Jason T. Huse
A5024476694- Glioma Diagnosis and Treatment
- Epigenetics and DNA Methylation
- Cancer Genomics and Diagnostics
- MicroRNA in disease regulation
- Chromatin Remodeling and Cancer
- Immune cells in cancer
- RNA modifications and cancer
- Neuroblastoma Research and Treatments
- Cancer, Hypoxia, and Metabolism
- Nanoparticle-Based Drug Delivery
- Radiomics and Machine Learning in Medical Imaging
- Brain Metastases and Treatment
- Neuroinflammation and Neurodegeneration Mechanisms
- Ferroptosis and cancer prognosis
- Single-cell and spatial transcriptomics
- Cancer-related molecular mechanisms research
- Cancer and Skin Lesions
- Microtubule and mitosis dynamics
- Nonmelanoma Skin Cancer Studies
- Nanoplatforms for cancer theranostics
- DNA Repair Mechanisms
- Protein Degradation and Inhibitors
- Cytomegalovirus and herpesvirus research
- Histone Deacetylase Inhibitors Research
- Meningioma and schwannoma management
The University of Texas MD Anderson Cancer Center
2017-2025
The University of Texas Health Science Center at Houston
2023-2024
Memorial Sloan Kettering Cancer Center
2011-2023
Neurology, Inc
2022
Anderson University - South Carolina
2012-2021
Kettering University
2015-2019
Baylor College of Medicine
2019
NorthShore University HealthSystem
2017
University of Calgary
2014-2017
Massachusetts General Hospital
2017
Diffuse low-grade and intermediate-grade gliomas (which together make up the lower-grade gliomas, World Health Organization grades II III) have highly variable clinical behavior that is not adequately predicted on basis of histologic class. Some are indolent; others quickly progress to glioblastoma. The uncertainty compounded by interobserver variability in diagnosis. Mutations IDH, TP53, ATRX codeletion chromosome arms 1p 19q (1p/19q codeletion) been implicated as clinically relevant...
The prediction of clinical behavior, response to therapy, and outcome infiltrative glioma is challenging. On the basis previous studies tumor biology, we defined five molecular groups with use three alterations: mutations in TERT promoter, IDH, codeletion chromosome arms 1p 19q (1p/19q codeletion). We tested hypothesis that within based on these features, tumors would have similar variables, acquired somatic alterations, germline variants.We scored as negative or positive for each markers...
Another pathway to cancer resistance Therapies targeting the tumor microenvironment show promise for treating cancer. For example, antibodies colony-stimulating factor-1 receptor (CSF-1R) inhibit protumorigenic macrophages and regress tumors in mouse models of glioblastoma multiforme (GBM), a deadly form brain Quail et al. found that although CSR-1R blockade prolonged survival GBM, more than 50% eventually recurred. Recurrence was correlated with elevated PI3-K activity tumors, driven by...
Activated oncogenic signaling is central to the development of nearly all forms cancer, including most common class primary brain tumor, glioma. Research over last two decades has revealed particular importance Akt pathway, and its molecular antagonist PTEN (phosphatase tensin homolog), in process gliomagenesis. Recent studies have also demonstrated that microRNAs (miRNAs) may be responsible for modulation cancer-implicated genes tumors. Here we report identification miR-26a as a direct...
The amyloidogenic Abeta peptide is liberated from the amyloid precursor protein (APP) by two proteolytic activities, beta-secretase and gamma-secretase. Recently, a type I membrane termed BACE (beta-site APP cleaving enzyme) with characteristics of an aspartyl protease has been identified as beta-secretase. We undertook series biochemical morphological investigations designed to characterize basic properties this protein. Initial studies indicated that undergoes N-linked glycosylation at...
Patients with 1p/19q codeleted anaplastic oligodendroglial tumors who participated in RTOG (Radiation Therapy Oncology Group) 9402 lived much longer after chemoradiotherapy (CRT) than radiation therapy (RT) alone. However, some patients noncodeleted also benefited from CRT; survival curves separated the median had been reached, and significantly more ≥ 10 years CRT RT. Thus, status may not identify all responders to CRT.Using trial data, we inquired whether an IDH mutation or germ-line...
Despite a multiplicity of clinical trials testing immune checkpoint inhibitors, the frequency expression potential predictive biomarkers is unknown in glioma.In this study, we profiled shared biomarker phenotypes. To clarify relationships among tumor mutational load (TML), mismatch repair (MMR), and expression, patients with glioma (n = 327), including glioblastoma (GBM) 198), whose samples had been submitted for analysis from 2009 to 2016. The calculation algorithm TML included...
Glioblastoma is highly enriched with macrophages, and osteopontin (OPN) expression levels correlate glioma grade the degree of macrophage infiltration; thus, we studied whether OPN plays a crucial role in immune modulation. Quantitative PCR, immunoblotting, ELISA were used to determine expression. Knockdown was achieved using complementary siRNA, shRNA, CRISPR/Cas9 techniques, followed by series vitro functional migration immunological assays. gene-deficient mice examine roles...
Exosomes can mediate a dynamic method of communication between malignancies, including those sequestered in the central nervous system and immune system. We sought to determine whether exosomes from glioblastoma (GBM)-derived stem cells (GSCs) induce immunosuppression. report that GSC-derived (GDEs) have predilection for monocytes, precursor macrophages. The GDEs traverse monocyte cytoplasm, cause reorganization actin cytoskeleton, skew monocytes toward suppresive M2 phenotype, programmed...
// Kasthuri Kannan 1,4 , Akiko Inagaki 2 Joachim Silber Daniel Gorovets Jianan Zhang Edward R. Kastenhuber Adriana Heguy 4 John H. Petrini Timothy A. Chan 3,4 and Jason T. Huse 1 Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA Molecular Biology, 3 Radiation Oncology, Human Oncology Pathogenesis Program, Correspondence: Huse, email: Keywords : glioma, astrocytoma, IDH, ATRX, whole-exome sequencing Received October 01, 2012, Accepted 09, Published 11, 2012...
Large-scale cancer genome projects, such as the Cancer Genome Atlas (TCGA) project, are comprehensive molecular characterization efforts to accelerate our understanding of biology and discovery new therapeutic targets. The accumulating wealth multidimensional data provides a paradigm for important research problems including subtype discovery. current standard approach relies on separate clustering analyses followed by manual integration. Results can be highly type dependent, restricting...
Macrophage subsets are dynamically altered during glioma response to radiotherapy, and their targeting delays tumor recurrence in preclinical trials.
// Sevin Turcan 1,* , Armida W. M. Fabius Alexandra Borodovsky 2 Alicia Pedraza 1 Cameron Brennan Jason Huse Agnes Viale 3 Gregory J. Riggins and Timothy A. Chan 1,4,5 Human Oncology Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. Department of Neurosurgery, School Medicine, Johns Hopkins University, Baltimore, MD. Genomics Core, 4 Dept. Radiation Oncology, 5 Brain Tumor * These authors contributed equally to this work Correspondence: Chan, email: Keywords :...
Abstract H3F3A mutations are seen in ∼30% of pediatric glioblastoma ( GBMs ) and involve either the lysine residue at position 27 K27M or glycine 34 G34R/V ). Sixteen genes encode histone H 3, each variant differing only a few amino acids. Therefore, how single 3 gene contribute to carcinogenesis is unknown. predicted alter methylation H3K27 . H3K27me3 repressive mark critical stem cell maintenance mediated by EZH2 , member polycomb‐group PcG family. We evaluated expression using...
Mutational inactivation of ATRX (α-thalassemia mental retardation X-linked) represents a defining molecular alteration in large subsets malignant glioma. Yet the pathogenic consequences deficiency remain unclear, as do tractable mechanisms for its therapeutic targeting. Here we report that loss isogenic glioma model systems induces replication stress and DNA damage by way G-quadruplex (G4) secondary structure. Moreover, these effects are associated with acquisition disease-relevant copy...