Effect of G-CSFR expression in bladder cancer

G-CSFR表达在膀胱癌中的作用

• 批准号: 6929878
• 负责人: ARUP CHAKRABORTY
• 金额: $ 13.12万
• 依托单位: BAYLOR COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-08-01 至 2006-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6929878
• 关键词: biological signal transduction; biomarker; bladder neoplasm; cell growth regulation; cell line; cell migration; cell proliferation; colony stimulating factor; gene expression; genetic regulation; genetically modified animals; growth factor receptors; intermolecular interaction; laboratory mouse; metastasis; microarray technology; molecular oncology; neoplasm /cancer genetics; protein structure function

DESCRIPTION (provided by applicant): An increasing number of molecular markers are being identified that correlate with cancer metastasis or a poor prognosis. Typically these markers were examined based on the potential for a biologic activity that would act to enhance cancer cell growth and metastasis. There are also reports of various cytokine or growth factor receptors that are constitutively activated via autocrine or paracrine loops thus supporting cancer cell growth. While granulocyte colony-stimulating factor (G-CSF) expression has been shown for a wide variety of cancer cell types, an increasing number of reports are being published regarding the aberrant expression of the G-CSF receptor (G-CSFR) by various non-hematopoietic human cancers and cancer cell lines. Our aim is to clearly demonstrate that G-CSF expression coupled with aberrant G-CSFR expression by transitional cell carcinoma (TCC) can be used as a predictor of more aggressive behavior. We will demonstrate the biological impact of G-CSF/G-CSFR expression in in vitro and also in vivo by using a murine TCC model. Thus the aberrant G-CSFR expression that is being demonstrated by an expanding variety of solid tumors may serve as both a marker of specific tumor cell capabilities impacting clinical outcome and as a mechanism for many of these tumor-enhancing functions.

描述（由申请人提供）：正在鉴定出越来越多的分子标记物与癌症转移或预后不良相关。通常，基于生物学活性的潜力来检查这些标记，该生物活性会起到癌细胞生长和转移的作用。还报告了各种细胞因子或生长因子受体的报道，这些因子或生长因子受体通过自分泌或旁分泌环的组成症激活，从而支持癌细胞的生长。虽然已经显示了多种癌细胞类型的粒细胞刺激因子（G-CSF）的表达，但各种非杂型人类癌细胞和癌细胞系正在发表越来越多的报告，越来越多地发布了有关G-CSF受体（G-CSFR）异常表达的报告。我们的目的是清楚地证明，通过过渡细胞癌（TCC）与异常的G-CSFR表达相结合的G-CSF表达可以用作更具侵略性行为的预测指标。我们将通过使用鼠TCC模型来证明G-CSF/G-CSFR表达在体外和体内的生物学影响。因此，通过扩展的实体瘤来证明的异常G-CSFR表达可能是影响临床结果的特定肿瘤细胞能力的标记，也可以作为许多这些肿瘤增强功能的机制。