About

Dr. Philip Fisher is the Diana Chen Professor of Early Childhood Learning in the Graduate School of Education at Stanford University and serves as the Director of the Stanford Center on Early Childhood. His research focuses on developing and evaluating scalable early childhood interventions in communities, translating scientific knowledge regarding healthy development under conditions of adversity for use in social policy and programs. He is particularly interested in the effects of early stressful experiences on children's development and in prevention and treatment programs aimed at improving children's functioning in areas such as relationships with caregivers and peers, social-emotional development, and academic achievement. Dr. Fisher is the lead investigator of the ongoing RAPID-EC project, a national survey on the well-being of households with young children during the COVID-19 pandemic. He has developed several evidence-based interventions supporting healthy child development in the context of social and economic adversity, including Treatment Foster Care Oregon for Preschoolers (TFCO-P), Kids in Transition to School (KITS), and the Filming Interactions to Nurture Development (FIND) video coaching program for supporting parenting and early childhood care professionals. He has published over 250 scientific papers in peer-reviewed journals and has received notable awards such as the 2012 Society for Prevention Research Translational Science Award and being named a Fellow of the American Psychological Society in 2019. His titles include Professor at the Graduate School of Education, courtesy Professor of Pediatrics, and member of the Wu Tsai Neurosciences Institute. His research interests encompass brain and learning sciences, child development, early childhood, leadership and organization, parents and family issues, poverty and inequality, professional development, psychology, and social-emotional learning.

Research topics

• Medicine
• Internal medicine
• Biology
• Genetics
• Cancer research
• Radiology
• Pathology
• Computer Science
• Artificial Intelligence
• Machine Learning
• Biochemistry
• Endocrinology
• Computational biology
• Oncology
• Bioinformatics

Selected publications

• A Qualitative Analysis of Physician Communication During Brain Death Conversations

  Neurology Clinical Practice · 2025-06-04

  article

  Background and Objectives: In recent decades, many legal cases have resulted from physicians ineffectively communicating to a family that their loved one is brain dead (brain dead/death by neurologic criteria [BD/DNC]). Although the definition of BD/DNC has recently undergone revision, little research has been conducted to establish optimal approaches in communicating BD/DNC status to families. The aim of this study was to characterize what highly experienced physicians perceive to be the best communication practices and language choices during BD/DNC conversations. Methods: In this qualitative study, we conducted semistructured, in-depth interviews with physician leaders in the field of BD/DNC between September 2023 and January 2024. All interviews were conducted through Zoom. Twenty expert physician participants were recruited from multiple institutions across the United States through convenience sampling. Participants were current or former attending physicians whose practices at academic institutions involved communication with families about BD/DNC in either the pediatric or adult setting. Participants completed a Qualtrics form containing questions about their demographic background and practice characteristics, including an estimate of the number of times they communicated BD/DNC to patient families. Semistructured interviews were conducted with each of the participants and included hypothetical scenarios and views about best practices. Results: Using 20 qualitative interview transcripts, we identified multiple areas of agreement and disagreement among expert physicians regarding best practices in communicating BD/DNC status. While physicians concurred on specific language to use and avoid, they differed on whether to use the word "coma," on when to introduce the possibility of brain death, and on whether to analogize with cardiac death. There was strong agreement on the utility of visualization through imaging and family attendance at BD/DNC testing. Finally, physicians were in consensus that multiple family meetings with the same providers are crucial for successful BD/DNC communication. Discussion: This study described main convergences and divergences in physician language during BD/DNC conversations and used qualitative data to present a "train journey" theory of ideal physician communication with families. By investigating and improving physician communication styles during BD/DNC conversations, the medical community may ameliorate the legal and medical fallout that results from clinical miscommunication.

  PublisherDOI

• Enriched phenotypes in rare variant carriers suggest pathogenic mechanisms in rare disease patients

  BioData Mining · 2025-01-17 · 1 citations

  articleOpen access

  BACKGROUND: The mechanistic pathways that give rise to the extreme symptoms exhibited by rare disease patients are complex, heterogeneous, and difficult to discern. Understanding these mechanisms is critical for developing treatments that address the underlying causes of diseases rather than merely the presenting symptoms. Moreover, the same dysfunctional series of interrelated symptoms implicated in rare recessive diseases may also lead to milder and potentially preventable symptoms in carriers in the general population. Seizures are a common and extreme phenotype that can result from diverse and often elusive pathways in patients with ultrarare or undiagnosed disorders. METHODS: In this pilot study, we present an approach to understand the underlying pathways leading to seizures in patients from the Undiagnosed Diseases Network (UDN) by analyzing aggregated genotype and phenotype data from the UK Biobank (UKB). Specifically, we look for enriched phenotypes across UKB participants who harbor rare variants in the same gene known or suspected to be causally implicated in a UDN patient's recessively manifesting disorder. Analyzing these milder but related associated phenotypes in UKB participants can provide insight into the disease-causing mechanisms at play in rare disease UDN patients. RESULTS: We present six vignettes of undiagnosed patients experiencing seizures as part of their recessive genetic condition. For each patient, we analyze a gene of interest: MPO, P2RX7, SQSTM1, COL27A1, PIGQ, or CACNA2D2, and find relevant symptoms associated with UKB participants. We discuss the potential mechanisms by which the digestive, skeletal, circulatory, and immune system abnormalities found in the UKB patients may contribute to the severe presentations exhibited by UDN patients. We find that in our set of rare disease patients, seizures may result from diverse, multi-step pathways that involve multiple body systems. CONCLUSIONS: Analyses of large-scale population cohorts such as the UKB can be a critical tool to further our understanding of rare diseases in general. Continued research in this area could lead to more precise diagnostics and personalized treatment strategies for patients with rare and undiagnosed conditions.

  PublisherOA PDFDOI

• CNSC-68. LEVETIRACETAM THERAPEUTICALLY TARGETS GABAERGIC SYNAPSES IN DIFFUSE MIDLINE GLIOMA

  Neuro-Oncology · 2025-11-01

  articleOpen access

  Abstract Pediatric high-grade gliomas (HGGs) are the leading cause of brain cancer-related death in children. HGGs include distinct subtypes defined by anatomical location as well as molecular characteristics that stratify into H3K27M-altered diffuse midline gliomas (DMG) and hemispheric HGGs such as isocitrate dehydrogenase-wild type (IDH-WT) glioblastoma. Neuronal activity drives HGG progression both through paracrine signaling and direct neuron-to-glioma synapses. Using whole-cell patch clamp electrophysiology, in vivo optogenetics, and patient-derived glioma xenograft mouse models, we identify functional, tumor-promoting GABAergic neuron-to-glioma synapses mediated by GABAA receptors in DMGs. GABAergic input has a depolarizing effect on DMG cells due to chloride uptake by the Na-K-2Cl cotransporter NKCC1 and consequent elevated intracellular chloride concentration. In contrast, depolarizing GABAergic currents were not detected in IDH-WT HGG. Membrane depolarization is known to increase glioma proliferation and accordingly, we find that the activity of GABAergic interneurons promotes DMG proliferation in vivo. Increasing GABA signaling with the benzodiazepine lorazepam increases glioma proliferation and reduces survival in xenograft models of DMG but not IDH-WT HGG. Conversely, we find that the anti-seizure medication levetiracetam attenuates low-frequency depolarizing GABAergic synaptic currents in a glioma-specific manner, reducing those in DMG but not in healthy neurons. The effect in DMG is independent of action on synaptic vesicle glycoprotein 2A (SV2A), the chief mechanism by which levetiracetam suppresses seizures. Levetiracetam reduces glioma proliferation and extends survival of mice bearing DMG xenografts, but not IDH-WT HGG xenografts. Retrospective real-world clinical data demonstrate longer overall survival for children with DMG who were taking levetiracetam, which was not evident in pediatric hemispheric HGG. These findings uncover growth-promoting GABAergic synaptic communication between GABAergic neurons and DMG cells, underscoring a tumor subtype-specific mechanism of brain cancer neurophysiology with potentially important implications for commonly used drugs in this disease context, which should be further studied in future prospective clinical studies.

  PublisherOA PDFDOI

• Monitoring Head Circumference is Fundamental to Clinical Diagnosis

  The Journal of Pediatrics · 2025-11-28

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Step Up After Concussion

  The Journal of Pediatrics · 2025-01-31

  article1st authorCorresponding
  PublisherDOI

• Large-scale mutational analysis identifies UNC93B1 variants that drive TLR-mediated autoimmunity in mice and humans

  The Journal of Experimental Medicine · 2024-05-23 · 34 citations

  articleOpen access

  Nucleic acid-sensing Toll-like receptors (TLR) 3, 7/8, and 9 are key innate immune sensors whose activities must be tightly regulated to prevent systemic autoimmune or autoinflammatory disease or virus-associated immunopathology. Here, we report a systematic scanning-alanine mutagenesis screen of all cytosolic and luminal residues of the TLR chaperone protein UNC93B1, which identified both negative and positive regulatory regions affecting TLR3, TLR7, and TLR9 responses. We subsequently identified two families harboring heterozygous coding mutations in UNC93B1, UNC93B1+/T93I and UNC93B1+/R336C, both in key negative regulatory regions identified in our screen. These patients presented with cutaneous tumid lupus and juvenile idiopathic arthritis plus neuroinflammatory disease, respectively. Disruption of UNC93B1-mediated regulation by these mutations led to enhanced TLR7/8 responses, and both variants resulted in systemic autoimmune or inflammatory disease when introduced into mice via genome editing. Altogether, our results implicate the UNC93B1-TLR7/8 axis in human monogenic autoimmune diseases and provide a functional resource to assess the impact of yet-to-be-reported UNC93B1 mutations.

  PublisherOA PDFDOI

• DIPG-47. SEQUENTIAL INTRAVENOUS AND INTRACEREBROVENTRICULAR GD2-CAR T-CELL THERAPY FOR H3K27M-MUTATED DIFFUSE MIDLINE GLIOMAS

  Neuro-Oncology · 2024-06-18

  articleOpen access

  Abstract BACKGROUND H3K27M-mutant diffuse midline gliomas (DMGs) express uniformly high levels of the GD2 disialoganglioside. In preclinical models, chimeric antigen receptor modified T-cells (CAR T-cells) targeting GD2 robustly regressed orthotopically xenografted DMGs. METHODS This Phase I trial (NCT04196413) administered one IV dose of autologous T-cells transduced with a GD2-CAR retroviral vector to patients with H3K27M-mutant pontine (DIPG) or spinal (sDMG) diffuse midline gliomas at two dose levels (DL1=1e6 GD2-CAR T-cells/kg; DL2=3e6 GD2-CAR T-cells/kg) following standard lymphodepleting (LD) chemotherapy. Patients with clinical or imaging benefit following IV infusion were eligible for subsequent intracerebroventricular (ICV) GD2-CAR T-cell infusions (10-30e6 GD2-CAR T-cells). Primary objectives were to determine feasibility of manufacturing, assess tolerability of IV GD2-CAR T-cells in patients with DIPG and sDMG, and identify a maximally tolerated dose of IV GD2-CAR T-cells following lymphodepleting chemotherapy. Secondary objectives included preliminary assessments of benefit. Here we report the final results of Arm A. RESULTS Thirteen patients enrolled and 11 received one IV GD2-CAR T infusion on study [n=3 DL1(3 DIPG); n=8 DL2(6 DIPG/2 sDMG). GD2-CAR T-cells were successfully manufactured for each patient. After IV infusion, no dose-limiting toxicities (DLTs) occurred on DL1, but three patients experienced DLT on DL2 due to grade 4 cytokine release syndrome (CRS). Nine patients received ICV infusions, which were not associated with DLTs. All patients exhibited tumor inflammation-associated neurotoxicity (TIAN). Four patients demonstrated major volumetric reductions of 52%, 54%, 91% and 100%. One patient exhibited a complete response durable for >30 months since therapy began. Eight patients demonstrated neurological benefit based upon a protocol-directed Clinical Improvement Score. CONCLUSIONS Sequential IV followed by ICV GD2-CAR T-cells infusions induced tumor regressions and neurological improvements. DL1 was established as the maximally tolerated IV GD2-CAR T-cell dose. Neurotoxicity was safely managed with intensive monitoring and close adherence to a management algorithm.

  PublisherOA PDFDOI

• LUSTR: a new customizable tool for calling genome-wide germline and somatic short tandem repeat variants

  BMC Genomics · 2024-01-26

  articleOpen access

  BACKGROUND: Short tandem repeats (STRs) are widely distributed across the human genome and are associated with numerous neurological disorders. However, the extent that STRs contribute to disease is likely under-estimated because of the challenges calling these variants in short read next generation sequencing data. Several computational tools have been developed for STR variant calling, but none fully address all of the complexities associated with this variant class. RESULTS: Here we introduce LUSTR which is designed to address some of the challenges associated with STR variant calling by enabling more flexibility in defining STR loci, allowing for customizable modules to tailor analyses, and expanding the capability to call somatic and multiallelic STR variants. LUSTR is a user-friendly and easily customizable tool for targeted or unbiased genome-wide STR variant screening that can use either predefined or novel genome builds. Using both simulated and real data sets, we demonstrated that LUSTR accurately infers germline and somatic STR expansions in individuals with and without diseases. CONCLUSIONS: LUSTR offers a powerful and user-friendly approach that allows for the identification of STR variants and can facilitate more comprehensive studies evaluating the role of pathogenic STR variants across human diseases.

  PublisherOA PDFDOI

• Comments and Controversies in Oncology: The Tribulations of Trials Developing ONC201

  Journal of Clinical Oncology · 2024-08-07 · 11 citations

  article

  Our international team highlights issues with efficacy reports in several studies on DMG with the new drug ONC201.

  PublisherDOI

• ALPHA2: A Phase 1b Study Evaluating the CD19 Allogeneic CAR T Cell Product Cemacabtagene Ansegedleucel (Cema-Cel) in Patients With Relapsed/ Refractory (R/R) Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL)

  Clinical Lymphoma Myeloma & Leukemia · 2024-08-26

  article
  PublisherDOI

Recent grants

• NIH Grant RC2CA148491

  NIH · $1.5M · 2013

• NIH Grant R01CA098712

  NIH · $1.8M · 2008

• NIH Grant K12NS049648

  NIH · $1.4M · 2011

• NIH Grant R01CA097318

  NIH · $2.8M · 2014

• Center for Undiagnosed Diseases at Stanford

  NIH · $6.2M · 2022–2023

Frequent coauthors

• Stewart Goldman

  Lurie Children's Hospital

  380 shared

• Maryam Fouladi

  The Ohio State University

  372 shared

• Ian F. Pollack

  University of Pittsburgh

  369 shared

• Roger J. Packer

  Children's National

  361 shared

• Girish Dhall

  University of Alabama at Birmingham

  355 shared

• Ira J. Dunkel

  Memorial Sloan Kettering Cancer Center

  336 shared

• Shengjie Wu

  Central South University

  335 shared

• Rishi Lulla

  Hasbro Children's Hospital

  329 shared

Education

• MD, Medicine

  UCSF Medical Center

• BA, Human Biology

  Stanford University

• MHS, School of Public Health and Hygiene

  Johns Hopkins University

Awards & honors

• 2012 Society for Prevention Research Translational Science A…
• 2019 Fellow of the American Psychological Society