About

Adam C. Resnick, Ph.D., is a Research Professor of Neurosurgery at the Perelman School of Medicine at the University of Pennsylvania and a member of the Abramson Cancer Center. He serves as the Director of the Children's Brain Tumor Network at the Children's Hospital of Philadelphia and is the Director of the CHOP/PENN Department of Neurosurgery Brain Tumor Tissue Biorepository. Dr. Resnick is also the Director of The Center for Data Driven Discovery in Biomedicine (D3b) at Children's Hospital of Philadelphia and holds the position of Scientific Chair for the Children's Brain Tumor Network. His research focuses on studying cell signaling cascades and their alterations in pediatric brain tumors. The goal of his laboratory is to elucidate the molecular and genetic underpinnings of pediatric brain tumors to identify and develop targeted therapies. Additional research interests include characterizing novel cell signaling pathways involved in cancer biology, such as inositol polyphosphates and their metabolism. Dr. Resnick leads open data initiatives aimed at genomic data sharing and supporting collaborative research efforts. His expertise extends to the study of brain development, molecular oncology, neuro-oncology, and transcriptional regulation, with a particular emphasis on brain tumors. He has contributed significantly to the understanding of pediatric brain tumor biology, including the genetic landscape of medulloblastoma and the molecular characterization of pediatric low-grade gliomas. Dr. Resnick is also the director of the Childhood Brain Tumor Tissue Consortium (CBTTC), a multi-institutional cooperative research program dedicated to improving outcomes for children with brain tumors through research on prognostic biomarkers and therapies. His work integrates informatics, biorepository development, and collaboration with leading experts to advance pediatric neuro-oncology research.

Research topics

• Biology
• Medicine
• Genetics
• Oncology
• Bioinformatics
• Internal medicine
• Computational biology
• Computer Science
• Pathology
• Artificial Intelligence
• Statistics
• Anatomy
• Cancer research
• Radiology

Selected publications

• Minimal Clinically Important Difference of the Sinonasal Outcome Test in Sinonasal Malignancy

  Annals of Otology Rhinology & Laryngology · 2026-03-25

  article

  Background: Sinonasal malignancies (SNM) are rare cancers associated with poor prognosis and impaired quality of life (QOL). The 22-question Sino-Nasal Outcome Test (SNOT-22) has been used to assess QOL in patients with SNM. Objective: To determine the minimal clinically important difference (MCID) for the SNOT-22 in patients with SNM. Methods: About 264 patients with SNM were drawn from a prospective, longitudinal, multi-institutional study. SNOT-22 scores were collected at pre-treatment baseline and follow-up through 5 years post-treatment. Cronbach’s alpha was used to assess the internal consistency of the SNOT-22. Distribution-based approaches were used to estimate the MCID. Multivariable regression identified factors associated with SNOT-22 improvement exceeding the determined MCID. Results: Cronbach’s alpha was >.85. The estimated MCIDs were: 1.44 (Cohen’s effect size), 1.32 (standard error of the mean), 10.45 (1/2 of baseline standard deviation), and 3.67 (minimum detectable change). The mean MCID across methods was 4.22. Multivariable regression demonstrated higher odds of clinically meaningful improvement from baseline in patients with early-stage disease (odds ratio (OR) 3.510, P = .035), no neck irradiation (OR 11.050, P = .014), and neoadjuvant therapy (OR 16.667, P = .047). Conclusions: The SNOT-22 MCID was estimated as 4.22 in a large multi-center cohort of patients with SNM, suggesting that relatively small QOL changes are clinically relevant. When applying the MCID to the current cohort, advanced stage, treatment of neck disease, and not requiring neoadjuvant therapy were predictive of worse QOL.

  PublisherDOI

• Table S2 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

  2025-02-18

  preprintOpen access

  <p>Individual patients with H3K27M-mutant DMG treated with ONC201.</p>

  PublisherDOI

• Germline pathogenic variation impacts somatic alterations and patient outcomes in pediatric central nervous system tumors

  Nature Communications · 2025-11-21

  articleOpen access

  The contribution of rare pathogenic/likely pathogenic (P/LP) germline variants to pediatric central nervous system (CNS) tumor development remains understudied. Here, we characterize the prevalence and biological significance of germline P/LP variants in cancer predisposition genes across 830 CNS tumor patients from the Pediatric Brain Tumor Atlas (PBTA). We identify germline P/LP variants in 23.3% (193/830) of patients and the majority (137/193) lack clinical reporting of genetic tumor syndromes. Among P/LP carriers, 34.6% have putative somatic second hits or loss of function tumor alterations. Finally, we link pathogenic germline variation with somatic events and patient survival to highlight the impact of germline variation on tumorigenesis and patient outcomes. The role of rare pathogenic/likely pathogenic (P/LP) germline variants in pediatric central nervous system (CNS) tumour development remains poorly understood. Here, the authors investigate the prevalence and clinical significance of germline P/LP variants in cancer predisposition genes across 830 CNS tumour patients.

  PublisherDOI

• Role of repulsive guidance signaling and GPR180 in pediatric low-grade glioma infiltration

  npj Precision Oncology · 2025-11-11 · 1 citations

  articleOpen access

  Pediatric low-grade gliomas (pLGGs) are the most common brain tumors in children with varying degrees of infiltration. Despite having a positive prognosis, if the standard treatment, gross total resection, is impossible due to tumor location or diffuseness, outcomes worsen. Development of targeted therapeutics for diverse subtypes of pLGGs is limited by a lack of genetic models. We generated five fly pLGG models using patient-derived fusion genes to investigate molecular subtype-specific pathology, and found glial overexpression of QKI::RAF1, associated with pilocytic astrocytomas and glioneuronal tumors, induced aberrant glial migration and infiltration. Both repulsive guidance signaling and GPR180/CG9304 mediated glial infiltration, which was suppressed by glial overexpression of Robo2 or PlexA/B, or knockdown of GPR180/CG9304. ROBO2 and GPR180/CG9304 were down and upregulated, respectively, in flies and patients with RAF fusions. Our study provides mechanistic insights into pLGG tumorigenesis and suggests targeting repulsive guidance signaling and GPR180/CG9304 as potential therapeutics for pLGG subtypes.

  PublisherOA PDFDOI

• The children's brain tumor network (CBTN) - Accelerating research in pediatric central nervous system tumors through collaboration and open science

  UNC Libraries · 2025-07-26

  articleOpen access
  PublisherDOI

• Artificial Intelligence for Response Assessment in Pediatric Neuro-Oncology (AI-RAPNO), part 2: challenges, opportunities, and recommendations for clinical translation

  The Lancet Oncology · 2025-10-28 · 4 citations

  review
  PublisherDOI

• Abstract 1117: cBioPortal for cancer genomics

  Cancer Research · 2025-04-21

  article

  Abstract cBioPortal for Cancer Genomics is a widely used platform for exploratory, interactive visualization and analysis of large-scale clinico-genomic datasets. cBioPortal provides a range of visualizations and analyses including interactive cohort exploration, OncoPrints, mutation “lollipop” plots, survival analysis, alteration enrichment analysis, and detailed patient-level visualizations. cBioPortal also integrates variant annotations from a variety of sources to facilitate interpretation. The public cBioPortal (https://www.cbioportal.org) is accessed by >40,000 unique visitors each month and hosts data from >460 studies. All data is also available in the cBioPortal Datahub: https://github.com/cBioPortal/datahub. In 2024 we added 76 new studies (∼30,000 samples), including data from the NCI Genomic Data Commons. In addition, >94 instances of cBioPortal are installed at academic institutions and companies worldwide. cBioPortal partners with AACR Project GENIE to provide access to the GENIE cohort in a dedicated instance (https://genie.cbioportal.org). Users can explore the full GENIE cohort of >229,000 clinically sequenced samples from 19 institutions, as well as cohorts with comprehensive clinical annotations including response, outcome, and treatment history, from the GENIE Biopharma Collaborative (BPC). BPC cohorts for NSCLC (∼2,000 samples) and colorectal cancer (∼1,500 samples) are available, with more to come. The past year has brought a variety of enhancements to cBioPortal. A new data type selector on the home page enables users to find studies with specific types of data. The interactive cohort exploration has new ways to explore data with the addition of gene-specific charts to summarize the types of mutations in a gene and the integration of the Plots tab for customizable graphs of any two data attributes. The OncoPrint can now display per group alteration frequency based on any categorical attribute. Variant interpretation is enhanced with the integration of AlphaMissense as a novel annotation source and an update to the latest MutationAssessor data. The patient page also has new visualizations, including mutational signatures and the integration of Chromoscope to visualize structural variations. We also made significant changes to the backend code to improve both the developer and user experience. The backend code was repackaged and upgraded to simplify and improve the development process. In addition, we are working on switching to an Online Analytical Processing (OLAP) database which will bring significant performance improvements. cBioPortal is open source: https://github.com/cBioPortal. Development is a collaborative effort among groups at Memorial Sloan Kettering Cancer Center, Dana-Farber Cancer Institute, Children’s Hospital of Philadelphia, Princess Margaret Cancer Centre, Caris Life Sciences, Bilkent University, SE4BIO and The Hyve. We welcome open source contributions from others in the cancer research community. Citation Format: Ino de Bruijn,Tali Mazor,Rima AlHamad,Calla Chennault,Corey Dubin,Jeremy Easton-Marks,Zhaoyuan Fu,Benjamin Gross,Charles Haynes,David M. Higgins,Jason Hwee,Prasanna K. Jagannathan,Mirella Kalafati,Karthik Kalletla,Zeynep Karagöz,James Ko,Tim Kuijpers,Sowmiyaa Kumar,Priti Kumari,Ritika Kundra,Bryan Lai,Xiang Li,James Lindsay,Aaron Lisman,Qi-Xuan Lu,Ramyasree Madupuri,Zain-ul-Abideen Nasir,Angelica Ochoa,Yusuf Ziya Özgül,Oleguer Plantalech,Matthijs N. Pon,Baby A. Satravada,Jessica Singh,Selcuk Onur Sumer,Pim van Nierop,Floris Vleugels,Avery Wang,Manda Wilson,Hongxin Zhang,Gaofei Zhao,Ugur Dogrusoz,Allison Heath,Adam Resnick,Trevor J. Pugh,Chris Sander,Ethan Cerami,JianJiong Gao,Nikolaus Schultz. cBioPortal for cancer genomics [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 1117.

  PublisherDOI

• Supplementary Data S2 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

  2025-02-18

  preprintOpen access

  <p>Protocol for NCT03134131, ONC201-018: Expanded Access to ONC201 for Patients with H3K27M-mutant and/or Midline High Grade Gliomas.</p>

  PublisherDOI

• Supplementary Figures 1-15 from Clinical Efficacy of ONC201 in H3K27M-Mutant Diffuse Midline Gliomas Is Driven by Disruption of Integrated Metabolic and Epigenetic Pathways

  2025-02-18

  preprintOpen access

  <p>Contains supplementary data and table titles and as well as supplementary figures with associated titles and legends.Fig. S1. Selection method for planned efficacy analysis of ONC201 in patients with H3K27MDMG.Fig. S2. Progression-free survival from diagnosis of trial patients with non-recurrent H3K27MDMG treated with ONC201.Fig. S3. Swimmers’ plot of ONC201 response by recurrence status, tumor location, and ONC201 trial.Fig. S4. ONC201 efficacy is independent of TP53 mutation status and chromosomal instability.Fig. S5. Cox proportional hazard regression to assess the effect of ONC201 after adjusting for confounders.Fig. S6. Survival of patients with H3K27M-DMG treated with ONC201 versus ONC201untreated historical controls.Fig. S7. Survival of patients with H3K27M-DMG treated with ONC201 versus ONC201untreated patients (PNOC003 or HERBY Phase II trials).Fig. S8. Molecular attributes of patients with H3K27M-DMG treated with ONC201.Fig. S9: Survival of H3K27M-DMG mice models treated with ONC201.Fig. S10. Integrative analysis of in vitro and human tumor metabolic gene expression in response to ONC201.Fig. S11. ONC201-mediated L2HG production increases H3K27me3 in H3K27M-DMG cells.Fig. S12. ONC201-induced increase in H3K27me3 is mediated by lactate dehydrogenase.Fig. S13. ONC201 alters genomic chromatin accessibility and H3K27ac distribution in H3K27M-DMG cells.Fig. S14. ONC201 increases global H3K27me3 in patient samples.Fig. S15. ONC201 does not cause hypermethylation leading to a glioma CpG island methylator phenotype.</p>

  PublisherDOI

• Abstract LB340: Analyzing both germline and somatic variants using Variant WorkBench in the Kids First Data Resource Portal: Children’s Brain Tumor Network as an example

  Cancer Research · 2025-04-25

  articleSenior author

  Abstract Aiming at facilitating researchers to uncover new insights into the biology of childhood cancers and structural birth defects, the Gabriella Miller Kids First Pediatric Research Program (Kids First) is initiated. The Kids First Data Resource Center (KFDRC) developed the Kids First Data Resource Portal (KFDRP; https://portal.kidsfirstdrc.org/), a centralized data platform for both Kids First and collaborative cohorts. On behalf of KFDRC, we present as part of KFDRP the upgraded Variant WorkBench (VWB) with more data incorporated, on a more efficient platform, in a more streamlined data flow design, and capable of analyzing both germline and somatic genomic variants. First, the current collection of Kids First data include reharmonized genomics data of over 922,000 files in more than 35,400 participants from 35 studies. We also provide updated variant/gene annotation databases from more than 50 public resources (e.g. gnomAD, ClinVar, HPO etc.). Second, VWB is running on Velsera’s Cavatica Data Studio platform with a new Spark version 3.5.1 plus Python 3.11, achieving a ∼10 fold acceleration in terms of executing PySpark codes when compared to previous versions. Third, we redesigned the data flow from KFDRP to VWB, where portal users can now import Kids First data with which they have dbGaP approval directly to a Cavatica project and start analyzing in VWB. As an example, we show how to use VWB to identify deleterious variants within the same genes in both germline and somatic genomes of the same participant from the Children’s Brain Tumor Network, the largest Kid First cohort so far. In conclusion, the upgraded Variant WorkBench enables accelerated exploration of pediatric disease genomics under the Kids First program. Citation Format: Yiran Guo, Jared Rozowsky, Jean-Philippe Thibert, Qi Li, Jeremy Costanza, Michele Mattioni, Eric Wenger, David Higgins, Yuankun Zhu, Allison Heath, Vincent Ferretti, Adam Resnick. Analyzing both germline and somatic variants using Variant WorkBench in the Kids First Data Resource Portal: Children’s Brain Tumor Network as an example [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 LB340.

  PublisherDOI

Recent grants

• NIH Grant K99CA134914

  NIH · $137k · 2009

• CAREER:Discovery and characterization of inositol polyphosphates as mediators of protein pyrophosphorylation

  NSF · $525k · 2013–2018

• Precision Medicine For Pediatric Low-Grade Gliomas

  NIH · $2.1M · 2015–2020

• Data Resource Core

  NIH · $5.9M · 2017–2022

• NIH Grant R00CA134914

  NIH · $738k · 2012

Frequent coauthors

• Phillip B. Storm

  Children's Hospital of Philadelphia

  230 shared

• Javad Nazarian

  216 shared

• Sabine Mueller

  211 shared

• Cassie Kline

  Children's Hospital of Philadelphia

  147 shared

• Angela J. Waanders

  Lurie Children's Hospital

  140 shared

• Sebastian M. Waszak

  École Polytechnique Fédérale de Lausanne

  128 shared

• Stefan M. Pfister

  University Hospital Heidelberg

  118 shared

• Jacques Grill

  113 shared

Education

• B.S., Neuroscience

  University of Florida

  1998

• B.A., English and Literature

  University of Florida

  1999

• Ph.D., Neuroscience

  Johns Hopkins School of Medicine

  2006