M Golam Mohi

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, NRB1038, 330 Brookline Ave, Boston, Massachusetts 02215, USA
    Nat Med 10:849-57. 2004
  2. ncbi Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations
    M Golam Mohi
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, 77 Avenue Louis Pasteur, NRB 1030, Boston, Massachusetts 02115, USA
    Cancer Cell 7:179-91. 2005
  3. ncbi Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs
    M Golam Mohi
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, New Research Building, 330 Brookline Avenue, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 101:3130-5. 2004
  4. ncbi Combining an mTOR antagonist and receptor tyrosine kinase inhibitors for the treatment of prostate cancer
    David Masiello
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 300 Brookline Avenue, Boston, MA 02215, USA
    Cancer Biol Ther 6:195-201. 2007
  5. ncbi Critical role for Gab2 in transformation by BCR/ABL
    Martin Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Cancer Cell 1:479-92. 2002
  6. ncbi Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences
    Shu Yue Ren
    Molecular Carcinogenesis Section, Center for Biotechnology, College of Science and Technology, Temple University, BLSB 419, 1900 N 12th Street, Philadelphia, PA 19122, USA
    Mol Cell Biol 25:8001-8. 2005
  7. ncbi The role of Shp2 (PTPN11) in cancer
    M Golam Mohi
    Department of Pharmacology, SUNY Upstate Medical University, WHA 3319, 750 East Adams Street, Syracuse, NY 13020, USA
    Curr Opin Genet Dev 17:23-30. 2007

Detail Information

Publications7

  1. ncbi Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation
    Toshiyuki Araki
    Cancer Biology Program, Division of Hematology Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, NRB1038, 330 Brookline Ave, Boston, Massachusetts 02215, USA
    Nat Med 10:849-57. 2004
    ....
  2. ncbi Prognostic, therapeutic, and mechanistic implications of a mouse model of leukemia evoked by Shp2 (PTPN11) mutations
    M Golam Mohi
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, 77 Avenue Louis Pasteur, NRB 1030, Boston, Massachusetts 02115, USA
    Cancer Cell 7:179-91. 2005
    ..Shp2 mutants also cause myeloproliferation in Drosophila. Mek or Tor inhibitors potently inhibit transformation, suggesting new approaches to JMML therapy...
  3. ncbi Combination of rapamycin and protein tyrosine kinase (PTK) inhibitors for the treatment of leukemias caused by oncogenic PTKs
    M Golam Mohi
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, New Research Building, 330 Brookline Avenue, Boston, MA 02215, USA
    Proc Natl Acad Sci U S A 101:3130-5. 2004
    ..Similar strategies may be useful for treating solid tumors associated with mutant and/or overexpressed PTKs...
  4. ncbi Combining an mTOR antagonist and receptor tyrosine kinase inhibitors for the treatment of prostate cancer
    David Masiello
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 300 Brookline Avenue, Boston, MA 02215, USA
    Cancer Biol Ther 6:195-201. 2007
    ....
  5. ncbi Critical role for Gab2 in transformation by BCR/ABL
    Martin Sattler
    Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Cancer Cell 1:479-92. 2002
    ..Our results identify Gab2 and its associated proteins as key determinants of the lineage and severity of BCR/ABL transformation...
  6. ncbi Phosphatidylinositol 3-kinase p85{alpha} subunit-dependent interaction with BCR/ABL-related fusion tyrosine kinases: molecular mechanisms and biological consequences
    Shu Yue Ren
    Molecular Carcinogenesis Section, Center for Biotechnology, College of Science and Technology, Temple University, BLSB 419, 1900 N 12th Street, Philadelphia, PA 19122, USA
    Mol Cell Biol 25:8001-8. 2005
    ..In conclusion, we have identified the domains of p85alpha responsible for the interaction with the FTK protein network and transduction of leukemogenic signaling...
  7. ncbi The role of Shp2 (PTPN11) in cancer
    M Golam Mohi
    Department of Pharmacology, SUNY Upstate Medical University, WHA 3319, 750 East Adams Street, Syracuse, NY 13020, USA
    Curr Opin Genet Dev 17:23-30. 2007
    ..Understanding how Shp2 and other PTPs contribute to oncogenesis should provide new insights into pathogenesis and might suggest new targets for anti-neoplastic drugs...