Kenneth E Hung

Summary

Affiliation: Tufts Medical Center
Country: USA

Publications

  1. pmc Comprehensive proteome analysis of an Apc mouse model uncovers proteins associated with intestinal tumorigenesis
    Kenneth E Hung
    Department of Medicine, Tufts Medical Center, Boston, Massachusetts, USA
    Cancer Prev Res (Phila) 2:224-33. 2009
  2. pmc Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment
    Kenneth E Hung
    Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 107:1565-70. 2010
  3. pmc Concomitant BRAF and PI3K/mTOR blockade is required for effective treatment of BRAF(V600E) colorectal cancer
    Erin M Coffee
    Division of Gastroenterology, Tufts Medical Center, Boston, Massachusetts 02111, USA
    Clin Cancer Res 19:2688-98. 2013
  4. pmc Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation
    Eric S Martin
    Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Clin Cancer Res 19:2929-40. 2013
  5. pmc Combination PI3K/MEK inhibition promotes tumor apoptosis and regression in PIK3CA wild-type, KRAS mutant colorectal cancer
    Jatin Roper
    Tufts Medical Center, Division of Gastroenterology, Department of Medicine, Boston, MA, United States Tufts Medical Center, Molecular Oncology Research Institute, Boston, MA, United States Electronic address
    Cancer Lett 347:204-11. 2014
  6. pmc In vivo optical molecular imaging of matrix metalloproteinase activity following celecoxib therapy for colorectal cancer
    Rahul A Sheth
    Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02114, USA
    Mol Imaging 11:417-25. 2012
  7. ncbi Mass spectrometry-based study of the plasma proteome in a mouse intestinal tumor model
    Kenneth E Hung
    Gastrointestinal Unit, Massachusetts General Hospital, 55 Fruit Street, Boston, 02114, USA
    J Proteome Res 5:1866-78. 2006
  8. pmc mTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1
    Anthony C Faber
    1Massachusetts General Hospital Cancer Center 2Department of Medicine, Harvard Medical School 3Division of Gastroenterology, Department of Medicine, Tufts Medical Center 4Department of Pathology, Massachusetts General Hospital, Boston and 5Radiation Oncology, Steele Lab for Tumor Biology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts
    Cancer Discov 4:42-52. 2014
  9. pmc Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models
    Ryan B Corcoran
    Massachusetts General Hospital Cancer Center, Boston, MA 02129, USA
    Cancer Cell 23:121-8. 2013
  10. pmc Colon-specific tumorigenesis in mice driven by Cre-mediated inactivation of Apc and activation of mutant Kras
    Alexander J Byun
    Vitamins and Carcinogenesis Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
    Cancer Lett 347:191-5. 2014

Collaborators

Detail Information

Publications17

  1. pmc Comprehensive proteome analysis of an Apc mouse model uncovers proteins associated with intestinal tumorigenesis
    Kenneth E Hung
    Department of Medicine, Tufts Medical Center, Boston, Massachusetts, USA
    Cancer Prev Res (Phila) 2:224-33. 2009
    ..Our results show that integrated analysis of the plasma proteome and tumor transcriptome of genetically engineered mouse models is a powerful approach for the identification of tumor-related plasma proteins...
  2. pmc Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment
    Kenneth E Hung
    Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 107:1565-70. 2010
    ..These studies suggest that mTOR inhibitors should be further explored as potential colorectal cancer therapies in patients whose tumors do not have activating mutations in KRAS...
  3. pmc Concomitant BRAF and PI3K/mTOR blockade is required for effective treatment of BRAF(V600E) colorectal cancer
    Erin M Coffee
    Division of Gastroenterology, Tufts Medical Center, Boston, Massachusetts 02111, USA
    Clin Cancer Res 19:2688-98. 2013
    ..Although selective BRAF inhibitors are effective for treatment of melanoma, comparable efforts in CRC have been disappointing. Here, we investigated potential mechanisms underlying this resistance to BRAF inhibitors in BRAF(V600E) CRC...
  4. pmc Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation
    Eric S Martin
    Dana Farber Cancer Institute, Boston, Massachusetts, USA
    Clin Cancer Res 19:2929-40. 2013
    ....
  5. pmc Combination PI3K/MEK inhibition promotes tumor apoptosis and regression in PIK3CA wild-type, KRAS mutant colorectal cancer
    Jatin Roper
    Tufts Medical Center, Division of Gastroenterology, Department of Medicine, Boston, MA, United States Tufts Medical Center, Molecular Oncology Research Institute, Boston, MA, United States Electronic address
    Cancer Lett 347:204-11. 2014
    ..These findings implicate mitochondrial-dependent apoptotic mechanisms as determinants for the efficacy of PI3K/MEK inhibition in the treatment of PIK3CA wild-type, KRAS mutant cancer. ..
  6. pmc In vivo optical molecular imaging of matrix metalloproteinase activity following celecoxib therapy for colorectal cancer
    Rahul A Sheth
    Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital, Boston, MA 02114, USA
    Mol Imaging 11:417-25. 2012
    ..This method may provide for the improved identification of patients for whom COX-2 inhibition therapy is indicated by allowing one to balance the patient's cardiovascular risk with the cancer's responsiveness to celecoxib...
  7. ncbi Mass spectrometry-based study of the plasma proteome in a mouse intestinal tumor model
    Kenneth E Hung
    Gastrointestinal Unit, Massachusetts General Hospital, 55 Fruit Street, Boston, 02114, USA
    J Proteome Res 5:1866-78. 2006
    ..These studies suggest that mass spectrometry-based approaches to examine the plasma proteome may prove to be a valuable method for determining the presence of intestinal tumors...
  8. pmc mTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1
    Anthony C Faber
    1Massachusetts General Hospital Cancer Center 2Department of Medicine, Harvard Medical School 3Division of Gastroenterology, Department of Medicine, Tufts Medical Center 4Department of Pathology, Massachusetts General Hospital, Boston and 5Radiation Oncology, Steele Lab for Tumor Biology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts
    Cancer Discov 4:42-52. 2014
    ..These data suggest that the combination of BCL-2/BCL-XL inhibitors with TORC1/2 inhibitors constitutes a promising targeted therapy strategy to treat these recalcitrant cancers. ..
  9. pmc Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models
    Ryan B Corcoran
    Massachusetts General Hospital Cancer Center, Boston, MA 02129, USA
    Cancer Cell 23:121-8. 2013
    ....
  10. pmc Colon-specific tumorigenesis in mice driven by Cre-mediated inactivation of Apc and activation of mutant Kras
    Alexander J Byun
    Vitamins and Carcinogenesis Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA
    Cancer Lett 347:191-5. 2014
    ..Despite the apparent lack of invasion, the geographical correctness, complete penetrance and intermediate tumor burden make this model a promising addition to our toolkit for the study of colorectal cancer treatment and prevention. ..
  11. pmc The dual PI3K/mTOR inhibitor NVP-BEZ235 induces tumor regression in a genetically engineered mouse model of PIK3CA wild-type colorectal cancer
    Jatin Roper
    Division of Gastroenterology, Department of Medicine, Tufts Medical Center, Boston, Massachusetts, United States of America
    PLoS ONE 6:e25132. 2011
    ..To examine the in vitro and in vivo efficacy of the dual PI3K/mTOR inhibitor NVP-BEZ235 in treatment of PIK3CA wild-type colorectal cancer (CRC)...
  12. pmc In vivo wide-area cellular imaging by side-view endomicroscopy
    Pilhan Kim
    Wellman Center for Photomedicine, Department of Dermatology, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA
    Nat Methods 7:303-5. 2010
    ..We monitored cell infiltration, vascular changes and tumor progression during inflammation and tumorigenesis in colon over several months...
  13. doi Overview of genetically engineered mouse models of colorectal carcinoma to enable translational biology and drug development
    Jatin Roper
    Division of Gastroenterology and Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts
    Curr Protoc Pharmacol 65:14.29.1-10. 2014
    ..Detailed in this overview are the salient features of several useful colorectal cancer GEMMs and their value as tools for translational biology and preclinical drug development...
  14. pmc EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib
    Ryan B Corcoran
    Massachusetts General Hospital Cancer Center, Boston, MA 02129, USA
    Cancer Discov 2:227-35. 2012
    ..These findings support evaluation of combined RAF and EGFR inhibition in BRAF mutant CRC patients...
  15. doi Priceless GEMMs: genetically engineered mouse models for colorectal cancer drug development
    Jatin Roper
    Gastroenterology Division, Department of Medicine, Tufts Medical Center, Boston, MA 02111, USA
    Trends Pharmacol Sci 33:449-55. 2012
    ..With the increasing sophistication of GEMMs, our preclinical armamentarium provides new hope for the ongoing war against CRC...
  16. pmc Cathepsin B expression and survival in colon cancer: implications for molecular detection of neoplasia
    Andrew T Chan
    Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
    Cancer Epidemiol Biomarkers Prev 19:2777-85. 2010
    ..Proteases play a critical role in tumorigenesis and are upregulated in colorectal cancer and neoplastic polyps. In animal models, cathepsin B (CTSB)-activatable imaging agents show high enzyme activity within intestinal tumors...
  17. pmc Oncogenic transformation of diverse gastrointestinal tissues in primary organoid culture
    Xingnan Li
    Department of Medicine, Hematology Division, Stanford University School of Medicine, Stanford, California, USA
    Nat Med 20:769-77. 2014
    ..These studies demonstrate the general utility of a highly tractable primary organoid system for cancer modeling and driver oncogene validation in diverse gastrointestinal tissues. ..