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Investigating Breast Cancer Collective Invasion

调查乳腺癌集体侵袭

基本信息

批准号：
8621982
负责人：
Gray W Pearson
金额：
$ 32万
依托单位：
UT SOUTHWESTERN MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
起止时间：
2011-03-01 至 2016-02-28
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8621982
关键词：
Address Animal Model Architecture Basement membrane Biological Breast Cancer Cell Breast Carcinoma Cancer Patient Cell Line Cells Cessation of life Characteristics Conditioned Culture Media Connective Tissue Cytoskeleton Development Distant Distant Metastasis Duct (organ) structure Epithelium Event Fibroblasts Goals Growth Human Image In Situ Lesion Individual Invaded Lesion Life Lobule Malignant Epithelial Cell Mammary Ductal Carcinoma Mammary Neoplasms Mammary gland MicroRNAs Modeling Molecular Neoplasm Metastasis Noninfiltrating Intraductal Carcinoma Paracrine Communication Pathology Patients Population Resolution Risk Role Sampling Signal Pathway Site Staging Stromal Cells System Therapeutic Intervention Time Tumor Cell Invasion Tumor Pathology Xenograft Model cancer cell cell behavior cell motility cellular imaging clinically significant epithelial to mesenchymal transition genetic regulatory protein in vivo intercalation loss of function malignant breast neoplasm neoplastic neoplastic cell public health relevance transcription factor tumor tumor microenvironment tumor progression

项目摘要

DESCRIPTION (provided by applicant): During tumor progression the well-ordered architecture of the mammary gland becomes disrupted as hyperproliferative cells accumulate in the luminal space of ducts and lobules. Over time the neoplastic cells can invade into the stroma where they can access the vasculature system and disseminate to distant sites throughout the body. Although the induction of invasive growth is a key step in the metastatic cascade, how breast cancer cells become invasive remains poorly understood. Using an organotypic culture system and animal models we propose to determine (1) how cell motility is regulated by intracellular signaling pathways during collective invasion; (2) how mammary fibroblasts induce collective invasion and (3) how subpopulations of neoplastic cells trigger collective invasion. Deciphering the requirements for breast cancer invasion could identify targets for therapeutic intervention in both the tumor and the microenvironment.

描述(申请人提供)：在肿瘤进展过程中，乳腺的有序结构被破坏，因为过度增殖的细胞聚集在导管和小叶的管腔空间。随着时间的推移，肿瘤细胞可以侵入基质，在那里它们可以进入血管系统，并扩散到全身较远的部位。尽管诱导侵袭性生长是转移级联过程中的关键一步，但乳腺癌细胞如何变得侵袭性仍然知之甚少。利用器官类型培养系统和动物模型，我们建议确定(1)在集体侵袭过程中细胞内信号通路如何调节细胞运动；(2)乳腺成纤维细胞如何诱导集体侵袭；(3)肿瘤细胞亚群如何触发集体侵袭。破译乳腺癌侵袭的要求可以确定在肿瘤和微环境中进行治疗干预的目标。