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Treatment of multiple myeloma using oncolytic myxoma virus

使用溶瘤粘液瘤病毒治疗多发性骨髓瘤

基本信息

批准号：
9187445
负责人：
Eric Carter Bartee
金额：
$ 34.2万
依托单位：
MEDICAL UNIVERSITY OF SOUTH CAROLINA
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-12-01 至 2020-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9187445
关键词：
Adverse event Apoptotic Autologous Binding Cancerous Cell Death Cells Cellular biology Clinical Data Defect Dependence Diagnosis Disease Dose Genetic Goals Hematopoietic Hematopoietic Neoplasms Human Immune response Immune system Immunologics In Vitro Light Malignant Neoplasms Mediating Methods Modality Molecular Molecular Biology Multiple Myeloma Myxoma Myxoma virus Nature Non-Malignant Normal Cell Oncolytic Oncolytic viruses Oryctolagus cuniculus Outcome Pathway interactions Patients Play Population Poxviridae Pre-Clinical Model Property Proteins Public Health Recombinant Proteins Relapse Residual Tumors Residual state Resistance Role Sampling Site Solid Neoplasm Systemic disease Therapeutic Translating Translations Transplantation Tumor Debulking Viral Viral Envelope Proteins Virus Virus Shedding Work base design improved improved outcome in vivo intravenous injection killings novel novel therapeutics prevent public health relevance response success

项目摘要

DESCRIPTION (provided by applicant): Oncolytic viruses, such as the rabbit-specific myxoma virus (MYXV), represent promising, novel methods to treat patients diagnosed with cancer. While the field of oncolytics has traditionally focused on solid tumors, our recent data demonstrates that the MYXV can also effectively treat the hematopoietic malignancy multiple myeloma. Specifically, MYXV discriminates myeloma cells from normal cells based on differential binding and subsequently eliminates these cells by inducing a rapid apoptotic response. This results in MYXV therapy completely preventing myeloma relapse associated with contamination of autologous transplant samples as well as eradicating residual myeloma in vivo through an apparent immunological mechanism. Unfortunately, the translation of this promising therapy is currently prevented by a lack of understanding concerning the mechanisms involved in treatment. This lack of understanding raises concerns about the accurate prediction of patient responses as well as the potential for treatment to generate adverse events. We therefore put forth the current proposal designed to advance the use of MYXV in a clinical setting by identifying the molecular mechanisms mediating: 1) the induction of an anti-myeloma immune response by systemic MYXV treatment, 2) the mechanisms mediating resistance of myeloma cells to MYXV therapy, and 3) the role that viral binding plays in delivery of MYXV to sites of residual disease. The successful completion of this project could have a significant impact on public health in a variety of ways. First it would advance the use of MYXV as a promising therapeutic for the treatment of patients with myeloma. Additionally, information generated in this proposal might be used to improve treatments with other oncolytic viruses by shedding light on the mechanisms mediating successful in vivo therapy.