A5073331883- Neuroblastoma Research and Treatments
- Polyamine Metabolism and Applications
- Renal and related cancers
- Pancreatic function and diabetes
- Renal cell carcinoma treatment
- Ethics and Legal Issues in Pediatric Healthcare
- Chronic Myeloid Leukemia Treatments
- Immunodeficiency and Autoimmune Disorders
- Urological Disorders and Treatments
- Pneumocystis jirovecii pneumonia detection and treatment
- Erythrocyte Function and Pathophysiology
- Anesthesia and Sedative Agents
- Cancer, Hypoxia, and Metabolism
- Childhood Cancer Survivors' Quality of Life
- Cancer Genomics and Diagnostics
- Neutropenia and Cancer Infections
- Drug-Induced Adverse Reactions
- Anesthesia and Neurotoxicity Research
- Chemotherapy-induced organ toxicity mitigation
- Renal Diseases and Glomerulopathies
- Tumors and Oncological Cases
- Intensive Care Unit Cognitive Disorders
Children's Hospital of Philadelphia
2008-2025
UNSW Sydney
2016
University of Pennsylvania
2009
Connecticut Children's Medical Center
2000
University of Connecticut
2000
Abstract Neuroblastoma is a frequently lethal childhood tumor in which MYC gene deregulation, commonly as MYCN amplification, portends poor outcome. Identifying the requisite biopathways downstream of may provide therapeutic opportunities. We used transcriptome analyses to show that MYCN-amplified neuroblastomas have coordinately deregulated myriad polyamine enzymes (including ODC1, SRM, SMS, AMD1, OAZ2, and SMOX) enhance biosynthesis. High-risk tumors without amplification also overexpress...
Deregulated MYC drives oncogenesis in many tissues yet direct pharmacologic inhibition has proven difficult. coordinately regulates polyamine homeostasis as these essential cations support functions, and drugs that antagonize sufficiency have synthetic-lethal interactions with Neuroblastoma is a lethal tumor which the homologue MYCN, ODC1, rate-limiting enzyme synthesis, are frequently deregulated so we tested optimized depletion regimens for activity against neuroblastoma.We used...
Objective: To evaluate age, TNW, or tumor diameter (TD) as continuous prognostic variables for outcomes in early stage FHWT after accounting biology and treatment. Summary of Background Data: Patient age (< 2 vs. ≥ years) nephrectomy weight (TNW; < 550g 550 grams) have been used to risk stratify children with I favorable histology Wilms (FHWT) on Children’s Oncology Group (COG) studies select patients omission chemotherapy. Methods: Included had II per central review were treated only,...
We describe a case of Pneumocystis jirovecii pneumonia in an 18-year-old female individual with refractory primary mediastinal B-cell lymphoma treated the immune checkpoint inhibitor pembrolizumab. She received 11 doses pembrolizumab without immune-related adverse events (irAEs) before diagnosis P. pneumonia. However, prophylactic trimethoprim/sulfamethoxazole was discontinued 6 months postautologous stem cell transplant per standard guidelines. This report highlights importance judicious...
Abstract Introduction The prognostic impact of positive lymph nodes (LN+) and/or singular loss heterozygosity (LOH) 1p or 16q were assessed in children with stage III favorable histology Wilms tumor (FHWT) enrolled on AREN0532 AREN03B2 alone. Patients and Methods A total 635 FHWT vincristine/dactinomycin/doxorubicin (DD4A)–treated patients met inclusion criteria. Event‐free survival (EFS) overall are reported by LN sampling, status, LOH 1p, 16q, a combination status LOH. unknown combined...
<div>Abstract<p>Neuroblastoma is a frequently lethal childhood tumor in which <i>MYC</i> gene deregulation, commonly as <i>MYCN</i> amplification, portends poor outcome. Identifying the requisite biopathways downstream of may provide therapeutic opportunities. We used transcriptome analyses to show that <i>MYCN</i>-amplified neuroblastomas have coordinately deregulated myriad polyamine enzymes (including <i>ODC1, SRM, SMS, AMD1,...
Supplementary Figure Legends 1-3 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 1 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 3 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 2 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure Legends 1-3 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 3 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 2 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
Supplementary Figure 1 from <i>ODC1</i> Is a Critical Determinant of <i>MYCN</i> Oncogenesis and Therapeutic Target in Neuroblastoma
<p>Supplementary Methods, Tables and Figures</p>
<div>Abstract<p><b>Purpose:</b> Deregulated <i>MYC</i> drives oncogenesis in many tissues yet direct pharmacologic inhibition has proven difficult. coordinately regulates polyamine homeostasis as these essential cations support functions, and drugs that antagonize sufficiency have synthetic-lethal interactions with <i>MYC</i>. Neuroblastoma is a lethal tumor which the homologue <i>MYCN</i>, <i>ODC1</i>, rate-limiting...