Brian C Lewis

Summary

Affiliation: University of Massachusetts Medical School
Country: USA

Publications

  1. ncbi The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer
    Brian C Lewis
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genes Dev 17:3127-38. 2003
  2. ncbi The absence of p53 promotes metastasis in a novel somatic mouse model for hepatocellular carcinoma
    Brian C Lewis
    University of Massachusetts Medical School, 364 Plantation St, LRB 521, Worcester, MA 01605, USA
    Mol Cell Biol 25:1228-37. 2005
  3. ncbi Development of the pancreas and pancreatic cancer
    Brian C Lewis
    Program in Gene Function and Expression, University of Massachusetts Medical School, 364 Plantation Street, LRB 521, Worcester, MA 01605 USA
    Endocrinol Metab Clin North Am 35:397-404, xi. 2006
  4. ncbi Trp53 deletion stimulates the formation of metastatic pancreatic tumors
    Jennifer P Morton
    University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    Am J Pathol 172:1081-7. 2008
  5. ncbi p19Arf inhibits the invasion of hepatocellular carcinoma cells by binding to C-terminal binding protein
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Cancer Res 68:476-82. 2008
  6. ncbi Differential roles of insulin-like growth factor receptor- and insulin receptor-mediated signaling in the phenotypes of hepatocellular carcinoma cells
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Neoplasia 11:835-45. 2009
  7. ncbi Loss of p53 and Ink4a/Arf cooperate in a cell autonomous fashion to induce metastasis of hepatocellular carcinoma cells
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Cancer Res 67:7589-96. 2007
  8. ncbi Assessing tumor progression factors by somatic gene transfer into a mouse model: Bcl-xL promotes islet tumor cell invasion
    Yi Chieh Nancy Du
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    PLoS Biol 5:e276. 2007
  9. ncbi The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis
    Mihir Rajurkar
    Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Proc Natl Acad Sci U S A 109:E1038-47. 2012
  10. ncbi The alternative reading frame tumor suppressor antagonizes hypoxia-induced cancer cell migration via interaction with the COOH-terminal binding protein corepressor
    Seema Paliwal
    Department of Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    Cancer Res 67:9322-9. 2007

Collaborators

Detail Information

Publications13

  1. ncbi The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer
    Brian C Lewis
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genes Dev 17:3127-38. 2003
    ..Our model appears to be useful for elucidating the genetic alterations, target cells, and signaling pathways that are important in the genesis of different types of pancreatic cancer...
  2. ncbi The absence of p53 promotes metastasis in a novel somatic mouse model for hepatocellular carcinoma
    Brian C Lewis
    University of Massachusetts Medical School, 364 Plantation St, LRB 521, Worcester, MA 01605, USA
    Mol Cell Biol 25:1228-37. 2005
    ..Tumors induced in p53 null, TVA transgenic mice by PyMT mutants with changes in specific tyrosine residues fail to form metastases, indicating that metastasis is dependent on both the oncogene and the absence of p53...
  3. ncbi Development of the pancreas and pancreatic cancer
    Brian C Lewis
    Program in Gene Function and Expression, University of Massachusetts Medical School, 364 Plantation Street, LRB 521, Worcester, MA 01605 USA
    Endocrinol Metab Clin North Am 35:397-404, xi. 2006
    ..These findings indicate that developmentally regulated gene expression programs are important in the pathogenesis of pancreatic cancer...
  4. ncbi Trp53 deletion stimulates the formation of metastatic pancreatic tumors
    Jennifer P Morton
    University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    Am J Pathol 172:1081-7. 2008
    ....
  5. ncbi p19Arf inhibits the invasion of hepatocellular carcinoma cells by binding to C-terminal binding protein
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Cancer Res 68:476-82. 2008
    ..Thus, our data indicate a novel role for the Arf tumor suppressor protein in regulating phenotypes associated with tumor progression and metastasis in HCC cells...
  6. ncbi Differential roles of insulin-like growth factor receptor- and insulin receptor-mediated signaling in the phenotypes of hepatocellular carcinoma cells
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Neoplasia 11:835-45. 2009
    ..Finally, we identify matrix metalloproteinase 2 as a mediator of the invasive phenotype downstream of IGF1R-induced signaling. Thus, our studies demonstrate the importance of IGF2-induced signaling in the dissemination of HCC cells...
  7. ncbi Loss of p53 and Ink4a/Arf cooperate in a cell autonomous fashion to induce metastasis of hepatocellular carcinoma cells
    Ya Wen Chen
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Cancer Res 67:7589-96. 2007
    ..Thus, our data illustrate a new model system amenable for the analysis of HCC metastasis...
  8. ncbi Assessing tumor progression factors by somatic gene transfer into a mouse model: Bcl-xL promotes islet tumor cell invasion
    Yi Chieh Nancy Du
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    PLoS Biol 5:e276. 2007
    ..In addition, myosin Va was identified as a novel Bcl-xL-interacting protein that might mediate the effects of Bcl-xL on tumor cell migration and invasion...
  9. ncbi The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesis
    Mihir Rajurkar
    Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Proc Natl Acad Sci U S A 109:E1038-47. 2012
    ....
  10. ncbi The alternative reading frame tumor suppressor antagonizes hypoxia-induced cancer cell migration via interaction with the COOH-terminal binding protein corepressor
    Seema Paliwal
    Department of Cancer Biology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    Cancer Res 67:9322-9. 2007
    ..Thus, ARF can suppress cell migration by antagonizing CtBP2 and the phosphatidylinositol 3-kinase pathway, and these data may explain the increased aggressiveness of ARF-null tumors in mouse models...
  11. ncbi Shh signaling and pancreatic cancer: implications for therapy?
    Jennifer P Morton
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts, USA
    Cell Cycle 6:1553-7. 2007
    ..Here we discuss the significance of these findings and the implications for therapy...
  12. ncbi Sonic hedgehog acts at multiple stages during pancreatic tumorigenesis
    Jennifer P Morton
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Proc Natl Acad Sci U S A 104:5103-8. 2007
    ..Collectively, our findings demonstrate crucial roles for Shh signaling in multiple stages of pancreatic carcinogenesis...
  13. ncbi KRAS(G12D)- and BRAF(V600E)-induced transformation of murine pancreatic epithelial cells requires MEK/ERK-stimulated IGF1R signaling
    Victoria A Appleman
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA
    Mol Cancer Res 10:1228-39. 2012
    ....

Research Grants12

  1. Molecular dissection of pancreatic ductal adenocarcinoma
    Brian Lewis; Fiscal Year: 2009
    ..Such gene expression signatures may potentially be used as diagnostic tools, as well as surrogate markers for response to targeted therapeutic interventions. ..
  2. Molecular dissection of pancreatic ductal adenocarcinoma
    Brian C Lewis; Fiscal Year: 2010
    ..Such gene expression signatures may potentially be used as diagnostic tools, as well as surrogate markers for response to targeted therapeutic interventions. ..
  3. Molecular mediators of metastasis in hepatocellular carcinoma
    Brian C Lewis; Fiscal Year: 2010
    ..abstract_text> ..
  4. Molecular dissection of pancreatic ductal adenocarcinoma
    Brian Lewis; Fiscal Year: 2009
    ..Such gene expression signatures may potentially be used as diagnostic tools, as well as surrogate markers for response to targeted therapeutic interventions. ..
  5. Molecular mediators of metastasis in hepatocellular carcinoma
    Brian Lewis; Fiscal Year: 2009
    ..abstract_text> ..
  6. A flexible somatic and sporadic mouse model for pancreatic ductal adenocarcinoma
    Brian Lewis; Fiscal Year: 2007
    ..Such an advance would benefit public health by reducing the mortality associated with this disease. ..
  7. Molecular mediators of metastasis in hepatocellular carcinoma
    Brian Lewis; Fiscal Year: 2007
    ....
  8. Molecular dissection of pancreatic ductal adenocarcinoma
    Brian C Lewis; Fiscal Year: 2010
    ..Such gene expression signatures may potentially be used as diagnostic tools, as well as surrogate markers for response to targeted therapeutic interventions. ..