Kelly D Getz
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 1985–2026
About
Kelly D Getz, PhD, MPH, is an Assistant Professor of Epidemiology in Biostatistics and Epidemiology at the Perelman School of Medicine at the University of Pennsylvania. He is an investigator at the Center for Real-world Evidence on the Effectiveness and Safety of Therapeutics (CREST) and a Senior Scholar at the Center for Clinical Epidemiology & Biostatistics. His research interests broadly focus on the treatment and supportive care of children and young adults with cancer, with an emphasis on understanding and balancing therapeutic benefits and toxicity risks. He has a specific interest in the emerging field of cardio-oncology, particularly in the early detection of cardiotoxic side effects of cancer treatments and in mitigating cardiac disease as a barrier to effective cancer therapy. Additionally, he is engaged in identifying and reducing disparities in the treatment and outcomes of pediatric cancers. Dr. Getz's educational background includes a BS in Biology from Millersville University, an MPH in Epidemiology from Boston University School of Public Health, and a PhD in Epidemiology from the same institution. His work contributes to advancing knowledge in pediatric oncology, cardio-oncology, and health disparities, with numerous publications in these areas.
Research topics
- Medicine
- Internal medicine
- Oncology
- Immunology
- Cardiology
Selected publications
Air Pollution and Cardiac Remodeling and Function in Patients With Breast Cancer
JAMA Network Open · 2026-01-15
articleOpen accessImportance: The relationship between air pollution and cardiac remodeling in patients with cancer treated with cardiotoxic therapy is undefined. Objective: To assess the associations between air pollutants and changes in cardiac function, structure, and remodeling in patients with breast cancer treated with anthracyclines and/or trastuzumab therapy. Design, Setting, and Participants: This longitudinal prospective cohort study included patients with breast cancer enrolled at multiple sites of a quaternary health care system from July 1, 2010, to November 1, 2018. All participants were initiating anthracyclines and/or trastuzumab. Data were analyzed from December 1, 2024, to April 30, 2025. Exposures: Three-year average census tract-level concentrations of fine particulate matter with diameter of 2.5 µm or less (PM2.5), particulate matter with diameter of 10 µm or less (PM10), nitrogen dioxide (NO2), and ozone (O3). Main Outcomes and Measures: Core laboratory-quantified, echocardiography-derived measures of cardiac remodeling and function and incidence of cardiac dysfunction, defined as a left ventricular ejection fraction (LVEF) decline of 10% or more from baseline to less than 50%. Multivariable linear regression and generalized estimating equations defined the cross-sectional and longitudinal associations between air pollution and measures of cardiac remodeling and function. Cause-specific hazard models defined the adjusted associations between air pollution and cardiac dysfunction. Results: Across 580 female patients (median age, 50 years [IQR, 42-58 years]), 3642 echocardiograms were obtained at standardized time intervals over a median of 3.1 years (IQR, 2.3-3.6 years) and centrally quantified. Cardiac dysfunction was observed in 98 of 574 participants (17.1%). Concentrations of PM2.5 (median, 9.26 μg/m3 [IQR, 8.49-10.17 μg/m3]) and O3 (median, 47.00 parts per billion [ppb] [IQR, 45.50-48.19 ppb]) were each associated with cardiac dysfunction and adverse remodeling, cross-sectionally and longitudinally. Over time, each IQR-increment increase in PM2.5 (1.68 μg/m3) and O3 (2.69 ppb) was associated with a mean LVEF change of -1.3% (95% CI, -1.8% to -0.8%) and -1.4% (95% CI, -1.8% to -1.0%), respectively; worse longitudinal strain (-1.0% [95% CI, -1.3% to -0.7%] and -1.1% [95% CI, -1.3% to -0.8%], respectively); and left ventricular mass increase of 4.8 g/m2 (95% CI, 3.1-6.5 g/m2) and 3.2 g/m2 (95% CI, 2.1-4.3 g/m2), respectively. Patients in the highest tertiles of PM2.5 (adjusted hazard ratio [AHR], 2.03; 95% CI, 1.17-3.52) and O3 (AHR, 2.15; 95% CI, 1.23-3.78) exposure were at a significantly higher risk of cardiac dysfunction compared with those in the lowest tertile. Neither PM10 (AHR, 0.84; 95% CI, 0.49-1.44) nor NO2 (AHR, 0.92; 95% CI, 0.50-1.70) showed significant associations with cardiac dysfunction. Conclusions and Relevance: In this cohort study, PM2.5 and O3 exposure was independently associated with worse cardiac remodeling and function in patients with breast cancer treated with cardiotoxic therapy. These findings highlight the importance of modifying environmental exposures to mitigate cardiovascular disease risk.
SSRN Electronic Journal · 2026-01-01
preprintOpen accessTransplantation and Cellular Therapy · 2026-02-01
articleJNCI Journal of the National Cancer Institute · 2026-01-28
articleOpen accessMore than 60% of adult survivors of childhood cancer report medical financial hardship due to the cumulative costs of cancer-directed therapy and related chronic health conditions. Whether neurocognitive impairment as a late effect is associated with increased financial hardship is unknown. In a large national cohort of 3023 adult survivors of childhood cancer, we observed a dose-dependent relationship between neurocognitive impairment and financial hardship outcomes. Individuals with 4 impaired neurocognitive domains had over 3-fold increased odds of debt collection (OR = 3.12, 95% CI = 1.91-5.09) and bankruptcy (OR = 3.77, 95% CI = 2.01-7.07) compared to individuals with no impaired neurocognitive domains. After adjusting for education, employment, and household income, the independent association between neurocognitive impairment and financial hardship outcomes persisted suggesting that other mechanisms may be at play. Neurocognitive impairment is an important risk factor for medical financial hardship in this patient population and should be considered for targeted screening and intervention.
JAMA Oncology · 2025-10-23
articleSenior authorThis cohort study examines trends in dexrazoxane and cardiovascular health care use for children with acute myeloid leukemia (AML) in the US.
Pediatric Hematology and Oncology · 2025-12-13
articleOpen accessfollowed at a single center before and after guideline publication. CVD was defined as the first of abnormal transcranial Doppler ultrasound, silent cerebral infarct, steno-occlusive vasculopathy, or arterial ischemic stroke. Among 530 patients with SCD, hydroxyurea prescriptions rose post-guideline, with lower age at initiation. CVD was lower post-guideline (2.2/100py) versus pre-guideline (4.4/100py). However, MRI screening also decreased post-guideline, leading to lower CVD detection. Results suggest decreased CVD, including silent cerebral infarcts, in the era of early hydroxyurea use; further analyses addressing age at hydroxyurea initiation and relevant confounders are needed to confirm whether earlier hydroxyurea initiation improves protection against CVD.
Journal of Clinical Oncology · 2025-05-28
article10055 Background: Adult survivors of childhood cancer are at high risk for financial hardship due to the cumulative lifetime costs of cancer-directed therapy and chronic health conditions. Whether neurocognitive impairment increases the risk for financial hardship is unknown. Methods: Childhood cancer survivors (≥ 5-year survivors, diagnosed < 21 years of age between 1970-1999) enrolled in CCSS completed a validated self-report Neurocognitive Questionnaire (NCQ) in 2014 and a subsequent financial hardship survey (age ≥ 26 at survey completion) 3 years later. The NCQ measured neurocognitive impairment in four domains: (1) memory ; (2) task efficiency; (3) organization; (4) emotional regulation. NCQ was the exposure and operationalized as the number of impaired domains (0-4); in each domain, impairment was defined as a Z-score >90 th percentile. Financial hardship outcomes were measured in behavioral (e.g., delaying care due to cost), material (e.g., high out-of-pocket costs), and psychological (e.g., worry about financial situation) domains, as well as two discrete outcomes of debt collection and bankruptcy. Multivariable linear and logistic regressions were used to analyze associations adjusting for age, sex, and race/ethnicity. Results: 3023 survivors completed the NCQ (mean age 38.8, SD=8.6 years) and a subsequent financial hardship survey (mean age 41.5, SD=8.7 years). 13.9%, 8.1%, 6.0%, and 2.6% of survivors had neurocognitive impairments in 1-4 domains, respectively. Individuals with NCQ impairment had significantly higher mean standardized scores across all three financial hardship domains than those without NCQ impairments (Table). Each ordinal increase in the number of impaired NCQ domains was associated with a higher mean standardized score for both behavioral and material financial hardship. Individuals with impairments in all four NCQ domains were more likely to be sent to debt collection (54% vs. 25%, OR=3.82, 95% CI: 2.27-6.43) and file for bankruptcy protection (21% vs. 8%, OR=2.81, 95% CI: 1.53-5.17) compared to those without impairments. Conclusions: Cancer survivors with neurocognitive impairment are particularly vulnerable to financial hardship. This survivor population should be specifically assessed for these outcomes and offered support to prevent and mitigate financial challenges. Standardized mean differences (SMD) of each financial hardship domain by number of NCQ impairments compared to no NCQ impairments. Number of NCQ domains impaired Behavioral Domain SMD (95% CI) Material DomainSMD (95% CI) Psychological DomainSMD (95% CI) 1 0.21 (0.11-0.31) 0.20 (0.10-0.29) 0.41 (0.31-0.50) 2 0.39 (0.27-0.51) 0.32 (0.20-0.44) 0.38 (0.25-0.50) 3 0.48 (0.34-0.63) 0.35 (0.20-0.49) 0.44 (0.30-0.58) 4 0.72 (0.51-0.93) 0.72 (0.52-0.94) 0.74 (0.53-0.94)
BMC Cancer · 2025-10-20
articleOpen accessDown syndrome (DS) is a common genetic disorder resulting from an extra copy of genetic material from all or part of chromosome 21. Individuals with DS have a higher burden of co-occurring structural birth defects, neurocognitive delay, and chronic health conditions when compared to those without DS, as well as a 10 to 20-fold excess risk for acute leukemia (AL). Few studies have reported the late effects of cancer treatment in DS-AL survivors, and even fewer have compared outcomes to children with DS and no cancer history. The Children’s Oncology Group study ALTE22C1 was developed to address this knowledge gap. This study leverages both registry and site-based DS-AL survivor recruitment and a prospective/retrospective cohort design to compare chronic health conditions and neurocognitive outcomes experienced by DS-AL survivors to age and sex-matched individuals enrolled to a DS cohort for which cancer is exclusionary. Survivors 6–39 years old, ≥ 3 years from end of AL treatment, and in remission are eligible. Participants complete a medical conditions survey and neuropsychological battery by parent proxy and may also participate in an in-person physical and neurocognitive assessment. Biological samples are collected to evaluate molecular features associated with outcomes. This cooperative group study will identify the prevalence and severity of medical and neurocognitive outcomes in DS-AL survivors compared with non-DS AL and DS controls without cancer history. Results are anticipated to inform clinical practice guidelines for DS-AL survivors and improve survivor outcomes through mitigation of outcome disparities in this vulnerable population. Children’s Oncology Group study ALTE22C1 is registered under the ClinicalTrials.gov identifier NCT05702645.
Blood · 2025-11-03
articleOpen accessSenior authorAbstract Introduction: Non-Hispanic Black (NHB) and Hispanic children with acute myeloid leukemia (AML) have historically had worse overall survival (OS) compared to their non-Hispanic White (NHW) peers. While our prior work demonstrated comparable risk of relapse by race/ethnicity, it remains unknown whether there are differential outcomes post-relapse which could drive OS disparities. In a large, multi-institutional real-world cohort of children with AML, we evaluated by race/ethnicity (1) post-relapse OS, and (2) potential mechanistic drivers of post-relapse outcomes including frontline treatment history and clinical features at relapse. Methods: We conducted a retrospective cohort analysis of patients in the REAL-AML cohort, a multi-institutional real-world cohort including pediatric (&lt;19 years old) patients treated for de novo AML at 17 US institutions from 2011-2024. Patients with acute promyelocytic leukemia were excluded. This analysis was restricted to patients who experienced relapse following an initial complete remission (CR1) and who were identified as NHB, Hispanic, or NHW in the medical record. Multi-racial and other racial/ethnic groups were excluded from analyses due to small sample sizes. Kaplan Meier survival curves were generated for post-relapse OS (time elapsed between date of first relapse and death from any cause). Cox models compared the hazard of death by race/ethnicity adjusting for a priori determined factors of age at relapse, sex, and cytomolecular risk profile at relapse. We performed pairwise comparisons between NHB and Hispanic patients against NHW patients (reference group) using chi-square and Fisher's exact tests for frontline therapy characteristics (history of bacteremia/sepsis, CTCAE Grade ≥2 cardiotoxicity, dexrazoxane receipt, hematopoietic stem cell transplant [HSCT] receipt in CR1, completion of frontline therapy) and clinical characteristics at relapse (early vs. late relapse, cytomolecular risk profile, body mass index [BMI], acuity, Grade ≥2 cardiotoxicity measured by echocardiogram within 7 days of relapse). Early relapse was defined as &lt;1 year from diagnosis. Cytomolecular risk profile was operationalized as only favorable markers vs. both favorable and unfavorable vs. neutral vs. only unfavorable. Acuity was defined as requiring ICU-level of care within initial 72 hours of relapse presentation. Results: A total of 268 patients (16.0% NHB, 29.9% Hispanic, median follow up 29.2 months) were included in the analytic cohort. Overall, the 3-year post-relapse OS was 41.0% (NHB 34.9%, Hispanic 40.0%, NHW 43.4%). In adjusted multivariable analyses, NHB patients experienced increased hazard of death (HR 1.64, 95% CI: 1.06-2.56) while Hispanic patients had similar outcomes (HR 1.14, 95% CI: 0.79-1.63) compared to NHW patients. This effect was restricted to outcomes for patients experiencing early relapse (NHB 3-year post-early relapse OS 8.7% vs. Hispanic 25.6% vs. NHW 25.3%). The incidence of early relapse was comparable across race/ethnicity (NHB 53.5%, Hispanic 53.8%, NHW 54.5%). We did not observe any statistically significant racial/ethnic differences in frontline bacteremia/sepsis, cardiotoxicity, dexrazoxane receipt, HSCT in CR1, rates of frontline therapy completion, or acuity at time of relapse. At relapse, NHB patients were more likely to have only favorable cytomolecular markers (23.8% vs. 9.8% in NHW patients, p=0.03). Compared to NHW patients (29.8%), both Hispanic (47.1%, p=0.03) and NHB (56.2%, p=0.01) patients were more likely to be overweight/obese. Seven percent of NHB patients had Grade ≥2 left ventricular systolic dysfunction on their most recent echo at relapse; this dysfunction was not observed in any of the NHW or Hispanic patients.Conclusion: NHB children with AML experience greater than 50% increased hazard of death post-relapse compared to NHW children, driven by poor outcomes after early relapse. This survival disparity occurs despite comparable rates of several major frontline therapy characteristics and overall rates of frontline therapy completion, suggesting that downstream intermediates are driving OS differences. Our data indicate potential differences in cardiovascular risk at the time of relapse, including elevated BMI and cardiac dysfunction. An expanded analysis will examine whether these differences mediate survival through re-induction regimen selection, relapse treatment response, HSCT receipt, and treatment-related mortality.
JCO Oncology Practice · 2025-09-19
articlePURPOSE: Current care guidelines for children with AML recommend hospitalization during severe neutropenia. However, selected patients discharged before neutrophil recovery have similar chemotherapy course-specific bacteremia and mortality rates to those who remain hospitalized. On the basis of published literature, we developed a toolkit to guide outpatient care after myelosuppressive AML chemotherapy and piloted its implementation at a single institution. We present the pilot clinical and implementation outcomes. METHODS: The AML Care at Home toolkit includes a discharge eligibility assessment tool and outpatient management guidelines for pediatric patients with AML and was implemented on November 15, 2022. Toolkit reach, defined as the proportion of postinduction 1 courses with toolkit use (target: 60%), was the coprimary implementation outcome, and total inpatient days per course was the coprimary clinical outcome. Chart abstractions were used to ascertain total inpatient days per course and other clinical outcome designations. RESULTS: During this pilot implementation program, 22 patients underwent 48 postinduction 1 chemotherapy courses. The toolkit was used in 33 (68.8%) courses. Appropriate toolkit use allowed for early discharge in 21 (43.8%) courses and directed inpatient recovery in 11 (22.9%). Median total inpatient days were markedly fewer for toolkit-guided early-discharge courses (8 days, IQR, 5.5-14.5) than toolkit-guided inpatient-only courses (26 days, IQR, 22-39) or when the toolkit was not used as intended (31 days, IQR, 25.3-34.8). CONCLUSION: Pilot implementation of the AML Care at Home toolkit exceeded our target reach goal and led to fewer inpatient days per course than expected on the basis of previous studies of outpatient neutropenia management. These data reflect the utility of a toolkit created on the basis of published data to identify and support appropriate patients for early hospital discharge and safe outpatient monitoring.
Recent grants
NIH · $2.3M · 2022–2027
NIH · $716k · 2018–2024
Frequent coauthors
- 208 shared
Richard Aplenc
Hospital for Sick Children
- 152 shared
Yimei Li
Children's Hospital of Philadelphia
- 132 shared
Brian T. Fisher
University of Pennsylvania
- 96 shared
Tamara P. Miller
Children's Healthcare of Atlanta
- 93 shared
Alix E. Seif
Children's Hospital of Philadelphia
- 69 shared
M. Monica Gramatges
Texas Children's Hospital
- 52 shared
Todd A. Alonzo
Children's Oncology Group
- 50 shared
Yuan‐Shung Huang
Children's Hospital of Philadelphia
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