The JAK2 V617F mutation within B cells and T cells leads to a pro-tumor microenvironment

B 细胞和 T 细胞内的 JAK2 V617F 突变导致促肿瘤微环境

• 批准号: 9903606
• 负责人: KENNETH J. PIENTA
• 金额: $ 7.38万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-08-29 至 2021-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9903606
• 关键词: Address; Adhesives; Arizona; B-Lymphocytes; Biological; Biomedical Engineering; Biophysics; Cancer Biology; Cancer Center; Cancer Patient; Cell Adhesion; Cells; Cessation of life; Clinical; Clinical Medicine; Collaborations; Collagen; Cues; DNA Sequence Alteration; Disseminated Malignant Neoplasm; Distant; Drug resistance; Ecology; Engineering; Epigenetic Process; Hypoxia; Individual; JAK2 gene; Laboratories; Leadership; Life; Mediating; Methods; Modification; Molecular; Mutation; Neoplasm Metastasis; Organ; Oxygen; Pennsylvania; Physics; Pilot Projects; Primary Neoplasm; Publishing; Role; Scientist; T-Lymphocyte; Therapeutic; Tumor Cell Invasion; Universities; Washington; anticancer research; biophysical techniques; cancer cell; epigenomics; extracellular; innovation; insight; mechanical force; medical schools; migration; oncology; outcome forecast; physical science; prevent; sarcoma; stem; success

In collaboration with cancer cell biologists at the Washington University School of Medicine and the University of Pennsylvania Abramson Cancer Center, as well as computational biophysicists at the University of Arizona, bioengineers and clinicians at Johns Hopkins University propose to create the Johns Hopkins Physical Sciences Oncology Center (PSOC). This PSOC will develop an integrated approach for a systematic, quantitative understanding of the forces mediating local invasion from the hypoxic primary tumor to distant organs, through single and collective invasion into the stromal matrix and confined migration along confining tracks, some of the early critical step in the metastatic cascade. To address the complexity of the combined effects of hypoxia, matrix microstructure and confinement on tumor cell invasion, we have developed three inter-related projects. Computational biophysicists will establish a computational core to systematically develop a quantitative understanding of forces in the metastatic cascade. PSOC projects will share innovative biophysical methods and experts. This PSOC takes a trans-disciplinary, integrated approach, combining the fields of physics, biomedical engineering, cancer biology, ecology, and clinical medicine, to transform our understanding of metastatic cancer, opening new paradigms for prognosis and treatment.

与华盛顿大学医学院和大学的癌细胞生物学家合作 宾夕法尼亚州阿布拉姆森癌症中心的研究人员，以及亚利桑那大学的计算生物物理学家， 约翰霍普金斯大学的生物工程师和临床医生提议创造约翰霍普金斯大学的物理 肿瘤科学中心(PSOC)。该PSOC将开发一种集成的方法， 对缺氧原发肿瘤局部侵袭远距离影响因素的定量认识 器官，通过单一和集体侵入基质基质和限制沿限制迁移 轨道是转移级联过程中的一些早期关键步骤。要解决合并后的 缺氧、基质微结构和限制对肿瘤细胞侵袭的影响，我们发展了三个 相互关联的项目。计算生物物理学家将建立一个计算核心来系统地开发 对转移级联中的力有一个定量的理解。PSoC项目将分享创新 生物物理方法和专家。该PSOC采取跨学科、集成的方法，结合 物理学、生物医学工程、癌症生物学、生态学和临床医学领域，以改变我们的 了解转移性癌症，为预后和治疗开辟新的范式。