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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 存在与侵入层次的非肌肉浸润性膀胱癌的管理有关的争议（PT1）。膀胱癌的这一阶段具有复发和进展的显着倾向。我们需要进一步了解免疫疗法的作用和/或是否应优化这种形式的治疗，以改善早期膀胱癌的治疗干预，尤其是在辅助BCG治疗的情况下，其肿瘤复发的患者。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，我们为“免疫血管静脉曲张”术语创造了它们在促进肿瘤回归中的潜在生物学作用。 最近，我们确定了免疫血管静脉曲张的生物学在介导与肾细胞癌相关的肿瘤回归中的重要性。在该提案中，我们假设免疫血管症的生物学对于非肌肉浸润性膀胱癌患者的BCG辅助免疫疗法的全部成功至关重要。此外，我们假设在对这种类型的辅助治疗的患者中，失败是由于他们无法表现出对肿瘤的完全免疫血管静脉作用。 后一个概念还表明，可能存在可以进一步优化的免疫血管机制，以便在这些肿瘤中完全介导免疫血管静脉曲张。提交审查的方案将用于确定在非肌肉浸润性膀胱患者中，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，以预测那些会反应反应的患者，而对免疫疗法的反应。