Hyung-Do Kim

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[[Image: Hyung_Do_Kim.jpg|200px|right]]
[[Image: Hyung_Do_Kim.jpg|200px|right]]
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'''Hyung-Do Kim''' (BE doctoral), in collaboration with Prof. Frank Gertler (Biology, MIT)
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'''Hyung-Do Kim''' (BE Doctoral) [mailto:hyungdo@mit.edu Email] [http://web.mit.edu/hyungdo/Public/HDK_CV.pdf CV]
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Ph.D. 2008  Biological Engineering, Massachusetts Institute of Technology <br/>
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B.S. 2003  Biomedical Engineering, Johns Hopkins University <br/>
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''Current affiliation:''<br/>
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McKinsey & Company<br/>
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''Research advisors:''<br/>
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Douglas Lauffenburger (Biological Engineering, MIT)<br/>
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Frank Gertler (Biology, MIT)
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''Research summary:''
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"Quantitative Analysis of 2D and 3D Models for Epidermal Growth Factor Receptor-Dependent Cell Migration in the Context of the Extracellular Microenvironment"
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Current models of the early stages of tumor metastasis suggest that carcinomas undergo an epithelial-mesenchymal-transition to become motile and invade complex neighboring tissue consisting of the 3D extracellular matrix. This invasion environment consists of multiple biochemical and biophysical cues that affects the success of tumor cell invasion.  The epidermal growth factor receptor (EGFR) expression is correlated with tumor progression and invasiveness in many cancers and is in the center of regulating the invasion process.  Due to the multivariate nature of this process, the detailed analysis of cell migration in the context of the invasion microenvironment compels a quantitative approach.  My work involves assessing EGFR dependent cell migration in the context of various extracellular cues. 
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''Publications (* co-first):''
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Kim HD*, Sileika TS*, Maniak P, Messersmith PB. ''Antibacterial performance of polydopamine modified polymer surfaces containing passive and active components.'' ''Submitted.'' 2011
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Kim HD, Peyton SR. ''Bio-inspired materials for parsing matrix physicochemical control of cell migration.'' Integr Biol. ''Accepted.'' 2011
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Kim HD*, Hause RJ*, Leung K*, Jones RA. ''Targeted protein-omic methods are bridging the gap between proteomic and hypothesis-driven protein analysis approaches.'' Expert Rev Proteomics. ''Accepted.'' 2011
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Kim HD, Meyer AS, Wagner JP, Alford SK, Wells A, Gertler FB, Lauffenburger DA. ''Signaling network state predicts Twist-mediated effects on breast cell migration across diverse growth factor contexts.''  Mol Cell Proteomics. ''Accepted.'' 2011
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Philippar U, Roussos ET, Oser M, Yamaguchi H, Kim HD, Giampieri S, Wang Y, Goswami S, Wyckoff JB, Lauffenburger DA, Sahai E, Condeelis JS, Gertler FB.  ''A Mena invasion isoform potentiates EGF-induced carcinoma cell invasion and metastasis.'' Dev Cell. 2008 Dec;15(6):813-28. [http://dx.doi.org/10.1016/j.devcel.2008.09.003 DOI]
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Kim HD, Guo TW, Wu AP, Wells A, Gertler FB, Lauffenburger DA.  ''Epidermal growth factor-induced enhancement of glioblastoma cell migration in 3D arises from an intrinsic increase in speed but an extrinsic matrix- and proteolysis-dependent increase in persistence.''  Mol Biol Cell. 2008 Oct;19(10):4249-59. [http://dx.doi.org/10.1091/mbc.E08-05-0501 DOI]
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Kim HD*, Harley BA*, Zaman MH, Yannas IV, Lauffenburger DA, Gibson LJ.  ''Microarchitecture of three-dimensional scaffolds influences cell migration behavior via junction interactions.''  Biophys J. 2008 Oct;95(8):4013-24. [http://dx.doi.org/10.1529/biophysj.107.122598 DOI]
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Kumar N, Afeyan R, Kim HD, Lauffenburger DA.  ''Multipathway model enables prediction of kinase inhibitor cross-talk effects on migration of Her2-overexpressing mammary epithelial cells.''  Mol Pharmacol. 2008 Jun;73(6):1668-78. [http://dx.doi.org/10.1124/mol.107.043794 DOI]
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Wolf-Yadlin A, Kumar N, Zhang Y, Hautaniemi S, Zaman M, Kim HD, Grantcharova V, Lauffenburger DA, White FM.  Effects of HER2 overexpression on cell signaling networks governing proliferation and migration.  Mol Syst Biol. 2006;2:54. [http://dx.doi.org/10.1038/msb4100094 DOI]
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Kumar N, Zaman MH, Kim HD, Lauffenburger DA.  ''A high-throughput migration assay reveals HER2-mediated cell migration arising from increased directional persistence.''  Biophys J. 2006 Aug 15;91(4):L32-4. [http://dx.doi.org/10.1529/biophysj.106.088898 DOI]
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''Quantitative analysis of EGFR signaling-mediated tumor cell migration in three-dimensional matrices''.  Development of data-driven cue-signal-response models to characterize the role of EGFR signaling in 3D motility biophysics and cell-matrix interactions.  Development of experimental platforms using current imaging techniques for quantitative studies of cell migration in 3D matrices.
 
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Current revision

Lauffenburger Lab

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Hyung-Do Kim (BE Doctoral) Email CV



Ph.D. 2008 Biological Engineering, Massachusetts Institute of Technology
B.S. 2003 Biomedical Engineering, Johns Hopkins University


Current affiliation:
McKinsey & Company


Research advisors:
Douglas Lauffenburger (Biological Engineering, MIT)
Frank Gertler (Biology, MIT)


Research summary:

"Quantitative Analysis of 2D and 3D Models for Epidermal Growth Factor Receptor-Dependent Cell Migration in the Context of the Extracellular Microenvironment"

Current models of the early stages of tumor metastasis suggest that carcinomas undergo an epithelial-mesenchymal-transition to become motile and invade complex neighboring tissue consisting of the 3D extracellular matrix. This invasion environment consists of multiple biochemical and biophysical cues that affects the success of tumor cell invasion. The epidermal growth factor receptor (EGFR) expression is correlated with tumor progression and invasiveness in many cancers and is in the center of regulating the invasion process. Due to the multivariate nature of this process, the detailed analysis of cell migration in the context of the invasion microenvironment compels a quantitative approach. My work involves assessing EGFR dependent cell migration in the context of various extracellular cues.


Publications (* co-first):

Kim HD*, Sileika TS*, Maniak P, Messersmith PB. Antibacterial performance of polydopamine modified polymer surfaces containing passive and active components. Submitted. 2011

Kim HD, Peyton SR. Bio-inspired materials for parsing matrix physicochemical control of cell migration. Integr Biol. Accepted. 2011

Kim HD*, Hause RJ*, Leung K*, Jones RA. Targeted protein-omic methods are bridging the gap between proteomic and hypothesis-driven protein analysis approaches. Expert Rev Proteomics. Accepted. 2011

Kim HD, Meyer AS, Wagner JP, Alford SK, Wells A, Gertler FB, Lauffenburger DA. Signaling network state predicts Twist-mediated effects on breast cell migration across diverse growth factor contexts. Mol Cell Proteomics. Accepted. 2011

Philippar U, Roussos ET, Oser M, Yamaguchi H, Kim HD, Giampieri S, Wang Y, Goswami S, Wyckoff JB, Lauffenburger DA, Sahai E, Condeelis JS, Gertler FB. A Mena invasion isoform potentiates EGF-induced carcinoma cell invasion and metastasis. Dev Cell. 2008 Dec;15(6):813-28. DOI

Kim HD, Guo TW, Wu AP, Wells A, Gertler FB, Lauffenburger DA. Epidermal growth factor-induced enhancement of glioblastoma cell migration in 3D arises from an intrinsic increase in speed but an extrinsic matrix- and proteolysis-dependent increase in persistence. Mol Biol Cell. 2008 Oct;19(10):4249-59. DOI

Kim HD*, Harley BA*, Zaman MH, Yannas IV, Lauffenburger DA, Gibson LJ. Microarchitecture of three-dimensional scaffolds influences cell migration behavior via junction interactions. Biophys J. 2008 Oct;95(8):4013-24. DOI

Kumar N, Afeyan R, Kim HD, Lauffenburger DA. Multipathway model enables prediction of kinase inhibitor cross-talk effects on migration of Her2-overexpressing mammary epithelial cells. Mol Pharmacol. 2008 Jun;73(6):1668-78. DOI

Wolf-Yadlin A, Kumar N, Zhang Y, Hautaniemi S, Zaman M, Kim HD, Grantcharova V, Lauffenburger DA, White FM. Effects of HER2 overexpression on cell signaling networks governing proliferation and migration. Mol Syst Biol. 2006;2:54. DOI

Kumar N, Zaman MH, Kim HD, Lauffenburger DA. A high-throughput migration assay reveals HER2-mediated cell migration arising from increased directional persistence. Biophys J. 2006 Aug 15;91(4):L32-4. DOI

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