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.

在与华盛顿大学医学院的癌细胞生物学家和 宾夕法尼亚州艾布拉姆森癌症中心的科学家，以及亚利桑那大学的计算生物药理学家， 约翰霍普金斯大学的生物工程师和临床医生建议创建约翰霍普金斯物理 肿瘤科学中心（PSOC）。该方案支助业务委员会将制定一种综合办法， 定量了解介导缺氧原发性肿瘤局部侵袭到远处的力 器官，通过单个和集体侵入基质基质和局限迁移沿着局限 跟踪，一些早期的关键步骤，在转移级联。为了解决复杂的组合 缺氧，基质微结构和限制对肿瘤细胞侵袭的影响，我们已经开发了三个 相关项目。计算生物药理学家将建立一个计算核心， 对转移级联中的力的定量理解。PSOC项目将分享创新 生物物理方法和专家。该PSOC采用跨学科的综合方法，将 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例。