Signaling and Tumor Microenvironment (STME)

项目总结/摘要（信号和肿瘤微环境） 密歇根大学（U-M）Rogel癌症中心（Rogel）信号传导和肿瘤 微环境（STME）计划与九项Rogel交叉研究中的五项保持一致 主题：肿瘤微环境与代谢;分子决定因素;炎症，微生物与免疫; 目标和治疗;预防和早期检测。STME，以前称为癌症生物学（CB）， 重新命名，以反映会员国的优势和重点领域。STME计划的成员包括 致力于了解改变的信号网络的肿瘤内在和微环境效应。 STME计划由来自密歇根大学28个系和4所学校的55名成员组成。 STME成员每年有1530万美元的癌症相关赠款资金（DC），其中88%来自同行。 审查来源（36% NCI，44%其他NIH来源）。调查人员参与方案内和方案间的 互动，并积极与Rogel癌症中心的研究人员在基础科学， 转化和临床研究，癌症控制和人口科学计划。期间 截至2017年1月1日和2021年12月31日，成员共撰写了910篇癌症相关出版物，其中30.7%发表在期刊上 影响因素> 10。计划成员的共同研究兴趣反映在该计划的 总体科学目标：1）阐明细胞命运和可塑性在组织稳态和癌症中的作用 2）定义驱动肿瘤上皮生长和治疗反应的异细胞相互作用， 3)表征影响癌症和生长进展的代谢和代谢物相互作用。目标将 鉴定改变肿瘤起始的基本方面的细胞自主和微环境因素， 扩张、侵袭和转移。我们的主要目标是将机制发现转化为改善癌症 预防、诊断和治疗。

PROJECT SUMMARY/ABSTRACT (SIGNALING AND TUMOR MICROENVIRONMENT) Members of the University of Michigan (U-M) Rogel Cancer Center (Rogel) Signaling and Tumor Microenvironment (STME) Program share interests that align with five of the nine Rogel cross-cutting research themes: Tumor Microenvironment & Metabolism; Molecular Determinants; Inflammation, Microbes & Immunity; Targets & Therapeutics; and Prevention & Early Detection. STME, formerly known as the Cancer Biology (CB), was renamed to reflect the areas of strength and focus of the membership. Members of the STME Program are engaged in understanding both tumor-intrinsic and microenvironmental effects of altered signaling networks. STME Program comprises 55 members from 28 departments and four schools at the University of Michigan. STME members have $15.3M in annual cancer-relevant grant funding (DC), 88% of which comes from peer- reviewed sources (36% NCI, 44% other NIH sources). Investigators are involved in intra- and inter-programmatic interactions and actively collaborate with Rogel Cancer Center researchers within the Basic Science, Translational and Clinical Research, and Cancer Control and Population Sciences Programs. During the period of 01/01/2017 and 12/31/2021, members authored a total of 910 cancer-relevant publications, 30.7% in journals with Impact Factors > 10. The shared research interests of program members are reflected in the program’s overall scientific aims: 1) Elucidate the role of cell fate and plasticity during tissue homeostasis and cancer progression, 2) Define the heterocellular interactions that drive tumor epithelial growth and treatment response, 3) Characterize metabolic and metabolite interactions that impact cancer and growth progression. The Aims will identify cell autonomous and microenvironmental factors that alter fundamental aspects of tumor initiation, expansion, invasion and metastasis. Our main goal is to translate the mechanistic findings to improve cancer prevention, diagnosis, and treatment.