Agnes Reschke, MD is a clinical fellow in the Division of Pediatric Hematology and Oncology at the Lucile Packard Children's Hospital, Stanford University School of Medicine. She obtained her bachelor of science and honors from Villanova University and after her family moved to Kentucky, went on to medical school at University of Kentucky College of Medicine. She completed a pediatric residency at Connecticut Children's Medical Center and during that time, focused on a clinical research project evaluating a proposed association between domestic radon levels and the development of sarcoma. Dr. Reschke ultimately came to Lucile Packard Children's Hospital for her pediatric hematology/oncology fellowship and during that time, discovered the emerging field of onco-critical care. Her fellowship research is in the lab of Tim Cornell, chief of pediatric critical care at Stanford. She is working to apply a real-time assay to measure cytokines in subsets of pediatric oncology patients to guide immunomodulatory therapies. By gaining a better understanding of these patients’ immune responses in real time, she believes that we will open the door for precision immunomodulatory therapy to treat critically ill patients, especially those experiencing sepsis or cytokine release syndrome. After completion of her hematology/oncology fellowship, Dr. Reschke will be pursuing a pediatric intensive care fellowship with the hope of becoming a leader and pioneer in onco-critical care.
- Pediatric Hematology/Oncology
- Onco-Critical Care
- Circulating cytokines
Honors & Awards
Inpatient Fellow Teaching Award, Pediatric Residency Program at LPCH/Stanford (2018-2019)
Member, Gold Humanism Honor Society
Residency, University of Connecticut, Pediatrics (2018)
MD, University of Kentucky College of Medicine (2015)
BS, Villanova University, Biology, Honors (2011)
Current Clinical Interests
- Critically Ill Oncology Patients
Dr. Reschke hopes to bring together the fields of pediatric oncology and critical care with the goal of ultimately impacting the clinical care and outcomes of critically ill pediatric oncology patients. While outcomes in these patients have improved with advances in intensive care and supportive treatments, novel therapies including emerging molecular therapies and immunotherapies bring significant new challenges. She hopes to address this developing need and envisions a career that translates lessons from the oncology networks to implement multicenter prospective interventional studies involving oncology patients in an ICU setting.
Timothy Cornell, (7/1/2019)
Development of clinical pathways to improve multidisciplinary care of high-risk pediatric oncology patients.
Frontiers in oncology
2022; 12: 1033993
Clinical pathways are evidence-based tools that have been integrated into many aspects of pediatric hospital medicine and have proven effective at reducing in-hospital complications from a variety of diseases. Adaptation of similar tools for specific, high-risk patient populations in pediatric oncology has been slower, in part due to patient complexities and variations in management strategies. There are few published studies of clinical pathways for pediatric oncology patients. Pediatric patients with a new diagnosis of leukemia or lymphoma often present with one or more "oncologic emergencies" that require urgent intervention and deliberate multidisciplinary care to prevent significant consequences. Here, we present two clinical pathways that have recently been developed using a multidisciplinary approach at a single institution, intended for the care of patients who present with hyperleukocytosis or an anterior mediastinal mass. These clinical care pathways have provided a critical framework for the immediate care of these patients who are often admitted to the pediatric intensive care unit for initial management. The goal of the pathways is to facilitate multidisciplinary collaborations, expedite diagnosis, and streamline timely treatment initiation. Standardizing the care of high-risk pediatric oncology patients will ultimately decrease morbidity and mortality associated with these diseases to increase the potential for excellent outcomes.
View details for DOI 10.3389/fonc.2022.1033993
View details for PubMedID 36523979
View details for PubMedCentralID PMC9744920
Genomic Microsatellite Signatures Identify Germline Mismatch Repair Deficiency and Risk of Cancer Onset.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
PURPOSE: Diagnosis of Mismatch Repair Deficiency (MMRD) is crucial for tumor management and early detection in patients with the cancer predisposition syndrome constitutional mismatch repair deficiency (CMMRD). Current diagnostic tools are cumbersome and inconsistent both in childhood cancers and in determining germline MMRD.PATIENTS AND METHODS: We developed and analyzed a functional Low-pass Genomic Instability Characterization (LOGIC) assay to detect MMRD. The diagnostic performance of LOGIC was compared with that of current established assays including tumor mutational burden, immunohistochemistry, and the microsatellite instability panel. LOGIC was then applied to various normal tissues of patients with CMMRD with comprehensive clinical data including age of cancer presentation.RESULTS: Overall, LOGIC was 100% sensitive and specific in detecting MMRD in childhood cancers (N = 376). It was more sensitive than the microsatellite instability panel (14%, P = 4.3 * 10-12), immunohistochemistry (86%, P = 4.6 * 10-3), or tumor mutational burden (80%, P = 9.1 * 10-4). LOGIC was able to distinguish CMMRD from other cancer predisposition syndromes using blood and saliva DNA (P < .0001, n = 277). In normal cells, MMRDness scores differed between tissues (GI > blood > brain), increased over time in the same individual, and revealed genotype-phenotype associations within the mismatch repair genes. Importantly, increased MMRDness score was associated with younger age of first cancer presentation in individuals with CMMRD (P = 2.2 * 10-5).CONCLUSION: LOGIC was a robust tool for the diagnosis of MMRD in multiple cancer types and in normal tissues. LOGIC may inform therapeutic cancer decisions, provide rapid diagnosis of germline MMRD, and support tailored surveillance for individuals with CMMRD.
View details for DOI 10.1200/JCO.21.02873
View details for PubMedID 36240479
MAJOR TUMOR REGRESSIONS IN H3K27M-MUTATED DIFFUSE MIDLINE GLIOMA (DMG) FOLLOWING SEQUENTIAL INTRAVENOUS (IV) AND INTRACEREBROVENTRICULAR (ICV) DELIVERY OF GD2-CAR T-CELLS
OXFORD UNIV PRESS INC. 2022: 20-21
View details for Web of Science ID 000840122400074
GD2-CAR T cell therapy for H3K27M-mutated diffuse midline gliomas.
Diffuse intrinsic pontine glioma (DIPG) and other H3K27M-mutated diffuse midline gliomas (DMG) are universally lethal paediatric central nervous system tumours1. We previously discovered that the disialoganglioside GD2 is highly expressed on H3K27M-mutant glioma cells and demonstrated promising preclinical efficacy of GD2-directed chimeric antigen receptor (CAR) T cells2, providing the rationale for a first-in-human Phase 1 clinical trial (NCT04196413). Because CAR T-cell-induced brainstem inflammation can result in obstructive hydrocephalus, increased intracranial pressure, and dangerous tissue shifts, neurocritical care precautions were incorporated. Here we present the clinical experience from the first four patients with H3K27M-mutant DIPG/DMG treated with GD2-CAR T cells (GD2-CART) at dose level 1 (1e6 GD2-CAR T cells/kg administered intravenously). Patients who exhibited clinical benefit were eligible for subsequent GD2-CAR T infusions administered intracerebroventricularly3. Toxicity was largely related to tumor location and reversible with intensive supportive care. On-target, off-tumor toxicity was not observed. Three of four patients exhibited clinical and radiographic improvement. Proinflammatory cytokines were increased in plasma and cerebrospinal fluid (CSF). Transcriptomic analyses of 65,598 single cells from CAR T cell products and CSF elucidate heterogeneity in response between subjects and administration routes. These early results underscore the promise of this approach for H3K27M+ DIPG/DMG therapy.
View details for DOI 10.1038/s41586-022-04489-4
View details for PubMedID 35130560
GD2 CAR T cells mediate clinical activity and manageable toxicity in children and young adults with DIPG and H3K27M-mutated diffuse midline gliomas.
AMER ASSOC CANCER RESEARCH. 2021
View details for Web of Science ID 000680263501014
- SINGLE CELL RNA SEQUENCING FROM THE CSF OF SUBJECTS WITH H3K27M+DIPG/DMG TREATED WITH GD2 CAR T-CELLULAR THERAPY OXFORD UNIV PRESS INC. 2021: 39
- GD2 CAR T-CELLS MEDIATE CLINICAL ACTIVITY AND MANAGEABLE TOXICITY IN CHILDREN AND YOUNG ADULTS WITH H3K27M-MUTATED DIPG AND SPINAL CORD DMG OXFORD UNIV PRESS INC. 2021: 49-50