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Integration of epidemiology, immunobiology, and translational research for brain tumors

Identifieur interne : 005F38 ( Main/Exploration ); précédent : 005F37; suivant : 005F39

Integration of epidemiology, immunobiology, and translational research for brain tumors

Auteurs : Hideho Okada [États-Unis] ; Michael E. Scheurer [États-Unis] ; Saumendra N. Sarkar [États-Unis] ; Melissa L. Bondy [États-Unis]

Source :

RBID : ISTEX:6ADF7CC53AFC2E5D53010794B97DF6C53A32AE48

Descripteurs français

English descriptors

Abstract

We recently identified a pivotal role for the host type I interferon (IFN) pathway in immunosurveillance against de novo mouse glioma development, especially through the regulation of immature myeloid cells (IMCs) in the glioma microenvironment. The present paper summarizes our published work in a number of areas. We have identified single‐nucleotide polymorphisms (SNPs) in human IFN genes that dictate altered prognosis of patients with glioma. One of these SNPs (rs12553612) is located in the promoter of IFNA8 and influences its activity. Conversely, recent epidemiologic data show that chronic use of nonsteroidal anti‐inflammatory drugs lowers the risk of glioma. We translated these findings back to our de novo glioma model and found that cyclooxygenase‐2 inhibition enhances antiglioma immunosurveillance by reducing glioma‐associated IMCs. Taken together, these findings suggest that alterations in myeloid cell function condition the brain for glioma development. Finally, in preliminary work, we have begun applying novel immunotherapeutic approaches to patients with low‐grade glioma with the aim of preventing malignant transformation. Future research will hopefully better integrate epidemiological, immunobiological, and translational techniques to develop novel, preventive approaches for malignant gliomas.

Url:
DOI: 10.1111/nyas.12115


Affiliations:


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<term>Biomarkers prev</term>
<term>Bone marrow</term>
<term>Brain tumors</term>
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<term>Hideho okada</term>
<term>High risk</term>
<term>Ifna8</term>
<term>Ifna8 promoter</term>
<term>Imcs</term>
<term>Immature myeloid cells</term>
<term>Immunologic factors</term>
<term>Immunological responses</term>
<term>International study</term>
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<term>Lggs</term>
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<term>Ndings</term>
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<term>Nonsteroidal drugs</term>
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<term>Peptide</term>
<term>Pilot study</term>
<term>Pivotal role</term>
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<term>Suppressor cells</term>
<term>System tumors</term>
<term>Translational</term>
<term>Translational research</term>
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<term>York academy</term>
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<term>Adult glioma</term>
<term>Allergy</term>
<term>Antiglioma immunosurveillance</term>
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<term>Biomarkers prev</term>
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<term>Brain tumors</term>
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<term>Relative luciferase</term>
<term>Risk factors</term>
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<div type="abstract">We recently identified a pivotal role for the host type I interferon (IFN) pathway in immunosurveillance against de novo mouse glioma development, especially through the regulation of immature myeloid cells (IMCs) in the glioma microenvironment. The present paper summarizes our published work in a number of areas. We have identified single‐nucleotide polymorphisms (SNPs) in human IFN genes that dictate altered prognosis of patients with glioma. One of these SNPs (rs12553612) is located in the promoter of IFNA8 and influences its activity. Conversely, recent epidemiologic data show that chronic use of nonsteroidal anti‐inflammatory drugs lowers the risk of glioma. We translated these findings back to our de novo glioma model and found that cyclooxygenase‐2 inhibition enhances antiglioma immunosurveillance by reducing glioma‐associated IMCs. Taken together, these findings suggest that alterations in myeloid cell function condition the brain for glioma development. Finally, in preliminary work, we have begun applying novel immunotherapeutic approaches to patients with low‐grade glioma with the aim of preventing malignant transformation. Future research will hopefully better integrate epidemiological, immunobiological, and translational techniques to develop novel, preventive approaches for malignant gliomas.</div>
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