About

Priya P. Chan, MD, is an Assistant Professor of Pediatrics at the University of Utah in the Division of Pediatric Hematology/Oncology. She received her medical degree from the University of Minnesota Medical School, completed her Pediatric Residency at the University of Wisconsin, and her Pediatric Hematology/Oncology Fellowship at the University of Utah. Following her fellowship, she completed a Pediatric Neuro-Oncology Fellowship at the University of Colorado/Children’s Hospital Colorado. Dr. Chan is a member of the neuro-oncology team at Primary Children’s Medical Center and specializes in the care of children and young adults with brain and spine tumors. Her research interests are focused on the development of early phase clinical trials for children with central nervous system tumors and the long-term care of patients who have survived these cancers. Her clinical and research work emphasizes improving treatment options and outcomes for pediatric patients with neuro-oncological conditions.

Research topics

• Medicine
• Internal medicine
• Computer Science
• Oncology
• Anatomy
• Cancer research
• Medical physics
• Pathology
• Biology

Selected publications

• LBA-02. Molecular Profiling-Guided Individualized Treatment in Children and Young Adults with Newly Diagnosed High-Grade Glioma (Excluding DIPG): A Pilot Trial Demonstrating Promising Outcomes (PNOC008)

  Neuro-Oncology Pediatrics · 2025-08-01

  articleOpen access

  Abstract Background PNOC008 was a single-arm, multi-center trial evaluating the feasibility, toxicity, and efficacy of molecularly guided, personalized treatment following upfront radiation for high-grade glioma (HGG), including non-pontine diffuse midline glioma (DMG). Methods Patients aged <21 years with newly diagnosed, localized, hemispheric HGG (Stratum A) or non-pontine DMG (Stratum B) were eligible. Comprehensive molecular profiling was performed (UCSF500 gene panel, WES, WGS, and mRNA-seq). Molecular data were reviewed by a specialized tumor board who recommended up to four FDA-approved drugs. Patients were followed for toxicity and efficacy. Central imaging review was completed. Results Fifty-five patients enrolled between 2018 and 2023 (median age 11 years [range 2-20], n = 31 female, n = 29 Stratum A), including H3K27-altered (n = 17), H3/IDH-wildtype diffuse pediatric-type (n = 16), and H3G34-mutant HGG (n = 12). In 44 patients who followed the recommended treatment, median overall survival (OS) from time of study enrollment was 26.5 months in Stratum A (n = 25, lower 95% CI18.5) and 23.5 months in Stratum B (n = 19, lower 95% CI16.8) with median follow-up of 34.5 months (lower 95% CI: 32.2). The median OS was 30 months in H3G34-mutant HGG (n = 10, lower 95% CI: 24.6) and 22.6 months in H3K27-altered DMG (n = 12, lower 95% CI: 19.3). The most common therapies for H3G34-mutant HGG and H3K27-altered DMG were: temozolomide and/or lomustine (18/22, 82%); everolimus (16/22, 73%); dasatinib (8/22, 36%); and olaparib (8/22, 36%). Novel combinations were well tolerated with grade 3 or 4 treatment-related adverse events being mostly hematologic. Fourteen patients (14/43, 33%) received re-irradiation. Clinical and biology correlates include 440 cell-free DNA samples, 350 MR images, 230 quality-of-life questionnaires, and 39 digitized tissue slides. Conclusions A molecularly guided, personalized treatment plan is feasible and well tolerated with encouraging clinical outcomes in children and young adults with HGG and non-pontine DMG. Volumetric tumor analysis and correlative studies are underway.

  PublisherDOI

• CTNI-78. PNOC008: A PILOT TRIAL TESTING THE CLINICAL BENEFIT OF USING MOLECULAR PROFILING TO DETERMINE AN INDIVIDUALIZED TREATMENT PLAN IN CHILDREN AND YOUNG ADULTS WITH NEWLY DIAGNOSED HIGH-GRADE GLIOMA (EXCLUDING DIFFUSE INTRINSIC PONTINE GLIOMA)

  Neuro-Oncology · 2024-11-01 · 1 citations

  articleOpen access

  Abstract BACKGROUND Despite multiple clinical trials in young patients with newly diagnosed high grade gliomas (HGG), survival remains poor. PNOC008 is a single-arm, multi-center pilot trial, investigating the feasibility, toxicity, and efficacy of a molecularly guided individualized treatment approach following radiotherapy. METHODS Patients aged ≤21 years with newly diagnosed, localized, hemispheric HGG (Stratum A) or non DIPG, diffuse midline glioma (DMG) (Stratum B) were eligible. Comprehensive molecular profiling (targeted gene panel, whole exome, and whole transcriptome sequencing) was performed on primary tumor tissue. The molecular data was reviewed by a dedicated tumor board that recommended an individualized treatment plan combining up to four FDA approved drugs. Patients were followed for toxicity and efficacy. Circulating tumor DNA (ctDNA), imaging, and quality of life (QOL) measures were collected at multiple timepoints. RESULTS Fifty-five HGG patients enrolled between 2018 and 2023 (median age 11 years [range 2-20], n=31 female, n=29 Stratum A), including H3K27-altered (n=17), H3/IDH-wildtype diffuse pediatric-type (n=16), and H3G34-mutant diffuse hemispheric glioma (n=12). In 44 patients that followed the recommended treatment, median overall survival (OS) from time of study enrollment was 26.5 months in Stratum A (lower 95% CI: 18.5) and 23.6 months in Stratum B (lower 95% CI: 16.8), and 30 months in H3G34-mutant patients (n=10, lower 95% CI:24.6) with median follow-up of 34.5 months for all patients (lower 95% CI: 32.2). The treatment recommendations most commonly included alkylator with targeted therapy combinations. The often novel drug combinations were generally well tolerated with grade 3 or 4 treatment-related adverse events being mostly hematologic. Central imaging, ctDNA, and QOL analyses are underway. CONCLUSIONS A personalized treatment approach using comprehensive transcriptomic and genomic analysis is feasible and well tolerated with encouraging survival data in children and young adults with HGG. Further analyses of molecular subgroups and correlatives are ongoing.

  PublisherOA PDFDOI

• A Simple and Scalable Zebrafish Model of Sonic Hedgehog Medulloblastoma

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-02-05

  preprintOpen access

  Summary Medulloblastoma (MB) is the most common malignant brain tumor in children and is stratified into three major subgroups. The Sonic hedgehog (SHH) subgroup represents ∼30% of all MB cases and has significant survival disparity depending upon TP53 status. Here, we describe the first zebrafish model of SHH MB using CRISPR to mutate ptch1 , the primary genetic driver in human SHH MB. These tumors rapidly arise adjacent to the valvula cerebelli and resemble human SHH MB by histology and comparative genomics. In addition, ptch1- deficient MB tumors with loss of tp53 have aggressive tumor histology and significantly worse survival outcomes, comparable to human patients. The simplicity and scalability of the ptch1 MB model makes it highly amenable to CRISPR-based genome editing screens to identify genes required for SHH MB tumor formation in vivo , and here we identify the grk3 kinase as one such target.

  PublisherOA PDFDOI

• NFS-30. ADJUVANT MEK INHIBITION TO PREVENT REBOUND GROWTH FOLLOWING PARTIAL RESECTION OF PLEXIFORM NEUROFIBROMAS

  Neuro-Oncology · 2024-06-18

  articleOpen access1st authorCorresponding

  Abstract BACKGROUND Plexiform neurofibromas (PNs) are benign peripheral nerve sheath tumors that occur in patients with neurofibromatosis type I. These tumors can cause significant morbidity leading to functional impairment, pain, and disfigurement. Management of PNs is challenging. Complete surgical resection is often not possible due to tumor growth along vital structures, and rebound growth is frequently experienced following subtotal resection (STR) of PNs. The mitogen-activated protein kinase (MAPK) pathway has been implicated in the growth of PNs, and the use of MAPK enzyme (MEK1/2) inhibitors has been shown to be an effective therapy in the treatment of PNs. Herein, we described our institutional experience using a short course of adjuvant MEK1/2 inhibitors in the treatment of pediatric patients with PNs following STR to prevent rebound growth. METHODS A single-institution retrospective record review of pediatric patients who underwent STR of their PN. RESULTS A total of 35 patients with 39 separate PNs had STR of their PNs. Fourteen PNs were treated with resection alone and 25 PNs were treated with a six-month course of adjuvant MEK1/2 inhibitors following STR. The number of patients requiring additional treatment with surgical resection or medical therapy was 11 of 14 patients (79%) in the resection only group and 6 of 25 patients (24%) in the adjuvant MEK1/2 inhibitor group. The mean time to additional treatment for the resection only group was 22 months, and the mean follow-up time for patients receiving adjuvant MEK1/2 inhibition was 29 months. Skin rash was the most common adverse effect seen with adjuvant MEK1/2 inhibition, and one patient experienced a dose-limiting thrombus. CONCLUSIONS A short course of MEK1/2 inhibitors following STR of PNs is effective in the short-term in preventing rebound growth when compared to STR alone. Treatment is well tolerated and should be considered as adjuvant therapy in pediatric patients.

  PublisherOA PDFDOI

• A simple and scalable zebrafish model of Sonic hedgehog medulloblastoma

  Cell Reports · 2024-07-29 · 8 citations

  articleOpen access

  Medulloblastoma (MB) is the most common malignant brain tumor in children and is stratified into three major subgroups. The Sonic hedgehog (SHH) subgroup represents ∼30% of all MB cases and has significant survival disparity depending upon TP53 status. Here, we describe a zebrafish model of SHH MB using CRISPR to create mutant ptch1, the primary genetic driver of human SHH MB. In these animals, tumors rapidly arise in the cerebellum and resemble human SHH MB by histology and comparative onco-genomics. Similar to human patients, MB tumors with loss of both ptch1 and tp53 have aggressive tumor histology and significantly worse survival outcomes. The simplicity and scalability of the ptch1-crispant MB model makes it highly amenable to CRISPR-based genome-editing screens to identify genes required for SHH MB tumor formation in vivo, and here we identify the gene encoding Grk3 kinase as one such target.

  PublisherDOI

• HGG-32. PNOC008: A PILOT TRIAL TESTING THE CLINICAL BENEFIT OF USING MOLECULAR PROFILING TO DETERMINE AN INDIVIDUALIZED TREATMENT PLAN IN CHILDREN AND YOUNG ADULTS WITH NEWLY DIAGNOSED HIGH-GRADE GLIOMA (EXCLUDING DIFFUSE INTRINSIC PONTINE GLIOMA)

  Neuro-Oncology · 2024 · 2 citations

  • Computer Science
  • Medicine
  • Oncology

  Abstract BACKGROUND Children and young adults diagnosed with high-grade glioma (HGG) face extremely poor prognoses. Despite multiple clinical trials testing new treatments in this population, a survival advantage has yet to be achieved. Herein we assessed, in a single-arm, multi-center pilot trial, the feasibility of molecular profiling of primary HGG tumor tissue to create an individualized treatment plan with up to four FDA approved medications. METHODS Patients aged <21 years with newly diagnosed, localized, hemispheric HGG (Stratum A) or midline HGG (non-DIPG; Stratum B) were eligible. Tumor tissue underwent comprehensive molecular profiling (targeted gene panel, whole exome, and whole transcriptome sequencing). Based on detailed review of the molecular data by a dedicated tumor board, an individualized treatment plan that combined up to four FDA approved drugs was recommended. Circulating tumor DNA (ctDNA), imaging, and quality of life (QOL) measures were collected at multiple timepoints. RESULTS Fifty-five patients enrolled between 2018 and 2023 (median age 11 years [range 2-20], n=31 female, n=29 Stratum A). The most common integrated diagnoses included H3K27-altered diffuse midline glioma (n=17), H3/IDH-wildtype diffuse pediatric-type HGG (n=16), and H3G34-mutant diffuse hemispheric glioma (n=12). Median overall survival (OS) from the time of study enrollment was 26.5 months in Stratum A (lower 95% CI: 18.7) and 21.7 months in Stratum B (lower 95% CI: 16.8), with a median follow-up of 35.4 months for all patients (lower 95% CI: 32.5). The most common grade 3 or 4 treatment-related adverse events were decreased neutrophils (n=28), decreased platelets (n=22), and decreased white blood cells (n=16). As of December 2023, seven patients remain on therapy. Central imaging, ctDNA, and QOL analyses are underway. CONCLUSIONS A personalized treatment recommendation for children and young adults with HGG based on comprehensive transcriptomic and genomic analysis is feasible. Current survival data are encouraging, and molecular subgroup analyses are ongoing.

  PublisherOA PDFDOI

• Thromboembolic toxicity observed with concurrent trametinib and lenalidomide therapy

  Pediatric Blood & Cancer · 2023 · 4 citations

  1st authorCorresponding
  • Medicine
  • Oncology
  • Internal medicine

  The event-free survival of pediatric low-grade gliomas is poor, and patients often require multiple treatment strategies. While MEK and RAF inhibitors are efficacious in early-phase trials, not all patients respond, and many experience progression following completion of therapy. Evaluating combination therapies that may enhance efficacy or prolong disease stabilization is warranted. We report our institutional experience using concurrent trametinib and lenalidomide in the treatment of primary pediatric central and peripheral nervous system tumors. Two of four patients using this combination therapy experienced severe thromboembolic events, necessitating discontinuation of therapy. This combination requires further investigation, and we urge caution if used.

  PublisherOA PDFDOI

• Recurrent ACVR1 mutations in posterior fossa ependymoma

  Acta Neuropathologica · 2022 · 18 citations

  • Medicine
  • Biology
  • Pathology
  PublisherOA PDFDOI

• LGG-42. Thromboembolic toxicity observed with concurrent trametinib and lenalidomide therapy

  Neuro-Oncology · 2022-06-01 · 1 citations

  articleOpen access1st authorCorresponding

  Abstract INTRODUCTION: Event-free survival of pediatric low-grade glioma (pLGG) is poor, and patients often require multiple treatment strategies. The hallmark of pLGGs are genetic aberrations of the mitogen-activated protein kinase pathway, which lead to constitutive pathway activation. MEK and RAF inhibitors target this pathway and are efficacious in early phase trials in recurrent pLGGs. However, not all patients respond to monotherapy, and many experience progression after completion of therapy. Evaluating combination therapies that may enhance efficacy or prolong disease stabilization is warranted. Lenalidomide is an immunomodulatory agent with an anti-tumor effect demonstrated in phase 1 trials in recurrent pediatric central nervous system (CNS) tumors. OBJECTIVE: To describe our institutional experience using concurrent trametinib and lenalidomide in the treatment of primary pediatric central and peripheral nervous system (PNS) tumors. METHODS: Retrospective review of patients’ medical records. RESULTS: Four patients with locally recurrent primary CNS or PNS tumors, three with WHO grade II pilomyxoid astrocytomas and one with a plexiform neurofibroma, were treated with trametinib and lenalidomide concurrently. Two patients developed severe thromboembolic events. One patient was treated with combination therapy for seven months until trametinib and lenalidomide were held after urgent ventriculoperitoneal shunt revision. Shortly following shunt revision, he experienced near-complete vision loss. MRI of the brain demonstrated a left posterior watershed territory hypoxic-ischemic injury. In a second patient, after four months of combination therapy, surveillance echocardiogram showed an incidental finding of severe biventricular dysfunction with a left ventricular ejection fraction (LVEF) of 17.7% and two mural thrombi in the left ventricular apex. She started losartan and enoxaparin and discontinued trametinib and lenalidomide. Her LVEF normalized four months later, and the mural thrombi resolved. CONCLUSIONS: Given the severe thromboembolic events experienced by these patients treated with concomitant trametinib and lenalidomide, this combination requires further investigation, and we urge caution if used concurrently.

  PublisherOA PDFDOI

• NFB-14. Post-operative use of MEK inhibitors to prevent rebound growth following partial resection of plexiform neurofibromas

  Neuro-Oncology · 2022-06-01

  articleOpen access1st authorCorresponding

  Abstract BACKGROUND: Plexiform neurofibromas (PNs) can cause significant morbidity leading to functional impairment, pain, and disfigurement. Management of PNs is challenging. Complete surgical resection is often not possible due to tumor growth along vital structures, and rebound growth is frequently experienced with partially resected PNs. The mitogen-activated protein kinase pathway has been implicated in the growth of PNs, and MEK1/2 inhibitors have been shown to be an effective treatment of PNs. OBJECTIVE: To describe our institutional experience using post-operative MEK1/2 inhibitors in the treatment of pediatric patients with PNs following subtotal resection (STR). METHODS: A single-institution retrospective record review. RESULTS: A total of 35 patients had STR of their PN. Fourteen patients underwent resection alone, ten patients received adjuvant mechanistic target of rapamycin (mTOR) inhibitors and eleven patients received adjuvant MEK1/2 inhibitors. The mean follow-up time was 5.1 years, but relatively shorter for patients receiving adjuvant MEK1/2 inhibitors. Mean time from resection to start of adjuvant therapy and mean duration of adjuvant therapy for patients in the mTOR inhibitor group was 3.3 weeks and 3.9 months, respectively, and for patients in the MEK1/2 inhibitor group was 3.1 weeks and 8.5 months, respectively. The number of patients in each group requiring additional treatment with surgical resection or medical therapy, was 11 of 14 patients (78.6%) in the resection only group, 7 of 10 patients (70%) in the adjuvant mTOR inhibitor group and 3 of 11 patients (27.3%) in the adjuvant MEK1/2 inhibitor group. CONCLUSIONS: A short course of MEK1/2 inhibitors following subtotal resection of PNs is effective in the short term in preventing rebound growth when compared to STR alone or adjuvant mTOR inhibitors. Treatment is well tolerated and should be considered as adjuvant therapy in pediatric patients. Long-term follow-up is necessary to judge the effectiveness of this approach.

  PublisherOA PDFDOI

Frequent coauthors

• Nathan Dahl

  University of Colorado Anschutz Medical Campus

  18 shared

• Nicholas K. Foreman

  18 shared

• Ashley Sabus

  Children's Hospital Colorado

  13 shared

• Molly Hemenway

  University of Colorado Denver

  12 shared

• Kathryn C. Chatfield

  9 shared

• Rodney A. Stewart

  Huntsman Cancer Institute

  8 shared

• Brooke French

  University of Colorado Anschutz Medical Campus

  8 shared

• Benjamin R. Myers

  University of Utah

  8 shared