CYCLOPHOSPHAMIDE AND TASTE

环磷酰胺和味道

• 批准号: 8168176
• 负责人: Eugene R Delay
• 金额: $ 3.84万
• 依托单位: UNIVERSITY OF VERMONT & ST AGRIC COLLEGE
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-08-01 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8168176
• 关键词: Adult; Adverse effects; Area; Behavioral; Cell Cycle; Cell physiology; Cells; Computer Retrieval of Information on Scientific Projects Database; Cyclophosphamide; DNA Damage; DNA Repair; Drug usage; Esthesia; Funding; Gene Family; Grant; Institution; Lead; Malnutrition; Methods; Molecular; Molecular Biology; Pharmaceutical Preparations; Recovery; Research; Research Personnel; Resources; Role; Sensory; Source; Stem cells; System; Taste Perception; Techniques; Testing; United States National Institutes of Health; Work; chemotherapy; interest; mouse model; repaired; tool

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Cyclophosphamide is the most commonly prescribed drug used for chemotherapy, but it like other chemotherapy drugs, has many adverse side effects such as altered or lost taste sensory abilities which can lead to malnutrition and poorer recovery. We are interested in what causes the changes in taste functions due to chemotherapy. We hypothesize that cyclophosphamide damages the DNA of stem cells or progenitor cells for new taste sensory cells. The cell cycle is arrested until the DNA repair is complete. Once repaired, new taste sensory cells are generated from the stem cells and taste sensations recover. To test this hypothesis, we propose four Specific Aims that will use a range of tools from behavioral techniques to molecular biology using a mouse model. We will use behavioral and molecular methods to assess the breadth of functional disruptions caused by cyclophosphamide. In addition we propose to study how the drug disrupts adult taste stem cell functioning and how the system recovers, including the role of the Sox family of genes. No previous work has been done in this area. Our work aims to fill some voids in the understanding of this often devastating side effect of chemotherapy.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 环磷酰胺是最常用的化疗药物，但与其他化疗药物一样，它具有许多不良副作用，例如味觉感觉能力改变或丧失，从而导致营养不良和恢复较差。我们感兴趣的是化疗导致味觉功能发生变化的原因。我们假设环磷酰胺会损害新味觉细胞的干细胞或祖细胞的 DNA。细胞周期被抑制，直到 DNA 修复完成。一旦修复，干​​细胞就会产生新的味觉细胞，味觉就会恢复。为了检验这一假设，我们提出了四个具体目标，将使用从行为技术到使用小鼠模型的分子生物学等一系列工具。我们将使用行为和分子方法来评估环磷酰胺引起的功能破坏的范围。此外，我们建议研究该药物如何破坏成体味觉干细胞功能以及系统如何恢复，包括 Sox 基因家族的作用。此前该领域尚未开展任何工作。我们的工作旨在填补对化疗这种经常具有破坏性的副作用的理解空白。