K562/GM-CSF VACCINATION

K562/GM-CSF 疫苗接种

• 批准号: 7378863
• 负责人: HYAM Isaac LEVITSKY
• 金额: $ 0.9万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7378863
• 关键词: K562; GM; CSF; VACCINATION

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. Description of Project for Release to Public- 03-08-12-05 CML is thought to an immunologically responsive disease based on the ability to cure the disease with allogeneic T cells as well as the demonstration of host immune responses to CML-associated antigens in patients who have responded to interferon-alpha. The dramatic clinical responses obtained with the selective tyrosine kinase inhibitor Imatinib Mesylate has provided a relatively non-toxic cytoreductive therapy, although complete molecular remissions remain rare. In this study, we are vaccinating CML patients who are in a complete hematologic remission, but have persistent cytogeneic or molecular evidence of disease, with a novel allogeneic tumor cell-based vaccine that expresses many of the antigens shown to be present in CML cells and to which T cell responses have been demonstrated. The vaccine is administered in conjunction with a topical agonist to Toll Like Receptor 9 (imiquimod). The two major objectives of this study will be to demonstrate the ability to generate and augment CML specific T cell responses in patients vaccinated while in remission on imatinib, and to test the hypothesis that such responses will lead to a measurable reduction in tumor burden (or its elimination) as assayed by quantitative RT-PCR of bcr/abl transcripts.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。发布项目描述- 03-08-12-05 CML被认为是一种免疫应答性疾病，其基础是用同种异体T细胞治愈疾病的能力以及在对α干扰素有应答的患者中对CML相关抗原的宿主免疫应答的证明。使用选择性酪氨酸激酶抑制剂甲磺酸伊马替尼获得的显著临床反应提供了相对无毒的细胞减少疗法，尽管完全的分子缓解仍然罕见。在这项研究中，我们正在接种CML患者谁是在一个完全的血液学缓解，但有持续的细胞遗传学或分子证据的疾病，与一种新的同种异体肿瘤细胞为基础的疫苗，表达许多抗原显示存在于CML细胞和T细胞反应已被证明。该疫苗与Toll样受体9的局部激动剂（咪喹莫特）联合施用。本研究的两个主要目的是证明在伊马替尼缓解期接种疫苗的患者中产生和增强CML特异性T细胞应答的能力，并检验通过bcr/abl转录物的定量RT-PCR测定的此类应答将导致肿瘤负荷可测量的降低（或其消除）的假设。