User talk:Dannielle Ryman: Difference between revisions
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Lab Info | |||
The mission of the Peyton lab is to learn how a variety of different cell types are able to process information from biochemical and biophysical cues from the ECM and make decisions about migration and phenotype. To do this, our lab uses both 2D and 3D biomaterial model systems, which can be engineered from the ground-up to instruct cells via both biochemical and biophysical signaling pathways. This broader mission will be focused onto different research avenues with applications toward: cardiovascular disease, where tissue homeostasis is normally maintained in a mechanically dynamic ECM; stem-cell therapeutics, where rational scaffold design may be the key to directing appropriate progenitor cell migration and differentiation for tissue regeneration; and cancer, where disruptions in the local ECM microenvironment may cause drastic changes in individual cell motility and phenotype. | |||
Research Info | |||
== Stiffness Sensing as a Metastatic Indicator == | |||
'''Collaboration with the Al Crosby Lab at the University of Massachusetts, Polymer Science'''<br> | |||
''Dannielle Ryman and Ravitheja Yelleswaru''<br> | |||
Metastasis is the leading cause of fatality for women diagnosed with breast cancer. It is well known that tumor environments stiffen: palpitation remains a powerful tool for early tumor detection. More recently, this matrix stiffening event at the sites of tumors has been linked to morphological changes in the tumor itself, and it is hypothesized by us and others that these stiffness changes may contribute to single cell metastasis. However, the mechanisms by which metastatic cells sense and respond to stiffness is unclear, and it is not yet known if metastatic cells respond to stiffness cues in a unique way. We are working with Yuri Ebata and Yujie Liu from Al Crosby's lab in PSE to make novel substrates with unique presentation of stiffness arrays and mechanical length scales. We are visualizing how breast cancer cells of varying known metastatic capability sense and respond (namely, migration and mitosis) to these changes in stiffness. From there, we will identify the molecular mechanisms by which these cells have either heightened or dampened stiffness sensing, in order to develop novel druggable targets to prevent metastasis in vivo. | |||
[[Image:DRyman_Screenshot.png|center|200px]] | |||
Revision as of 08:53, 20 July 2011
Lab Info The mission of the Peyton lab is to learn how a variety of different cell types are able to process information from biochemical and biophysical cues from the ECM and make decisions about migration and phenotype. To do this, our lab uses both 2D and 3D biomaterial model systems, which can be engineered from the ground-up to instruct cells via both biochemical and biophysical signaling pathways. This broader mission will be focused onto different research avenues with applications toward: cardiovascular disease, where tissue homeostasis is normally maintained in a mechanically dynamic ECM; stem-cell therapeutics, where rational scaffold design may be the key to directing appropriate progenitor cell migration and differentiation for tissue regeneration; and cancer, where disruptions in the local ECM microenvironment may cause drastic changes in individual cell motility and phenotype.
Research Info
Stiffness Sensing as a Metastatic Indicator
Collaboration with the Al Crosby Lab at the University of Massachusetts, Polymer Science
Dannielle Ryman and Ravitheja Yelleswaru
Metastasis is the leading cause of fatality for women diagnosed with breast cancer. It is well known that tumor environments stiffen: palpitation remains a powerful tool for early tumor detection. More recently, this matrix stiffening event at the sites of tumors has been linked to morphological changes in the tumor itself, and it is hypothesized by us and others that these stiffness changes may contribute to single cell metastasis. However, the mechanisms by which metastatic cells sense and respond to stiffness is unclear, and it is not yet known if metastatic cells respond to stiffness cues in a unique way. We are working with Yuri Ebata and Yujie Liu from Al Crosby's lab in PSE to make novel substrates with unique presentation of stiffness arrays and mechanical length scales. We are visualizing how breast cancer cells of varying known metastatic capability sense and respond (namely, migration and mitosis) to these changes in stiffness. From there, we will identify the molecular mechanisms by which these cells have either heightened or dampened stiffness sensing, in order to develop novel druggable targets to prevent metastasis in vivo.
