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）：越来越多的分子标志物被鉴定为与癌症转移或不良预后相关。通常，这些标志物是基于生物活性的潜力来检查的，该生物活性将起到增强癌细胞生长和转移的作用。还报道了通过自分泌或旁分泌环组成性激活的各种细胞因子或生长因子受体，从而支持癌细胞生长。虽然粒细胞集落刺激因子（G-CSF）的表达已被证明是多种癌细胞类型的，但越来越多的关于各种非造血系统人类癌症和癌细胞系的G-CSF受体（G-CSFR）的异常表达的报道正在发表。我们的目的是清楚地表明，G-CSF的表达加上异常G-CSFR表达的移行细胞癌（TCC）可以作为一个预测更积极的行为。我们将证明G-CSF/G-CSFR表达的生物学影响，在体外，也在体内通过使用小鼠TCC模型。因此，正在扩大的各种实体瘤所证明的异常G-CSFR表达可以作为影响临床结果的特定肿瘤细胞能力的标志物，也可以作为许多这些肿瘤增强功能的机制。