Lauffenburger:Laura Sontag

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'''Laura Sontag''' (CSB doctoral), in collaboration with Prof. Peter Sorger
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'''Laura Sontag''' (Computational and Systems Biology doctoral student), in collaboration with Prof. Peter Sorger (Biology/BE, MIT) and Prof. Tyler Jacks (Biology/Center for Cancer Research,
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(Biology/BE, MIT) and Prof. Tyler Jacks (Biology/Center for Cancer Research,
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MIT)
MIT)
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Computational and experimental analysis of mitogenic signaling pathways
Computational and experimental analysis of mitogenic signaling pathways
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activated by a mutation in the K-ras oncogene.  The Ras signaling cascade
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activated by mutations in the K-ras oncogene.  The Ras signaling cascade
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constitutes a major pathway shown to be misregulated due to activating
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constitutes a major pathway shown to be deregulated due to activating
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mutations in 30% of all human tumors.  The vast majority of mutations occur in
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mutations in 30% of all human tumors.  The vast majority of mutations occur in the
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K-ras.  We use genetically engineered mice that harbor a conditional,
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K-ras isoform.  We use genetically engineered mice that harbor a conditional,
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activatable allele of the K-ras oncogene as a model of human cancer.
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activatable K-ras allele as a model of human cancer.
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Email:  sontag {AT} mit {DOT} edu
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[http://www.mit.edu/~sontag/ Laura Sontag's Homepage]
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Revision as of 17:46, 6 January 2006

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Laura Sontag (Computational and Systems Biology doctoral student), in collaboration with Prof. Peter Sorger (Biology/BE, MIT) and Prof. Tyler Jacks (Biology/Center for Cancer Research, MIT)


Computational and experimental analysis of mitogenic signaling pathways activated by mutations in the K-ras oncogene. The Ras signaling cascade constitutes a major pathway shown to be deregulated due to activating mutations in 30% of all human tumors. The vast majority of mutations occur in the K-ras isoform. We use genetically engineered mice that harbor a conditional, activatable K-ras allele as a model of human cancer.


Email: sontag {AT} mit {DOT} edu

Laura Sontag's Homepage

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