(suppl 1):i60-i60. DOI:10.1093/annonc/mdv128.05 · 6.58 Impact Factor
  • Annals of Oncology 04/2015; 26(suppl 1):i32-i33. DOI:10.1093/annonc/mdv050.08 · 6.58 Impact Factor
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    ABSTRACT: Clinical variables associated with 30-day mortality after lung cancer surgery are well known. However, the effects of nonclinical factors, including insurance coverage, household income, education, type of treatment center, and area of residence, on short-term survival are less appreciated. We studied the National Cancer Data Base, a joint endeavor of the Commission on Cancer of the American College of Surgeons and the American Cancer Society, to identify disparities in 30-day mortality after lung cancer resection based on these nonclinical factors. We performed a retrospective cohort analysis of patients undergoing lung cancer resection from 2003 to 2011 using the National Cancer Data Base. Data were analyzed using a multivariable logistic regression model to identify risk factors for 30-day mortality. During our study period, 215,645 patients underwent lung cancer resection. We found that clinical variables, such as age, sex, comorbidity, cancer stage, preoperative radiation, extent of resection, positive surgical margins, and tumor size were associated with 30-day mortality after resection. Nonclinical factors, including living in lower-income neighborhoods with a lesser proportion of high school graduates, and receiving cancer care at a nonacademic medical center were also independently associated with increased 30-day postoperative mortality. This study represents the largest analysis of 30-day mortality for lung cancer resection to date from a generalizable national cohort. Our results demonstrate that, in addition to known clinical risk factors, several nonclinical factors are associated with increased 30-day mortality after lung cancer resection. These disparities require additional investigation to improve lung cancer patient outcomes. Published by Elsevier Inc.
    Journal of the American College of Surgeons 04/2015; 221(2). DOI:10.1016/j.jamcollsurg.2015.03.056 · 4.45 Impact Factor
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    ABSTRACT: The single-agent activity of rapalogs (rapamycin and its analogues) in most tumor types has been modest at best. The underlying mechanisms are largely unclear. In this report, we have uncovered a critical role of GSK3 in regulating degradation of some oncogenic proteins induced by rapalogs and cell sensitivity to rapalogs. The basal level of GSK3 activity was positively correlated with cell sensitivity of lung cancer cell lines to rapalogs. GSK3 inhibition antagonized rapamycin's growth inhibitory effects both in vitro and in vivo, while enforced activation of GSK3β sensitized cells to rapamycin. GSK3 inhibition rescued rapamcyin-induced reduction of several oncogenic proteins such as cyclin D1, Mcl-1 and c-Myc, without interfering with the ability of rapamycin to suppress mTORC1 signaling and cap binding. Interestingly, rapamycin induces proteasomal degradation of these oncogenic proteins, as evidenced by their decreased stabilities induced by rapamcyin and rescue of their reduction by proteasomal inhibition. Moreover, acute or short-time rapamycin treatment dissociated not only raptor, but also rictor from mTOR in several tested cell lines, suggesting inhibition of both mTORC1 and mTORC2. Thus, induction of GSK3-dependent degradation of these oncogenic proteins is likely secondary to mTORC2 inhibition; this effect should be critical for rapamycin to exert its anticancer activity.
    Oncotarget 03/2015; · 6.63 Impact Factor
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    ABSTRACT: Preclinical evidence supports the clinical investigation of inhibitors to the insulin-like growth factor receptor (IGFR) and the epidermal growth factor receptor (EGFR) either alone or in combination as treatment for patients with nonsmall cell lung cancer (NSCLC). Patients with chemotherapy-naïve, advanced NSCLC who had an Eastern Cooperative Oncology Group performance status of 0 or 1 were eligible. Patients were randomized to receive carboplatin intravenously at an area under the plasma drug concentration-time curve of 6.0 plus paclitaxel 200 mg/m(2) intravenously on day 1 every 3 weeks combined with either intravenous cetuximab weekly (arm A), intravenous cixutumumab every 2 weeks (arm B), or both (arm C). Patients who had nonprogessing disease after 12 weeks of therapy were permitted to continue on maintenance antibody therapy until they developed progressive disease. The primary endpoint was progression-free survival (PFS). The study design required 180 eligible patients and had 88% power to detect a 60% increase in median PFS for either comparison (arm A vs arm C or arm B vs arm C) using the log-rank test. From September 2009 to December 2010, 140 patients were accrued. The study was closed to accrual early because of an excessive number of grade 5 events reported on arms A and C. Thirteen patients died during treatment (6 patients on arm A, 2 patients on arm B, and 5 patients on arm C), including 9 within approximately 1 month of starting therapy. The estimated median PFS for arms A, B, and C were similar at 3.4 months, 4.2 months, and 4 months, respectively. On the basis of the apparent lack of efficacy and excessive premature deaths, the current results do not support the continued investigation of carboplatin, paclitaxel, and cixutumumab either alone or in combination with cetuximab for patients with advanced NSCLC. Cancer 2015. © 2015 American Cancer Society. © 2015 American Cancer Society.
    Cancer 03/2015; 121(13). DOI:10.1002/cncr.29308 · 4.90 Impact Factor
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    Fadlo R. Khuri · Suresh S. Ramalingam
    Cancer 03/2015; 121(14). DOI:10.1002/cncr.29361 · 4.90 Impact Factor
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    ABSTRACT: Treatment guidelines provide recommendations, but cannot account for the wide variability in patient-tumor characteristics in individual patients. We developed an online interactive decision tool to provide expert recommendations for specific patient scenarios in the first-line and maintenance settings for advanced NSCLC. We sought to determine how providing expert feedback would influence clinical decision-making. Five lung cancer experts selected treatment for 96 different patient cases based on tumor-specific features. These data were used to develop an online decision tool. Participant physicians entered variables for their patient scenario with treatment choices, and then received expert treatment recommendations for that scenario. To determine the impact on decision-making, users were asked whether the expert feedback impacted their original plan. A total of 442 individual physicians, of which 88% were from outside the USA, entered 653 cases, with report on impact in 389 cases. Expert feedback affected treatment choice in 73% of cases (23% changed, 50% confirmed decisions). For cases with EGFR mutation or ALK fusion, all experts selected targeted therapy while 51% and 58% of participants did not. Greater variability was seen between experts and participants for cases involving EGFR or ALK wild-type tumors. Participants were 2.5-fold more likely to change to expert recommended therapy for ALK fusions than for EGFR mutations (P = 0.017). This online tool for treatment decision-making resulted in a positive influence on clinician's decisions. This approach offers opportunities for improving quality of care and meets an educational need in application of new therapeutic paradigms.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 02/2015; Publish Ahead of Print. DOI:10.1097/JTO.0000000000000508 · 5.80 Impact Factor
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    ABSTRACT: Patients with squamous non-small-cell lung cancer that is refractory to multiple treatments have poor outcomes. We assessed the activity of nivolumab, a fully human IgG4 PD-1 immune checkpoint inhibitor antibody, for patients with advanced, refractory, squamous non-small-cell lung cancer. We did this phase 2, single-arm trial at 27 sites (academic, hospital, and private cancer centres) in France, Germany, Italy, and USA. Patients who had received two or more previous treatments received intravenous nivolumab (3 mg/kg) every 2 weeks until progression or unacceptable toxic effects. The primary endpoint was the proportion of patients with a confirmed objective response as assessed by an independent radiology review committee. We included all treated patients in the analyses. This study is registered with ClinicalTrials.gov, number NCT01721759. Between Nov 16, 2012, and July 22, 2013, we enrolled and treated 117 patients. 17 (14·5%, 95% CI 8·7-22·2) of 117 patients had an objective response as assessed by an independent radiology review committee. Median time to response was 3·3 months (IQR 2·2-4·8), and median duration of response was not reached (95% CI 8·31-not applicable); 13 (77%) of 17 of responses were ongoing at the time of analysis. 30 (26%) of 117 patients had stable disease (median duration 6·0 months, 95% CI 4·7-10·9). 20 (17%) of 117 patients reported grade 3-4 treatment-related adverse events, including: fatigue (five [4%] of 117 patients), pneumonitis (four [3%]), and diarrhoea (three [3%]). There were two treatment-associated deaths caused by pneumonia and ischaemic stroke that occurred in patients with multiple comorbidities in the setting of progressive disease. Nivolumab has clinically meaningful activity and a manageable safety profile in previously treated patients with advanced, refractory, squamous non-small cell lung cancer. These data support the assessment of nivolumab in randomised, controlled, phase 3 studies of first-line and second-line treatment. Bristol-Myers Squibb. Copyright © 2015 Elsevier Ltd. All rights reserved.
    The Lancet Oncology 02/2015; 16(3). DOI:10.1016/S1470-2045(15)70054-9 · 24.73 Impact Factor
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    ABSTRACT: The Lung Master Protocol (Lung-MAP, S1400) is a groundbreaking clinical trial designed to advance the efficient development of targeted therapies for squamous cell cancer (SCCA) of the lung. There are no approved targeted therapies specific to advanced lung SCCA, although The Cancer Genome Atlas (TCGA) project and similar studies have detected a significant number of somatic gene mutations/amplifications in lung SCCA, some of which are targetable by investigational agents. However, the frequency of these changes is low (5-20%), making recruitment and study conduct challenging in the traditional clinical trial setting. Here we describe our approach to development of a biomarker-driven phase 2/3 multi-substudy "Master Protocol," employing a common platform (Next Generation DNA Sequencing) to identify actionable molecular abnormalities, followed by randomization to the relevant targeted therapy versus standard of care. Copyright © 2015, American Association for Cancer Research.
    Clinical Cancer Research 02/2015; 21(7). DOI:10.1158/1078-0432.CCR-13-3473 · 8.19 Impact Factor
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    Clinical Cancer Research 02/2015; · 8.19 Impact Factor

Publication Stats

3k Citations
1,667.14 Total Impact Points

Institutions

  • 2008–2015
    • Emory University
      • Winship Cancer Institute
      Atlanta, Georgia, United States
  • 2012
    • University of Miami Miller School of Medicine
      Miami, Florida, United States
  • 2010
    • Penn State Hershey Medical Center and Penn State College of Medicine
      Hershey, Pennsylvania, United States
  • 2004–2010
    • University of Pittsburgh
      • • Department of Pharmacology and Chemical Biology
      • • Department of Medicine
      Pittsburgh, Pennsylvania, United States
  • 2007–2008
    • Fox Chase Cancer Center
      Filadelfia, Pennsylvania, United States