Peyton:Research: Difference between revisions
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== Signaling Network-Microenvironment Crosstalk in Metastasis == | == Signaling Network-Microenvironment Crosstalk in Metastasis == | ||
'''Collaboration with the Shannon Alford Lab at the University of Minnesota''' | |||
''Erinn Dandley and Jaclyn Somadelis''<br> | ''Erinn Dandley and Jaclyn Somadelis''<br> | ||
Metastasis is the leading cause of fatality for women diagnosed with breast cancer. While specific genetic signatures have been correlated with metastatic potential, and, in some cases, prediction of metastatic tissue site, there exists no biophysical explanation for metastatic site determination. Increasing evidence suggests that the physicochemical factors within the extracellular milieu may regulate tumor growth, morphology, and tumor cell motility. The overwhelmingly complex nature of the tumor microenvironment in vivo, which includes numerous extracellular matrix proteins, cell types, inflammatory chemokines, and proteolytic enzymes, presents a significant challenge in parsing the role of physicochemical cues involved in regulating metastasis. There exists a critical need for novel in vitro experimental systems that can mimic the metastatic niche in a well-defined, controllable, and reproducible manner. We are developing novel biomaterials to systematically measure breast cancer metastasis in response to physiologically relevant physiochemical cues. We are employing mathematical modeling tools to both describe and predict the relationship between physicochemical cues of the metastatic site and the predetermined signaling network within metastatic breast cancer cell lines. Within the scope of this project, we will identify components of intracellular signaling pathways involved in metastatic site preference. These pathways could serve as checkpoints for pharmaceutical intervention, and, in the long term, control of breast cancer metastasis. | Metastasis is the leading cause of fatality for women diagnosed with breast cancer. While specific genetic signatures have been correlated with metastatic potential, and, in some cases, prediction of metastatic tissue site, there exists no biophysical explanation for metastatic site determination. Increasing evidence suggests that the physicochemical factors within the extracellular milieu may regulate tumor growth, morphology, and tumor cell motility. The overwhelmingly complex nature of the tumor microenvironment in vivo, which includes numerous extracellular matrix proteins, cell types, inflammatory chemokines, and proteolytic enzymes, presents a significant challenge in parsing the role of physicochemical cues involved in regulating metastasis. There exists a critical need for novel in vitro experimental systems that can mimic the metastatic niche in a well-defined, controllable, and reproducible manner. We are developing novel biomaterials to systematically measure breast cancer metastasis in response to physiologically relevant physiochemical cues. We are employing mathematical modeling tools to both describe and predict the relationship between physicochemical cues of the metastatic site and the predetermined signaling network within metastatic breast cancer cell lines. Within the scope of this project, we will identify components of intracellular signaling pathways involved in metastatic site preference. These pathways could serve as checkpoints for pharmaceutical intervention, and, in the long term, control of breast cancer metastasis. | ||
[[Image:NSF_NCI.jpg|center|300px]] | [[Image:NSF_NCI.jpg|center|300px]] |
Revision as of 12:02, 18 November 2010
Matrix Physicochemical Cues as Chemotherapeutic Protective Agents in Hepatocellular CarcinomaThuy Nguyen Inflammatory Feedback Loops in CardiovascularWill Herrick
Signaling Network-Microenvironment Crosstalk in MetastasisCollaboration with the Shannon Alford Lab at the University of Minnesota Erinn Dandley and Jaclyn Somadelis |