PDGF RECEPTOR EXPRESSION IN GLIAL CELLS

胶质细胞中的 PDGF 受体表达

• 批准号: 2039081
• 负责人: CHIAYENG WANG
• 金额: $ 12.82万
• 依托单位: UNIVERSITY OF ILLINOIS AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-05-15 至 2001-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2039081
• 关键词: chimeric proteins; cyclic AMP; gel mobility shift assay; glia; glioma; globin; growth factor receptors; human genetic material tag; human tissue; neoplasm /cancer genetics; nucleic acid sequence; platelet derived growth factor; receptor expression; reporter genes; site directed mutagenesis

Gliomas are the most common and malignant of primary brain tumors in adults. Current treatments include surgical removal followed by chemotherapy. However,these procedures may themselves transform cells surrounding the lesion, leading to secondary tumors. The long-term goal of this research program seeks to identify mechanisms involved in transformation of glia. These studies will provide key insights into the development of gliomas and may identify novel targets for therapeutic intervention. The proposal focuses on the characterization of the mechanisms responsible for appropriate PDGFR expression during glial cell differentiation and examination of whether these mechanisms are defective in glial tumor cells. They physiological function of PDGFR is to control glial cell growth and differentiation during development. Overexpression of PDGFR is detected in both early and late stages of gliomas. Preliminary data suggest the PDGFR transcript does not respond to cAMP regulation in glioma cells as it does in normal glia. The hypothesis is that an altered response of PDGFR gene expression to cAMP regulation may underlie the uncontrolled proliferation of tumor cells. The specific aims of this proposal are to identify nucleotide sequences within the PDGFR gene and gene product ghat are involved in the cAMP- dependent regulatory mechanisms, and to establish a role for these factors in inducing aberrant PDGFR expression in glioma cells.

神经胶质瘤是最常见和恶性的原发性脑肿瘤 在成人中。 目前的治疗方法包括手术切除 通过化疗。 然而，这些程序本身可能 转化病变周围的细胞，导致继发性 肿瘤。 该研究计划的长期目标旨在 确定参与神经胶质细胞转化的机制。 这些 研究将为神经胶质瘤的发展提供重要见解 并可能确定治疗干预的新目标。 这 提案侧重于机制的特征 负责神经胶质细胞期间适当的 PDGFR 表达 区分并检查这些机制是否 神经胶质瘤细胞有缺陷。 它们的生理功能 PDGFR 的作用是控制神经胶质细胞的生长和分化 发展。 PDGFR 的过表达在早期和晚期均检测到。 和神经胶质瘤的晚期阶段。 初步数据表明 PDGFR 转录本不响应神经胶质瘤细胞中的 cAMP 调节 就像正常神经胶质细胞一样。 假设是改变了 PDGFR 基因表达对 cAMP 调节的反应可能是 肿瘤细胞不受控制的增殖。 具体目标 该提案的目的是鉴定内的核苷酸序列 PDGFR基因和基因产物ghat参与cAMP- 依赖的监管机制，并建立 这些因素诱导神经胶质瘤中PDGFR异常表达 细胞。