BLADDER TISSUE BANK

膀胱组织库

• 批准号: 8167199
• 负责人: DAN THEODORESCU
• 金额: $ 6.28万
• 依托单位: UNIVERSITY OF VIRGINIA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-03-01 至 2013-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167199
• 关键词: Adjuvant; Adjuvant Therapy; Biological; Biological Markers; Biology; Bladder; Bladder Tissue; CXC Chemokines; Coin; Computer Retrieval of Information on Scientific Projects Database; Failure; Funding; Grant; Immunity; Immunotherapy; Institution; Interferons; Invaded; Lamina Propria; Malignant neoplasm of urinary bladder; Mediating; Muscle; Patients; Protocols documentation; Recurrence; Renal Cell Carcinoma; Research; Research Personnel; Resources; Role; Source; Staging; Therapeutic Intervention; Tissue Banking; Tissue Banks; United States National Institutes of Health; angiogenesis; base; improved; success; tumor

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. There has been controversy related to the management of non-muscle invasive bladder cancer, which invades the lamina propria (pT1). This stage of bladder cancer has a significant propensity for recurrence and progression. We need to further understand the role of immunotherapy and/or whether this form of therapy should be optimized in order to improve therapeutic intervention of early stage bladder cancer, especially in those patients with recurrence of their tumor in the context of adjuvant BCG therapy. On the basis of the ability of interferon-inducible CXC chemokines to promote Th1 immunity and inhibit angiogenesis, we have coined the term, "immunoangiostasis" for their potential biological role in promoting tumor regression. Recently, we have identified the importance of the biology of immunoangiostasis in mediating tumor regression related to renal cell carcinoma. In this proposal, we hypothesize that the biology of immunoangiostasis is critical to the full success of adjuvant immunotherapy with BCG in patients with non-muscle invasive bladder cancer. Moreover, we postulated that in patients who fail to respond to this type of adjuvant therapy,, failure is due to their inability to manifest a full immunoangiostatic effect to their tumor. This latter concept would also suggest that there may be immunoangiostatic mechanisms that could be further optimized in order to fully mediate immunoangiostasis in these tumors. The protocol submitted for review will be used to determine whether the expression of interferon-inducible CXC chemokines in patients with non-muscle invasive bladder can be used as a biomarker to predict those patients that will respond vs. patients that will fail to respond to immunotherapy.

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。 对于侵犯固有层（pT1）的非肌层浸润性膀胱癌的治疗一直存在争议。此阶段的膀胱癌具有明显的复发和进展倾向。我们需要进一步了解免疫疗法的作用和/或是否应该优化这种治疗形式，以改善早期膀胱癌的治疗干预，特别是在辅助卡介苗治疗背景下肿瘤复发的患者。基于干扰素诱导的CXC趋化因子促进Th1免疫和抑制血管生成的能力，我们创造了术语“免疫血管抑制”，因为它们在促进肿瘤消退中具有潜在的生物学作用。 最近，我们已经确定了免疫血管抑制生物学在介导肾细胞癌相关肿瘤消退中的重要性。在本提案中，我们假设免疫血管抑制的生物学特性对于非肌层浸润性膀胱癌患者使用卡介苗进行辅助免疫治疗的完全成功至关重要。此外，我们假设，在对此类辅助治疗没有反应的患者中，失败是由于他们无法对肿瘤表现出完全的免疫血管抑制作用。 后一个概念还表明，可能存在可以进一步优化的免疫血管抑制机制，以充分介导这些肿瘤中的免疫血管抑制。提交审查的方案将用于确定非肌层浸润性膀胱患者中干扰素诱导的 CXC 趋化因子的表达是否可以用作生物标志物来预测对免疫治疗有反应的患者与对免疫治疗无反应的患者。