David Spencer Mangum
· Associate Professor (Clinical)VerifiedUniversity of Utah · Hematology & Oncology
Active 2007–2026
About
David Spencer Mangum, MD, is an Assistant Professor of Pediatrics at the University of Utah, specializing in Pediatric Hematology Oncology within the Division of Pediatric Hematology Oncology. He received his medical degree from the Albert Einstein College of Medicine, affiliated with Yeshiva University, and completed his Pediatric residency at Primary Children’s Hospital, affiliated with the University of Utah. His training includes a Pediatric Hematology Oncology Fellowship at St. Jude Children’s Research Hospital, affiliated with the University of Tennessee, followed by a two-year Physician Scientist Training Program fellowship at St. Jude, where he also continued patient care. Dr. Mangum’s academic interests have primarily focused on Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia. His clinical practice encompasses care for patients with Leukemias, Lymphomas, and histiocytic disorders, with the capability to treat the entire pediatric hematology oncology spectrum. His research contributions include characterizing children and adolescents with acute lymphoblastic leukemia, exploring genetic alterations in leukemia, and investigating outcomes related to specific deletions and mutations. His work aims to improve understanding and treatment of pediatric hematologic malignancies, contributing to the advancement of clinical care and scientific knowledge in this field.
Research topics
- Medicine
- Genetics
- Pathology
- Pediatrics
- Immunology
- Oncology
- Biology
- Internal medicine
Selected publications
Pediatric Blood & Cancer · 2026-05-08
articleOpen accessBACKGROUND: Blinatumomab is a bispecific T-cell engager approved for the treatment of pediatric B-cell acute lymphoblastic leukemia (B-ALL). Outpatient home infusion reduces hospitalization burden and optimizes resource utilization, but is logistically challenging. METHODS: Our institution developed a multidisciplinary outpatient blinatumomab protocol. The workflow included early prior authorization, home healthcare (HH) partnerships, and standardized procedures for outpatient management. Clinical and logistical data were prospectively collected from August 2024 to August 2025. RESULTS: Since initiation, 50 patients aged 1-23 years have received blinatumomab. Patients resided within five states across the Intermountain West, with distances to the treating hospital ranging from 4.8 to 640 miles (mean 109 miles). Thirty patients (60%) lived within 50 miles of the treating institution, four (8%) lived 50-100 miles away, and 16 (32%) resided more than 100 miles away. All patients were able to receive blinatumomab outpatient, with 96% of patients able to receive services locally for the majority of the infusion period. Ninety-eight percent of patients used HH for outpatient drug delivery and/or nursing care. Our workflow standardized agency responsibilities, bag change frequency, and emergency contact protocols. This model limited inpatient stays to 24-48 h for most patients, expanded access across a large geographic area, and decreased travel burden. CONCLUSIONS: Outpatient blinatumomab administration is feasible, safe, and resource-efficient when supported by a structured care coordination framework. Partnerships with HH providers, proactive insurance authorization, and standardized troubleshooting protocols are critical for success. This model has reduced costs, preserved hospital resources, and improved quality of life.
Complete Recovery of Severe Nelarabine Neurotoxicity in a Pediatric ETP‐ALL Patient
Pediatric Blood & Cancer · 2025-11-02 · 1 citations
articleSenior authorCorrespondingThe authors declare no conflicts of interest. Data sharing is not applicable to this article as no new datasets were generated or analyzed during the current study.
Pediatric Blood & Cancer · 2025-04-23
articleOpen access1st authorCorrespondingCells painted on glass under magnified light, Revealed the foe that you must soon fight. There's a chance for cure, I begin to explain, But a price will be paid when vial hits vein. What piece of you will be laid at that altar? Your heart, your lungs, the blood of another? But the cure you seek is not mine to give, I do not choose who dies, who lives. Day and night I will carefully plan To stack the odds the best I can. I'll mix my elixirs and brew my potions To win your place among the chosen. But if winning the battle were mine to choose, No life in my hands would ever lose. The cure you seek is not mine to give, I do not choose who dies, who lives. In sterile tubes, new cures await, But for you today, those cures are too late. Progress takes time and time can't be borrowed, My path goes on, as others will follow. While for this day our options are few, Tomorrow is ours to create something new. The cure you seek is not mine to give, But we will not stop, until it is. The author declares no conflicts of interest. Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
Blood Neoplasia · 2025-07-25 · 1 citations
articleOpen access• Enitociclib synergizes with MI-463 to effectively decrease HOXA9 protein levels in infant KMT2A-r leukemia cells. • Enitociclib potentiates the cytotoxicity of venetoclax in relatively venetoclax-resistant KMT2A-r leukemic cells. The KMT2A-rearranged (KMT2A-r) leukemia is one of the most challenging cancers to treat in children, owing to the higher relapse rates and chemoresistance frequently observed in this patient population. At the molecular level, chromosomal translocation in the KMT2A gene leads to a deregulated epigenetic landscape resulting in the upregulation of transcription factors like HOXA9 , consequently contributing to leukemogenesis. One crucial component of the oncogenic KMT2A-r complex is the involvement of positive transcription elongation factor b, which is composed of cyclin T and cyclin-dependent kinase 9 (CDK9), which leads to the dysregulation of transcriptional elongation. This study investigated the function of enitociclib, a small molecule CDK9 inhibitor in clinical development that has shown effective activity in other tumor types. Enitociclib showed growth inhibition and an on-target effect in KMT2A-r leukemic cells with a significant decrease in MYC and MCL-1 protein levels. Moreover, enitociclib was found to reduce the growth advantage provided to leukemic cells by the bone marrow microenvironment. In addition, it demonstrates the ability to synergize with menin inhibitors, leading to an effective decrease in HOXA9 protein levels in KMT2A-r infant leukemia cells. Enitociclib also potentiates the cytotoxicity of venetoclax in relatively venetoclax-resistant KMT2A-r leukemic cells. Overall, enitociclib has shown measurable in vitro antitumor activity in KMT2A-r infant leukemia and is a rational therapeutic option to explore in future clinical trials.
Journal of Clinical Oncology · 2025-05-28
articleTPS10075 Background: ROR1 is an oncofetal protein expressed in various blood and solid cancers. Zilovertamab vedotin (ZV) is an antibody-drug conjugate comprising a monoclonal antibody against ROR1, a proteolytically cleavable linker, and monomethyl auristatin E. LIGHTBEAM-U01A (NCT06395103) is a single-arm, open-label, phase 1/2 basket study designed to evaluate ZV in 4 disease cohorts: pediatric B-cell acute lymphoblastic leukemia (B-ALL), pediatric diffuse large B-cell lymphoma (DLBCL)/Burkitt lymphoma, pediatric neuroblastoma, and pediatric or young adult Ewing sarcoma. Methods: Pediatric participants (pts) are aged 0 to < 18 years; young adults are aged 18-25 years. Pts must have a confirmed diagnosis of B-ALL or DLBCL/Burkitt lymphoma per WHO criteria that has relapsed after ≥2 prior lines of therapy, or histologically confirmed neuroblastoma or Ewing Sarcoma that is refractory to frontline therapy. Pts with B-ALL must have ≥5% bone marrow blasts (M2 or M3), pts with DLBCL/Burkitt lymphoma must have radiographically measurable disease per IPNHL response criteria, and pts with neuroblastoma or Ewing sarcoma must have measurable disease per RECIST v1.1 (or MIBG-avid evaluable neuroblastoma). Pts aged ≤16 years must have a Lansky play-performance scale ≥50, pts aged > 16 to < 18 years must have a Karnofsky performance status of ≥50, and pts aged ≥18 years must have an ECOG performance status of 0 or 1. The study consists of 2 parts: dose escalation and confirmation (part 1) and efficacy expansion (part 2). Part 1 will enroll 3-12 pts per dose level. Also, ≥3 pts will be enrolled in 2 age groups: 1 to < 6 years and 6 to < 18 years. Pts will receive ZV at a starting dose of 2 mg/kg IV Q3W, escalating to 2.25 and 2.5 mg/kg or de-escalating to 1.75 mg/kg per a modified toxicity probability interval design-2. In part 2, eligibility will be expanded to ≥6 months for all cohorts and ≤25 years for Ewing sarcoma (if adequate safety and tolerability are shown, eligibility will expand to age 0 to < 6 months). In part 2, 10 pts will be enrolled in each cohort and will receive ZV at the preliminary RP2D determined in part 1. Disease assessments for pts with DLBCL/Burkitt lymphoma, neuroblastoma, or Ewing sarcoma will be performed Q8W for 6 months, then Q12W through 24 months, then Q24W through 5 years, then annually. Disease assessments for B-ALL will be performed at the end of each treatment cycle, at 6 months, at 1 year, then annually. Adverse events (AEs) will be monitored ≤30 days after last dose of study treatment (90 days for serious AEs; 30 days if new anticancer therapy is initiated) and will be graded per NCI CTCAE v5.0. Primary end points are safety and objective response rate. Secondary end points are pharmacokinetics, immunogenicity, duration of response, and eligibility for transplant/CAR-T therapy for pts with B-ALL or DLBCL/Burkitt lymphoma. Approximately 50-90 pts will be enrolled. Recruitment is underway. Clinical trial information: NCT06395103 .
Journal of the National Comprehensive Cancer Network · 2025-02-01 · 19 citations
articleThe NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Pediatric Acute Lymphoblastic Leukemia (ALL) were developed as a result of meetings convened by a multidisciplinary panel of pediatric ALL experts, with the goal of providing recommendations on standard treatment approaches based on current evidence. The NCCN Guidelines for pediatric ALL focus on risk assessment and stratification of risk-adapted therapy; treatment strategies for BCR::ABL1 (Philadelphia chromosome [Ph])-negative and BCR::ABL1-positive B-cell lineage, T-cell lineage, and infant ALL; and supportive care considerations. This selection from the NCCN Guidelines for pediatric ALL focuses on the diagnosis of and management of pediatric T-ALL.
Cancer Research · 2025-04-25
articleAbstract Background: Zilovertamab vedotin (ZV) is an antibody-drug conjugate comprising an anti-ROR1 antibody, a proteolytically cleavable linker, and monomethyl auristatin E. Substudy 01A of LIGHTBEAM-U01 (NCT06395103) is a single-arm, open-label, phase 1/2 basket study designed to determine the preliminary recommended phase 2 dose (RP2D), safety, and antitumor activity of ZV in 4 disease cohorts: pediatric patients (pts) with relapsed/refractory (R/R) B-cell acute lymphoblastic leukemia (B-ALL), diffuse large B-cell lymphoma (DLBCL)/Burkitt lymphoma, or neuroblastoma, and pediatric or young adult pts with Ewing sarcoma. Study Design and Methods: Eligible pts are aged 0 months to ≤25 years. Pts with B-ALL or DLBCL/Burkitt lymphoma must have relapsed after ≥2 prior lines of therapy and exhausted all therapies of known clinical benefit. Pts with B-ALL must have ≥5% (M2 or M3) bone marrow blasts. Pts with DLBCL/Burkitt lymphoma must have radiographically measurable disease per International Pediatric Non-Hodgkin Lymphoma staging system response criteria. Pts with neuroblastoma or Ewing sarcoma must have measurable disease per RECIST v1.1 (or MIBG-avid evaluable neuroblastoma) and be refractory to front-line therapy and for whom further standard therapy is not available/appropriate. All pts must also have a Lansky play-performance scale ≥50 if aged ≤16 years, a Karnofsky performance status ≥50 if aged &gt;16 to &lt;18 years, or an ECOG PS of 0 or 1 if aged ≥18 years. Approximately 50 to 90 pts will be enrolled across the study, which will consist of 2 parts: dose escalation and confirmation (part 1) and efficacy expansion (part 2). In part 1, ≥3 pts will be enrolled for 2 age groups: 1 to &lt;6 years and 6 to &lt;18 years. Pts will receive ZV at a starting dose of 2 mg/kg IV Q3W, with escalation to 2.25 and 2.5 mg/kg or de-escalation to 1.75 mg/kg per a modified toxicity probability interval design-2. In part 2, the age of pts will be expanded to ≥6 months for all indications and ≤25 years for R/R Ewing sarcoma. Approximately 10 pts will be enrolled in each cohort and will receive ZV at the preliminary RP2D determined in part 1. For all pts except those with B-ALL, imaging/disease assessments will be performed Q8W for 6 months, then Q12W through 24 months, Q24W through 5 years, and annually thereafter. Disease assessments for B-ALL will be performed at the end of each cycle, at 6 months and 1 year, and then annually. Adverse events (AEs) will be monitored throughout the study and for 30 days after the last dose of study treatment (90 days for serious AEs or 30 days if new anticancer therapy is initiated). AEs will be graded per NCI CTCAE v5.0. Primary end points are safety and tolerability and objective response rate. Secondary end points include pharmacokinetics, immunogenicity, duration of response, and eligibility for transplant/CAR-T therapy in pts with B-ALL or DLBCL/Burkitt lymphoma. Recruitment is ongoing. Citation Format: Hyoung Jin Kang, Pablo Berlanga, Quentin Campbell-Hewson, Steven G. DuBois, Kyung-Nam Koh, Christine Mauz-Koerholz, Michael Sullivan, David Mangum, Rachael Windsor, David S. Dickens, Alexandre Duarte, Farzana Pashankar, Shifra Ash, Andrew Bellantoni, Scott J. Diede, Rohini Singh, Yulia Sidi, Michal Yalon. Zilovertamab vedotin in pediatric and young adult hematologic malignancies or solid tumors: Phase 1/2 LIGHTBEAM-U01A study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_2):Abstract nr CT119.
Fusion-negative rhabdomyosarcoma with diffuse bony metastases and remarkable chemosensitivity
BMJ Case Reports · 2022-08-01 · 1 citations
articleOpen accessIn this report, we describe the case of an adolescent male with an unusual case of fusion-negative, paratesticular alveolar rhabdomyosarcoma who presented with spontaneous tumour lysis syndrome and diffuse bony metastases throughout the axial and appendicular skeleton with additional significant bone marrow involvement. Both spontaneous tumour lysis syndrome and diffuse bony metastases are extremely unusual for rhabdomyosarcoma. On the backbone of standard vincristine, dactinomycin and cyclophosphamide (VAC) chemotherapy, the only local control was orchiectomy at 15 weeks, with no radiation administered due to the initially diffuse nature of the disease and rapid response to chemotherapy. Following 43 weeks of VAC, a year-long maintenance phase with pazopanib was given which was well tolerated. The patient remains in remission now 4 years after completion of therapy.
Sporadic extranodal Rosai–Dorfman–Destombes disease treated with tocilizumab
Pediatric Blood & Cancer · 2022-04-29 · 2 citations
editorialPlease 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.
Pediatric Blood & Cancer · 2022-07-20 · 7 citations
articleSenior authorCorrespondingApproximately 25% of B-cell acute lymphoblastic leukemia (B-ALL) cases are defined by hyperdiploidy, with RAS mutations occurring in 30% of hyperdiploid B-ALL patients. It is believed that hyperdiploidy is an in utero event with RAS mutations occurring postnatally, but clinical evidence of this is based on relatively few patients. We present a case of monozygotic, monochorionic twins who developed concordant hyperdiploid B-ALL with identical chromosomal gains but different RAS mutations, adding further evidence that hyperdiploidy is occurring prenatally, with RAS mutations developing postnatally. Environmental exposures were reviewed with the family without identification of a clear association.
Frequent coauthors
- 9 shared
Johnathon D. Bishop
University of Tennessee Health Science Center
- 7 shared
Joshua D. Schiffman
Huntsman Cancer Institute
- 6 shared
Cheng Cheng
Daqing Oilfield General Hospital
- 6 shared
Ching‐Hon Pui
St. Jude Children's Research Hospital
- 6 shared
Anupam Verma
Inova Fairfax Hospital
- 6 shared
Mark Fluchel
- 6 shared
Anne C. Kirchhoff
- 6 shared
Charles G. Mullighan
St. Jude Children's Research Hospital
Labs
University of Utah Pediatric Hematology OncologyPI
Education
M.D.
Albert Einstein College of Medicine
Other
Primary Children's Hospital
Other
St. Jude Children’s Research Hospital
Other
St. Jude Children’s Research Hospital
Other
Sidney Kimmel Medical College
Other, Pediatric Hematology Oncology
University of Utah
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