MOLECULAR MECHANISTIC BASIS FOR RADIATION INDUCED PULMONARY LATE EFFECTS

辐射引起的肺迟发效应的分子机制基础

• 批准号: 6563658
• 负责人: Jacob N Finkelstein
• 金额: $ 15.75万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-02-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6563658
• 关键词: RNase protection assay; allergic pneumonitis; alveolar macrophages; cell cell interaction; cell type; chemokine; cytokine; enzyme linked immunosorbent assay; fibroblast growth factor; gene expression; genetic strain; immunocytochemistry; in situ hybridization; ionizing radiation; laboratory mouse; medical complication; molecular pathology; neoplasm /cancer radiation therapy; protein biosynthesis; pulmonary fibrosis /granuloma; radiation dosage; radiation genetics; radiation sensitivity; respiratory epithelium; vascular endothelium

Description: (Applicant?s Description)The general goal of this program is directed at gaining a deeper understanding of the molecular mechanisms which are the basis for the normal tissue late effects which are observed in the lung following radiation. Previous CERRIS programs have led to the paradigm of radiation late effects being dependent upon the "conversation" which takes place between a number of injured cells, rather than the classic concept of a single target cell. In pursuit of this goal, they mean to further define the conversation, which they have hypothesized as a "cytokine cascade", in terms of the spatial and temporal release of proinflammatory and profibrotic cytokines and growth factors, and their genetic context. Expansion of this paradigm has led them to postulate the role of the immune system in the development of late tissue effects and this will be explored in more detail. Modulation of the cytokine cascade(s) and/or the immune system will be investigated as a means of both elucidating the roles of specific cytokines, as well as suggesting routes of amelioration.

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