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dc.contributor.advisorScott R. Manalis.en_US
dc.contributor.authorWeng, Yaochungen_US
dc.contributor.otherMassachusetts Institute of Technology. Computational and Systems Biology Program.en_US
dc.date.accessioned2012-09-11T17:28:42Z
dc.date.available2012-09-11T17:28:42Z
dc.date.copyright2012en_US
dc.date.issued2012en_US
dc.identifier.urihttp://hdl.handle.net/1721.1/72638
dc.descriptionThesis (Ph. D.)--Massachusetts Institute of Technology, Computational and Systems Biology Program, 2012.en_US
dc.descriptionThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.en_US
dc.descriptionCataloged from student submitted PDF version of thesis.en_US
dc.descriptionIncludes bibliographical references.en_US
dc.description.abstractUnderstanding the effectiveness of a drug therapy on halting disease progression is an essential aspect of cancer biology. Conventional assays that study cell behavior after a drug intervention report the average response of a cell population which can mask the heterogeneity and dynamics of seemingly identical cells. Recently, many single-cell techniques have been developed, but there are currently no methods that can fully characterize the long-term effects of drug treatment on cancer cell growth. To accomplish such, we developed an instrument to measure single-cell growth before and after drug treatment. In order to achieve femtogram-level mass resolution, we employed the suspended microchannel resonator (SMR), a vacuum-packaged cantilever with an embedded channel. Here, we describe three implementations that involve different technologies (optical trap, mechanical trap, and dynamic ow trapping) to capture a cell for repeated measurements and to perform drug delivery. Applying the technique we developed based on the dynamic ow trapping, we were able to monitor one or more generations of a cancer cell before and after drug treatment. We investigated the growth of mouse leukemia cells in response to drugs that inhibit the mammalian target of rapamycin (mTOR) pathway, induce apoptosis, or prevent translational activity directly at the ribosome. Our method was able to discern a particular growth signature for each drug investigated and to discover a new phenotype in cells following mTOR inhibition. Furthermore, our data demonstrates that the instantaneous growth rate changes following a drug treatment could potentially predict the long-term inhibitory effect on cellular biogenesis and mass accumulation.en_US
dc.description.statementofresponsibilityby Yaochung Weng.en_US
dc.format.extent122 p.en_US
dc.language.isoengen_US
dc.publisherMassachusetts Institute of Technologyen_US
dc.rightsM.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.en_US
dc.rights.urihttp://dspace.mit.edu/handle/1721.1/7582en_US
dc.subjectComputational and Systems Biology Program.en_US
dc.titleMeasuring the effects of drugs on single cancer cell growthen_US
dc.typeThesisen_US
dc.description.degreePh.D.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Computational and Systems Biology Program.en_US
dc.identifier.oclc806957124en_US


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