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NIH RePORTER · NIH · U54 · $172,073 · view on reporter.nih.gov ↗

Abstract

Enhancing antigen and cytokine expression to break immune tolerance and improve antitumor response Gliomas, like other solid tumors, restrict immune recognition of aberrant cancer cells. Further complicating this, pediatric cancers also have lower mutation rates than adult tumors making them more difficult to generate an immunotherapeutic response. This proposal addresses three mechanisms contributing to immune resistance in pediatric tumors: 1) low mutational loads, 2) myeloid immunosuppressive environment, and 3) MHC downregulation (immuno-editing). We have developed a multimodal virus based vaccine platform that uses the virus’s natural ability to recruit immune cells and break immune tolerance to improve immune activity against the tumor. By encoding tumor associated self-antigens within the viral genome so that they are expressed during infection our results show that we can convert the antiviral response into an anti-tumor response. The studies described in our proposal seek to improve our virus-based multi-modal vaccine approach to overcome immune restriction in one of the most difficult to treat solid tumors, malignant glioma. We propose testing our hypothesis that: Engineered viral modifications that enhance native and adoptive immune cell activity will improve durable anti-tumor activity in treatment resistant pediatric gliomas by the following aims.

Key facts

NIH application ID
10707767
Project number
3U54CA232561-01A1S5
Recipient
RESEARCH INST NATIONWIDE CHILDREN'S HOSP
Principal Investigator
TIMOTHY P CRIPE
Activity code
U54
Funding institute
NIH
Fiscal year
2022
Award amount
$172,073
Award type
3
Project period
2022-05-01 → 2024-08-31