Bio

Bio


Justin Nathaniel Carter earned his B.A. in 2014 from Columbia University. While attending Columbia, he volunteered as tour-guide, a student-life ambassador, a member of the student council, and was elected University Senator. As a Senator, he served on the Student Affairs (SAC), Budget & Finance, Housing, and Alumni Affairs committees. He also served on the Columbia University Trustee?s Advisory Committee for Socially Responsible Investing (ACSRI) and as the Undergraduate Representative to the Columbia Alumni Association (CAA) Board. While living in New York, he was a New York City Emergency Medical Technician, A New York State EMT Instructor, and served as Chief of Operations for Columbia University's Emergency Medical Service.

Justin initially joined Stanford through the Department of Radiation Oncology as a Clinical Research Assistant and Research Coordinator. He assisted the Thoracic Radiation Oncology Group, working primarily with Drs. Bill Loo and Max Diehn on biomarker, immunotherapy, and translative imaging in thoracic cancers. He has presented at several conferences and symposiums, and has contributed to publications in various oncology related journals. Justin now supports the departments of Urology, Cardio-Thoracic Surgery, and Otolaryngology as a Research Process Manager representing the Research Management Group.

Justin is a 2013 Columbia Health Services Summer Fellowship recipient where he focused on a multifaceted project addressing the modernization, sustainability, and continuity of operating a prehospital emergency medical service in bustling New York City. For several years he volunteered as a skills instructor with Stanford's Department of Emergency Medicine EMT Program. Drawing on his previous medical and management roles, He has traveled several times to Nepal in coordination with Stanford's Nepal Medical Project to facilitate a recertification program for in-country EMT/pre-hospital providers and to assist with modernization and analysis of updates with the Nepal Ambulance Service

His interests include the intersections of communications & outreach, medicine, government & health policy, and strategic management. He continues to work with several PIs conducting medical research and is pursuing a Master's degree.

Honors & Awards


  • Honorable Service Award, Columbia University Emergency Medical Service (2014)
  • Graduating Head Senior Marshal, Columbia University (2014)
  • Graduating Honors, Columbia University Office of Multicultural Affairs (2014)
  • Spirit Award, Columbia University (2014)
  • Health Services Award, Columbia University (2012 - 2014)
  • Service Award, Columbia University (2012, 2013)
  • Permanent Member, Alpha Gamma Sigma Honor Society - Gamma Iota Chapter (2011)

Education & Certifications


  • BLS, American Red Cross
  • A.A., West Valley College (2011)
  • B.A., Columbia University (2014)
  • M.S., Columbia University
  • EMT-B, New York State Department of Health (2012)

Service, Volunteer and Community Work


  • Board Member, Columbia Alumni Association, Columbia University in the City of New York

    The CAA Board is the governing body of the Columbia Alumni Association and controls the management, policies, activities, funds and affairs of CAA. Outside of the Columbia University Senate, the CAA Board is the only group of individuals who's constituency is representative of all the colleges and schools from Columbia and seeks to keep alumni connected between and to the University at large. Learn more at: Alumni.Columbia.edu

    Location

    Based in New York, NY

  • Board Member, Columbia Club of NorCal

    Representing the largest community of Columbia University alumni outside of the New York/Tri-state area, the Columbia Club of NorCal aims to connect those with an affiliation to Alma Mater through networking, social, and humanitarian events. Learn more at: NorCal.Alumni.Columbia.edu

    Location

    San Francisco Bay Area

Publications

All Publications


  • Predicting Survival for Patients with Metastatic Disease. International journal of radiation oncology, biology, physics Benson, K. R., Aggarwal, S., Carter, J. N., von Eyben, R., Pradhan, P., Prionas, N. D., Bui, J. L., Soltys, S. G., Hancock, S., Gensheimer, M. F., Koong, A. C., Chang, D. T. 2019

    Abstract

    PURPOSE: This prospective study aimed to determine the accuracy of radiation oncologists in predicting the survival of patients with metastatic disease receiving radiotherapy and to understand factors associated with their accuracy.METHODS AND MATERIALS: This single-institution study surveyed 22 attending radiation oncologists to estimate patient survival. Survival predictions were defined as accurate if the observed survival (OS) was within the correct survival prediction category (0-6 months, >6-12 months, >12-24 months, and >24 months). The physicians made survival estimates for each course of radiation, yielding 877 analyzable predictions for 689 unique patients. Data analysis included Stuart's Tau C, logistic regression models, ordinal logistic regression models, and stepwise selection to examine variable interactions.RESULTS: Of the 877 radiation oncologists' predictions, 39.7% were accurate, 26.5% underestimations, and 33.9% overestimations. Stuart's Tau C showed low correlation between OS and survival estimates (0.3499), consistent with the inaccuracy reported in literature. However, results showed less systematic over-prediction than reported in the literature. Karnofsky performance status (KPS) was the most significant predictor of accuracy with greater accuracy for patients with shorter OS. Estimates were also more accurate for patients with lower KPS. Accuracy by patient age varied by primary site and race. Physician years of experience did not correlate with accuracy.CONCLUSIONS: The sampled radiation oncologists have relatively low accuracy in predicting patient survival. Future investigation should explore how survival estimates influence treatment decisions and how to improve survival prediction accuracy.

    View details for DOI 10.1016/j.ijrobp.2019.10.032

    View details for PubMedID 31682969

  • Circulating Tumor DNA Quantitation for Early Response Assessment of Immune Checkpoint Inhibitors for Metastatic Non-Small Cell Lung Cancer Chaudhuri, A. A., Nabet, B. Y., Merriott, D. J., Jin, M., Chen, E. L., Chabon, J. J., Newman, A. M., Stehr, H., Say, C., Carter, J. N., Walters, S., Becker, H., Das, M., Padda, S. K., Loo, B. W., Wakelee, H. A., Neal, J. W., Alizadeh, A. A., Diehn, M. ELSEVIER SCIENCE INC. 2018: E1?E2
  • 18F-EF5 Pet-Based Imageable Hypoxia Predicts for Local Control in Tumors Treated With Conformal Radiotherapy Qian, Y., Liu, Y., Von Eyben, R., Carter, J. N., Pollom, E. L., Harris, J. P., Prionas, N. D., Binkley, M. S., Simmons, A., Diehn, M., Chin, F. T., Shultz, D. B., Brown, J., Maxim, P. G., Koong, A. C., Graves, E. E., Loo, B. W. ELSEVIER SCIENCE INC. 2018: E17?E18
  • 18F-EF5 PET-based Imageable Hypoxia Predicts Local Recurrence in Tumors Treated With Highly Conformal Radiation Therapy. International journal of radiation oncology, biology, physics Qian, Y., Von Eyben, R., Liu, Y., Chin, F. T., Miao, Z., Apte, S., Carter, J. N., Binkley, M. S., Pollom, E. L., Harris, J. P., Prionas, N. D., Kissel, M., Simmons, A., Diehn, M., Shultz, D. B., Brown, J. M., Maxim, P. G., Koong, A. C., Graves, E. E., Loo, B. W. 2018

    Abstract

    Tumor hypoxia contributes to radiation resistance. A noninvasive assessment of tumor hypoxia would be valuable for prognostication and possibly selection for hypoxia-targeted therapies. 18F-pentafluorinated etanidazole (18F-EF5) is a nitroimidazole derivative that has demonstrated promise as a positron emission tomography (PET) hypoxia imaging agent in preclinical and clinical studies. However, correlation of imageable hypoxia by 18F-EF5 PET with clinical outcomes after radiation therapy remains limited.Our study prospectively enrolled 28 patients undergoing radiation therapy for localized lung or other tumors to receive pretreatment 18F-EF5 PET imaging. Depending on the level of 18F-EF5 tumor uptake, patients underwent functional manipulation of tumor oxygenation with either carbogen breathing or oral dichloroacetate followed by repeated 18F-EF5 PET. The hypoxic subvolume of tumor was defined as the proportion of tumor voxels exhibiting higher 18F-EF5 uptake than the 95th percentile of 18F-EF5 uptake in the blood pool. Tumors with a hypoxic subvolume ? 10% on baseline 18F-EF5 PET imaging were classified as hypoxic by imaging. A Cox model was used to assess the correlation between imageable hypoxia and clinical outcomes after treatment.At baseline, imageable hypoxia was demonstrated in 43% of all patients (12 of 28), including 6 of 16 patients with early-stage non-small cell lung cancer treated with stereotactic ablative radiation therapy and 6 of 12 patients with other cancers. Carbogen breathing was significantly associated with decreased imageable hypoxia, while dichloroacetate did not result in a significant change under our protocol conditions. Tumors with imageable hypoxia had a higher incidence of local recurrence at 12 months (30%) than those without (0%) (P < .01).Noninvasive hypoxia imaging by 18F-EF5 PET identified imageable hypoxia in about 40% of tumors in our study population. Local tumor recurrence after highly conformal radiation therapy was higher in tumors with imageable hypoxia.

    View details for PubMedID 29859786

  • Role of KEAP1/NRF2 and TP53 Mutations in Lung Squamous Cell Carcinoma Development and Radiation Resistance CANCER DISCOVERY Jeong, Y., Hoang, N. T., Lovejoy, A., Stehr, H., Newman, A. M., Gentles, A. J., Kong, W., Diana Truong, D., Martin, S., Chaudhuri, A., Heiser, D., Zhou, L., Say, C., Carter, J. N., Hiniker, S. M., Loo, B. W., West, R. B., Beachy, P., Alizadeh, A. A., Diehn, M. 2017; 7 (1): 86-101

    Abstract

    Lung squamous cell carcinoma (LSCC) pathogenesis remains incompletely understood, and biomarkers predicting treatment response remain lacking. Here, we describe novel murine LSCC models driven by loss of Trp53 and Keap1, both of which are frequently mutated in human LSCCs. Homozygous inactivation of Keap1 or Trp53 promoted airway basal stem cell (ABSC) self-renewal, suggesting that mutations in these genes lead to expansion of mutant stem cell clones. Deletion of Trp53 and Keap1 in ABSCs, but not more differentiated tracheal cells, produced tumors recapitulating histologic and molecular features of human LSCCs, indicating that they represent the likely cell of origin in this model. Deletion of Keap1 promoted tumor aggressiveness, metastasis, and resistance to oxidative stress and radiotherapy (RT). KEAP1/NRF2 mutation status predicted risk of local recurrence after RT in patients with non-small lung cancer (NSCLC) and could be noninvasively identified in circulating tumor DNA. Thus, KEAP1/NRF2 mutations could serve as predictive biomarkers for personalization of therapeutic strategies for NSCLCs.We developed an LSCC mouse model involving Trp53 and Keap1, which are frequently mutated in human LSCCs. In this model, ABSCs are the cell of origin of these tumors. KEAP1/NRF2 mutations increase radioresistance and predict local tumor recurrence in radiotherapy patients. Our findings are of potential clinical relevance and could lead to personalized treatment strategies for tumors with KEAP1/NRF2 mutations. Cancer Discov; 7(1); 86-101. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 1.

    View details for DOI 10.1158/2159-8290.CD-16-0127

    View details for Web of Science ID 000396017700024

    View details for PubMedCentralID PMC5222718

  • Early detection of molecular residual disease in localized lung cancer by circulating tumor DNA profiling. Cancer discovery Chaudhuri, A. A., Chabon, J. J., Lovejoy, A. F., Newman, A. M., Stehr, H., Azad, T. D., Khodadoust, M. S., Esfahani, M. S., Liu, C. L., Zhou, L., Scherer, F., Kurtz, D. M., Say, C., Carter, J. N., Merriott, D. J., Dudley, J. C., Binkley, M. S., Modlin, L., Padda, S. K., Gensheimer, M. F., West, R. B., Shrager, J. B., Neal, J. W., Wakelee, H. A., Loo, B. W., Alizadeh, A. A., Diehn, M. 2017

    Abstract

    Identifying molecular residual disease (MRD) after treatment of localized lung cancer could facilitate early intervention and personalization of adjuvant therapies. Here we apply Cancer Personalized Profiling by Deep Sequencing (CAPP-Seq) circulating tumor DNA (ctDNA) analysis to 255 samples from 40 patients treated with curative intent for stage I-III lung cancer and 54 healthy adults. In 94% of evaluable patients experiencing recurrence, ctDNA was detectable in the first post-treatment blood sample, indicating reliable identification of MRD. Post-treatment ctDNA detection preceded radiographic progression in 72% of patients by a median of 5.2 months and 53% of patients harbored ctDNA mutation profiles associated with favorable responses to tyrosine kinase inhibitors or immune checkpoint blockade. Collectively, these results indicate that ctDNA MRD in lung cancer patients can be accurately detected using CAPP-Seq and may allow personalized adjuvant treatment while disease burden is lowest.

    View details for PubMedID 28899864

  • Molecular profiling of single circulating tumor cells from lung cancer patients PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Park, S., Wong, D. J., Ooi, C. C., Kurtz, D. M., Vermesh, O., Aalipour, A., Suh, S., Pian, K. L., Chabon, J. J., Lee, S. H., Jamali, M., Say, C., Carter, J. N., Lee, L. P., Kuschner, W. G., Schwartz, E. J., Shrager, J. B., Neal, J. W., Wakelee, H. A., Diehn, M., Nair, V. S., Wang, S. X., Gambhir, S. S. 2016; 113 (52): E8379-E8386

    Abstract

    Circulating tumor cells (CTCs) are established cancer biomarkers for the "liquid biopsy" of tumors. Molecular analysis of single CTCs, which recapitulate primary and metastatic tumor biology, remains challenging because current platforms have limited throughput, are expensive, and are not easily translatable to the clinic. Here, we report a massively parallel, multigene-profiling nanoplatform to compartmentalize and analyze hundreds of single CTCs. After high-efficiency magnetic collection of CTC from blood, a single-cell nanowell array performs CTC mutation profiling using modular gene panels. Using this approach, we demonstrated multigene expression profiling of individual CTCs from non-small-cell lung cancer (NSCLC) patients with remarkable sensitivity. Thus, we report a high-throughput, multiplexed strategy for single-cell mutation profiling of individual lung cancer CTCs toward minimally invasive cancer therapy prediction and disease monitoring.

    View details for DOI 10.1073/pnas.1608461113

    View details for PubMedID 27956614

  • Role of KEAP1/NRF2 and TP53 Mutations in Lung Squamous Cell Carcinoma Development and Radiation Resistance. Cancer discovery Jeong, Y., Hoang, N. T., Lovejoy, A., Stehr, H., Newman, A. M., Gentles, A. J., Kong, W., Truong, D., Martin, S., Chaudhuri, A., Heiser, D., Zhou, L., Say, C., Carter, J. N., Hiniker, S. M., Loo, B. W., West, R. B., Beachy, P., Alizadeh, A. A., Diehn, M. 2016

    Abstract

    Lung squamous cell carcinoma (LSCC) pathogenesis remains incompletely understood, and biomarkers predicting treatment response remain lacking. Here, we describe novel murine LSCC models driven by loss of Trp53 and Keap1, both of which are frequently mutated in human LSCCs. Homozygous inactivation of Keap1 or Trp53 promoted airway basal stem cell (ABSC) self-renewal, suggesting that mutations in these genes lead to expansion of mutant stem cell clones. Deletion of Trp53 and Keap1 in ABSCs, but not more differentiated tracheal cells, produced tumors recapitulating histologic and molecular features of human LSCCs, indicating that they represent the likely cell of origin in this model. Deletion of Keap1 promoted tumor aggressiveness, metastasis, and resistance to oxidative stress and radiotherapy (RT). KEAP1/NRF2 mutation status predicted risk of local recurrence after RT in patients with non-small lung cancer (NSCLC) and could be noninvasively identified in circulating tumor DNA. Thus, KEAP1/NRF2 mutations could serve as predictive biomarkers for personalization of therapeutic strategies for NSCLCs.We developed an LSCC mouse model involving Trp53 and Keap1, which are frequently mutated in human LSCCs. In this model, ABSCs are the cell of origin of these tumors. KEAP1/NRF2 mutations increase radioresistance and predict local tumor recurrence in radiotherapy patients. Our findings are of potential clinical relevance and could lead to personalized treatment strategies for tumors with KEAP1/NRF2 mutations. Cancer Discov; 7(1); 86-101. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 1.

    View details for PubMedID 27663899

  • Pre-treatment non-target lung FDG-PET uptake predicts symptomatic radiation pneumonitis following Stereotactic Ablative Radiotherapy (SABR). Radiotherapy and oncology Chaudhuri, A. A., Binkley, M. S., Rigdon, J., Carter, J. N., Aggarwal, S., Dudley, S. A., Qian, Y., Kumar, K. A., Hara, W. Y., Gensheimer, M., Nair, V. S., Maxim, P. G., Shultz, D. B., Bush, K., Trakul, N., Le, Q., Diehn, M., Loo, B. W., Guo, H. H. 2016; 119 (3): 454-460

    Abstract

    To determine if pre-treatment non-target lung FDG-PET uptake predicts for symptomatic radiation pneumonitis (RP) following lung stereotactic ablative radiotherapy (SABR).We reviewed a 258 patient database from our institution to identify 28 patients who experienced symptomatic (grade ? 2) RP after SABR, and compared them to 57 controls who did not develop symptomatic RP. We compared clinical, dosimetric and functional imaging characteristics between the 2 cohorts including pre-treatment non-target lung FDG-PET uptake.Median follow-up time was 26.9 months. Patients who experienced symptomatic RP had significantly higher non-target lung FDG-PET uptake as measured by mean SUV (p < 0.0001) than controls. ROC analysis for symptomatic RP revealed area under the curve (AUC) of 0.74, with sensitivity 82.1% and specificity 57.9% with cutoff mean non-target lung SUV > 0.56. Predictive value increased (AUC of 0.82) when mean non-target lung SUV was combined with mean lung dose (MLD). We developed a 0-2 point model using these 2 variables, 1 point each for SUV > 0.56 or MLD > 5.88 Gy equivalent dose in 2 Gy per fraction (EQD2), predictive for symptomatic RP in our cohort with hazard ratio 10.01 for score 2 versus 0 (p < 0.001).Patients with elevated pre-SABR non-target lung FDG-PET uptake are at increased risk of symptomatic RP after lung SABR. Our predictive model suggests patients with mean non-target lung SUV > 0.56 and MLD > 5.88 Gy EQD2 are at highest risk. Our predictive model should be validated in an external cohort before clinical implementation.

    View details for DOI 10.1016/j.radonc.2016.05.007

    View details for PubMedID 27267049

  • Integrated digital error suppression for improved detection of circulating tumor DNA NATURE BIOTECHNOLOGY Newman, A. M., Lovejoy, A. F., Klass, D. M., Kurtz, D. M., Chabon, J. J., Scherer, F., Stehr, H., Liu, C. L., Bratman, S. V., Say, C., Zhou, L., Carter, J. N., West, R. B., Sledge, G. W., Shrager, J. B., Loo, B. W., Neal, J. W., Wakelee, H. A., Diehn, M., Alizadeh, A. A. 2016; 34 (5): 547-555

    Abstract

    High-throughput sequencing of circulating tumor DNA (ctDNA) promises to facilitate personalized cancer therapy. However, low quantities of cell-free DNA (cfDNA) in the blood and sequencing artifacts currently limit analytical sensitivity. To overcome these limitations, we introduce an approach for integrated digital error suppression (iDES). Our method combines in silico elimination of highly stereotypical background artifacts with a molecular barcoding strategy for the efficient recovery of cfDNA molecules. Individually, these two methods each improve the sensitivity of cancer personalized profiling by deep sequencing (CAPP-Seq) by about threefold, and synergize when combined to yield ?15-fold improvements. As a result, iDES-enhanced CAPP-Seq facilitates noninvasive variant detection across hundreds of kilobases. Applied to non-small cell lung cancer (NSCLC) patients, our method enabled biopsy-free profiling of EGFR kinase domain mutations with 92% sensitivity and >99.99% specificity at the variant level, and with 90% sensitivity and 96% specificity at the patient level. In addition, our approach allowed monitoring of NSCLC ctDNA down to 4 in 10(5) cfDNA molecules. We anticipate that iDES will aid the noninvasive genotyping and detection of ctDNA in research and clinical settings.

    View details for DOI 10.1038/nbt.3520

    View details for PubMedID 27018799

  • Tracheal Diverticulum Following Paratracheal Hypofractionated Radiotherapy in the Setting of Prior and Subsequent Bevacizumab. Cure¯us Chaudhuri, A. A., Chen, J. J., Carter, J. N., Binkley, M. S., Kumar, K. A., Dudley, S. A., Sung, A. W., Loo, B. W. 2016; 8 (4)

    Abstract

    We present the case of a 63-year-old woman with limited metastatic colorectal cancer to the lungs and liver treated with FOLFIRI-bevacizumab, followed by consolidative hypofractionated radiotherapy to right paratracheal metastatic lymphadenopathy. We treated the right paratracheal site with 60 Gy in 15 fractions (70 Gy equivalent dose in 2 Gy fractions). The patient tolerated the treatment well, and six months later started a five-month course of FOLFIRI-bevacizumab for new metastatic disease. She presented to our clinic six months after completing this, complaining of productive cough with scant hemoptysis, and was found to have localized tracheal wall breakdown and diverticulum in the region of prior high-dose radiation therapy, threatening to progress to catastrophic tracheovascular fistula. This was successfully repaired surgically after a lack of response to conservative measures. We urge caution in treating patients with vascular endothelial growth factor (VEGF) inhibitors in the setting of hypofractionated radiotherapy involving the mucosa of tubular organs, even when these treatments are separated by months. Though data is limited as to the impact of sequence, this may be particularly an issue when VEGF inhibitors follow prior radiotherapy.

    View details for DOI 10.7759/cureus.578

    View details for PubMedID 27226939

  • Severe Chest Wall Toxicity From Cryoablation in the Setting of Prior Stereotactic Ablative Radiotherapy. Cure¯us Chaudhuri, A. A., Binkley, M. S., Aggarwal, S., Qian, Y., Carter, J. N., Shah, R., Loo, B. W. 2016; 8 (2)

    Abstract

    We present the case of a 42-year-old woman with metastatic synovial sarcoma of parotid origin, treated definitively with chemoradiation, who subsequently developed oligometastatic disease limited to the lungs. She underwent multiple left and right lung wedge resections and left lower lobectomy, followed by right lower lobe stereotactic ablative radiotherapy (SABR), 54 Gy in three fractions to a right lower lobe lesion abutting the chest wall. Two years later, she was treated with cryoablation for a separate right upper lobe nodule abutting the chest wall. Two months later, she presented with acute shortness of breath, pleuritic chest pain, decreased peripheral blood O2 saturation, and productive cough. A computed tomography (CT) scan demonstrated severe chest wall necrosis in the area of recent cryoablation that, in retrospect, also received a significant radiation dose from her prior SABR. This case demonstrates that clinicians should exercise caution in using cryoablation when treating lung tumors abutting a previously irradiated chest wall. Note: Drs. Loo and Shah contributed equally as co-senior authors.

    View details for DOI 10.7759/cureus.477

    View details for PubMedID 27004154

    View details for PubMedCentralID PMC4780688

  • Stress and Burnout Among Residency Program Directors in United States Radiation Oncology Programs INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS Aggarwal, S., Kusano, A. S., Carter, J. N., Gable, L., Thomas, C. R., Chang, D. T. 2015; 93 (4): 746-753

    Abstract

    To evaluate stressors among radiation oncology residency program directors (PDs) and determine the prevalence and indicators of burnout.An anonymous, online, cross-sectional survey was offered to PDs of US radiation oncology programs in the fall of 2014. Survey content examined individual and program demographics, perceptions surrounding the role of PD, and commonly encountered stressors. Burnout was assessed using the validated Maslach Burnout Inventory-Human Services Survey.In total, 47 of 88 PDs (53%) responded to the survey. Although 78% of respondents reported feeling "satisfied" or "highly satisfied" with their current role, 85% planned to remain as PD for <5 years. The most commonly cited stressors were satisfying Accreditation Council for Graduate Medical Education/Residency Review Committee requirements (47%), administrative duties (30%) and resident morale (28%). Three-quarters of respondents were satisfied that they became PDs. Overall, 11% of respondents met criteria for low burnout, 83% for moderate burnout, and 6% for high burnout. Not having served as a PD at a prior institution correlated with high depersonalization (OR 6.75, P=.04) and overall burnout (odds ratio [OR], 15.6; P=.04). Having more years on faculty prior to becoming PD correlated with less emotional exhaustion (OR, 0.44, P=.05) and depersonalization (OR, 0.20, P=.04). Finally, having dedicated time for PD duties correlated with less emotional exhaustion (OR, 0.27, P=.04).Moderate levels of burnout are common in U.S. radiation oncology PDs with regulatory stressors being common. Despite this, many PDs are fulfilled with their role. Longitudinal studies assessing dynamic external factors and their influence on PD burnout would be beneficial.

    View details for DOI 10.1016/j.ijrobp.2015.08.019

    View details for PubMedID 26530741

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