Core A: Administrative Core

核心A：行政核心

• 批准号: 10249090
• 负责人: SELINA Y CHEN-KIANG
• 金额: $ 19.82万
• 依托单位: WEILL MEDICAL COLL OF CORNELL UNIV
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-09-18 至 2023-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10249090
• 关键词: Accounting; Administrator; Agreement; Animals; Basic Science; Bioinformatics; Biometry; Biostatistics Core; Budgets; CDK4 gene; Cancer Center; Cell Cycle; Cell Proliferation; Clinical; Clinical Trials; Combined Modality Therapy; Consult; Consultations; Cyclin D1; Decision Making; Disease; Disease Progression; Drug resistance; Electronic Mail; Equipment and supply inventories; Esters; Facilities and Administrative Costs; Failure; Funding; Genome; Genomics; Goals; Grant; Human; Human Resources; Individual; Institutional Review Boards; Investigational Therapies; Mantle Cell Lymphoma; Manuscripts; Medicine; Molecular; Non-Hodgkin' s Lymphoma; Ohio; Outcome; Pathology; Patient Care; Patients; Preparation; Principal Investigator; Progress Reports; Proliferating; Protocols documentation; Reagent; Reporting; Research; Research Personnel; Research Project Grants; Resistance; Rest; Role; Schedule; Shipping; Site; Specimen; Stratification; Teleconferences; Telephone; Time; Treatment Failure; Tumor Expansion; Universities; Videoconferencing; anticancer research; authority; base; chromatin remodeling; data sharing; drug development; inhibitor/antagonist; meetings; neoplastic cell; novel strategies; novel therapeutics; overexpression; programs; response; synergism; therapeutic target; tumor; virtual

Mantle cell lymphoma (MCL) is a non-Hodgkin's lymphoma that remains incurable due to the development of drug resistance, which is typically marked by unrestrained tumor cell proliferation. Cell cycle dysregulation is a hallmark of MCL. In particular, overexpression of CDK4, together with aberrant cyclin D1 expression, drives unrestrained proliferation of tumor cells that underlies disease progression and expansion of resistant clones. However, the molecular basis for drug resistance in MCL remains obscure. The overall goals of the program project are: 1) to develop superior, mechanism-based combination therapies that both control tumor expansion and enhance tumor killing in MCL, 2) to elucidate the mechanism(s) of drug resistance, and 3) to advance genome-based patient and therapy stratification for optimal and durable clinical responses. To achieve these goals, a team of investigators with strong, complementary expertise in basic science, cancer research, experimental therapeutics and patient care at Weill Cornell Medicine (WCM) and The Ohio State University OSU) have assembled three interactive projects to 1) target CDK4 in MCL therapy; 2) to elucidate the role of FOXO and chromatin remodeling in cell cycle therapy for MCL; and 3) to target PRMT5 in MCL. These projects are supported by four outstanding Cores: 1) Administrative Core, 2) Pathology Core; 3) Genomics and Bioinformatics Core; and 4) Biostatistics Core. The projects and cores are highly integrated at both the conceptual and technical levels, with ideas and unpublished data shared freely on a real-time basis. The PPG, led by the Principal Investigator, will hold scheduled bi-weekly meetings via video conferencing in addition to impromptu discussions, both face-to-face or via teleconferences and frequent phone calls and emails. The chain of authority for decision-making and administration rests with the Principal Investigator, in consultation with individual Project and Core leaders. The PPG is supported by an External Advisory Board composed of four distinguished investigators who will participate in the annual review meeting in which progress and plans for each Project and Core are presented for discussion and review. The PPG is further supported by Internal Advisory Boards at WCM and OSU, who are available as needed for consultation, either singly or as a panel. Synergy among Investigators, as well as between WCM and OSU, is the most outstanding feature of this PPG and will propel its progress.

套细胞淋巴瘤（MCL）是一种非霍奇金淋巴瘤，由于发展为恶性淋巴瘤， 耐药性，其通常以不受限制的肿瘤细胞增殖为标志。细胞周期失调是一种 MCL的标志。特别是，CDK 4的过表达，以及异常的细胞周期蛋白D1表达， 肿瘤细胞的无限制增殖是疾病进展和抗性克隆扩增的基础。 然而，MCL耐药的分子基础仍然不清楚。该计划的总体目标 项目是：1）开发上级的，基于机制的联合治疗， 增强MCL中的肿瘤杀伤，2）阐明耐药机制，3）推进 基于基因组的患者和治疗分层，以获得最佳和持久的临床反应。实现这些 目标，一支在基础科学、癌症研究， 威尔康奈尔医学（WCM）和俄亥俄州州立大学的实验治疗学和病人护理 OSU）已经组装了三个互动项目，1）靶向CDK 4在MCL治疗中的作用; 2）阐明CDK 4在MCL治疗中的作用。 F0 XO和染色质重塑在MCL的细胞周期疗法中的作用;以及3）靶向MCL中的PRMT 5。这些项目 由四个杰出的核心支持：1）行政核心，2）病理学核心，3）基因组学和 生物信息学核心;和4）生物统计学核心。项目和核心在两个方面都高度集成， 在概念和技术层面上，想法和未发表的数据可以实时自由共享。PPG， 由主要研究者领导，将通过视频会议举行预定的双周会议， 面对面或通过电话会议以及频繁的电话和电子邮件进行即兴讨论。的 决策和管理的权力链属于主要研究者， 与个别项目和核心领导人。PPG由外部咨询委员会提供支持，该委员会由以下人员组成： 四位杰出的研究者将参加年度审查会议， 为每个项目和核心提出了讨论和审查。PPG还得到了内部 WCM和OSU的咨询委员会，他们可以根据需要单独或作为小组进行咨询。 研究者之间以及WCM和OSU之间的协同作用是该PPG的最突出特征 并将推动其发展。