BLADDER TISSUE BANK

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 关于侵犯固有层(PT1)的非肌肉浸润性膀胱癌的治疗一直存在争议。这个阶段的膀胱癌有很大的复发和进展的倾向。我们需要进一步了解免疫治疗的作用和/或是否应该优化这种治疗形式，以改善对早期膀胱癌的治疗干预，特别是在辅助卡介苗治疗的情况下，对肿瘤复发的患者。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“免疫血管抑制”这一术语，因为它们在促进肿瘤消退方面具有潜在的生物学作用。最近，我们已经确认了免疫血管抑制生物学在介导与肾癌相关的肿瘤消退中的重要性。在这项建议中，我们假设免疫血管稳定的生物学对于卡介苗辅助免疫治疗在非肌肉浸润性膀胱癌患者中的完全成功至关重要。此外，我们推测，在对这种辅助治疗无效的患者中，失败是由于他们无法对肿瘤表现出完全的免疫血管抑制效应。后一个概念还表明，可能存在免疫血管抑制机制，可以进一步优化，以便在这些肿瘤中充分介导免疫血管稳定。提交审查的方案将用于确定干扰素诱导的CXC趋化因子在非肌肉侵袭性膀胱患者中的表达是否可以用作预测免疫治疗有效患者与无效患者的生物标志物。

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.