M M Moasser

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Phase II study of celecoxib and trastuzumab in metastatic breast cancer patients who have progressed after prior trastuzumab-based treatments
    Chau T Dang
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Clin Cancer Res 10:4062-7. 2004
  2. pmc Targeting HER proteins in cancer therapy and the role of the non-target HER3
    A C Hsieh
    Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    Br J Cancer 97:453-7. 2007
  3. pmc Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3
    Natalia V Sergina
    Department of Medicine, University of California, San Francisco 94143, USA
    Nature 445:437-41. 2007
  4. pmc Targeting the function of the HER2 oncogene in human cancer therapeutics
    M M Moasser
    Department of Medicine, Comprehensive Cancer Center, University of California, San Francisco, CA 94143 0875, USA
    Oncogene 26:6577-92. 2007
  5. pmc Improved tumor vascular function following high-dose epidermal growth factor receptor tyrosine kinase inhibitor therapy
    Mark M Moasser
    Department of Medicine, University of California, San Francisco, San Francisco, California 94143, USA
    J Magn Reson Imaging 26:1618-25. 2007
  6. pmc The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis
    M M Moasser
    Department of Medicine and Comprehensive Cancer Center, University of California, San Francisco, CA 94143 0875, USA
    Oncogene 26:6469-87. 2007
  7. ncbi request reprint The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells
    M M Moasser
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 61:7184-8. 2001
  8. ncbi request reprint Inhibition of Src kinases by a selective tyrosine kinase inhibitor causes mitotic arrest
    M M Moasser
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 59:6145-52. 1999
  9. ncbi request reprint Inhibition of heat shock protein 90 function by ansamycins causes the morphological and functional differentiation of breast cancer cells
    P N Munster
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 61:2945-52. 2001
  10. doi request reprint MRI methods for evaluating the effects of tyrosine kinase inhibitor administration used to enhance chemotherapy efficiency in a breast tumor xenograft model
    S O Aliu
    Department of Radiology and Biomedical Imaging, University of California at San Francisco, San Francisco, California 94107, USA
    J Magn Reson Imaging 29:1071-9. 2009

Collaborators

Detail Information

Publications26

  1. ncbi request reprint Phase II study of celecoxib and trastuzumab in metastatic breast cancer patients who have progressed after prior trastuzumab-based treatments
    Chau T Dang
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Clin Cancer Res 10:4062-7. 2004
    ....
  2. pmc Targeting HER proteins in cancer therapy and the role of the non-target HER3
    A C Hsieh
    Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    Br J Cancer 97:453-7. 2007
    ..This review presents the current evidence highlighting the role of HER3 in tumorigenesis and its role in mediating resistance to inhibitors of EGFR and HER2...
  3. pmc Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3
    Natalia V Sergina
    Department of Medicine, University of California, San Francisco 94143, USA
    Nature 445:437-41. 2007
    ..The biologic marker with which to assess the efficacy of HER TKIs should be the transphosphorylation of HER3 rather than autophosphorylation...
  4. pmc Targeting the function of the HER2 oncogene in human cancer therapeutics
    M M Moasser
    Department of Medicine, Comprehensive Cancer Center, University of California, San Francisco, CA 94143 0875, USA
    Oncogene 26:6577-92. 2007
    ..Here, I review the development of treatments that target HER2 in the context of the HER2 oncogene hypothesis, and where we stand with regards to the clinical translation of the HER2 oncogene hypothesis...
  5. pmc Improved tumor vascular function following high-dose epidermal growth factor receptor tyrosine kinase inhibitor therapy
    Mark M Moasser
    Department of Medicine, University of California, San Francisco, San Francisco, California 94143, USA
    J Magn Reson Imaging 26:1618-25. 2007
    ..Poor tumor vascular function limits the delivery and efficacy of cancer chemotherapeutics and HER family tyrosine kinases mediate tumor-endothelial signaling in both of these compartments...
  6. pmc The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis
    M M Moasser
    Department of Medicine and Comprehensive Cancer Center, University of California, San Francisco, CA 94143 0875, USA
    Oncogene 26:6469-87. 2007
    ..Here I review the evidence supporting the oncogenic function of HER2, the mechanisms that are felt to mediate its oncogenic functions, and the evidence that links the experimental evidence with human cancer pathogenesis...
  7. ncbi request reprint The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells
    M M Moasser
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 61:7184-8. 2001
    ..These studies suggest that HER2-overexpressing tumors are particularly susceptible to the inhibition of HER family tyrosine kinase signaling and suggest novel strategies to treat these particularly aggressive tumors...
  8. ncbi request reprint Inhibition of Src kinases by a selective tyrosine kinase inhibitor causes mitotic arrest
    M M Moasser
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 59:6145-52. 1999
    ..This compound defines a novel class of antimitotic drugs that work through inhibition of src kinases and possibly other protein kinases that are required for progression through the initial phases of mitosis...
  9. ncbi request reprint Inhibition of heat shock protein 90 function by ansamycins causes the morphological and functional differentiation of breast cancer cells
    P N Munster
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 61:2945-52. 2001
    ..G1 arrest is sufficient for some but not all aspects of the phenotype. Induction of differentiation may be responsible for some of the antitumor effects of this drug...
  10. doi request reprint MRI methods for evaluating the effects of tyrosine kinase inhibitor administration used to enhance chemotherapy efficiency in a breast tumor xenograft model
    S O Aliu
    Department of Radiology and Biomedical Imaging, University of California at San Francisco, San Francisco, California 94107, USA
    J Magn Reson Imaging 29:1071-9. 2009
    ..To evaluate whether quantitative MRI parameters are sensitive to the effects of the tyrosine kinase inhibitor gefitinib and can discriminate between two different treatment protocols...
  11. pmc Phosphorylation of Trask by Src kinases inhibits integrin clustering and functions in exclusion with focal adhesion signaling
    Danislav S Spassov
    Department of Medicine, University of California, San Francisco, San Francisco, CA 94143 1387, USA
    Mol Cell Biol 31:766-82. 2011
    ..These data provide considerable insight into how Trask functions to regulate cell adhesion and reveal a novel pathway through which Src kinases can oppose integrin-mediated cell adhesion...
  12. pmc The epidermal growth factor receptor family: biology driving targeted therapeutics
    M J Wieduwilt
    Department of Medicine, Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143 0875, USA
    Cell Mol Life Sci 65:1566-84. 2008
    ..Here we review the biology of ErbB receptors, including their structure, signaling, regulation, and roles in development and disease, then briefly touch on their increasing roles as targets for cancer therapy...
  13. ncbi request reprint Oral gossypol in the treatment of patients with refractory metastatic breast cancer: a phase I/II clinical trial
    C Van Poznak
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Breast Cancer Res Treat 66:239-48. 2001
    ..The cell cycle regulatory effects of gossypol suggest a potential role for gossypol as a modulating agent in conjunction with other cell cycle specific compounds...
  14. pmc A tumor-suppressing function in the epithelial adhesion protein Trask
    D S Spassov
    Department of Medicine, University of California, San Francisco, CA 94143, USA
    Oncogene 31:419-31. 2012
    ..These data identify Trask as one of several potential candidates for functionally relevant tumor suppressors on the 3p21.3 region of the genome frequently lost in human cancers...
  15. ncbi request reprint The use of molecular markers in farnesyltransferase inhibitor (FTI) therapy of breast cancer
    M M Moasser
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Breast Cancer Res Treat 73:135-44. 2002
    ..Although these studies do not identify any single molecular marker that can accurately predict FTI sensitivity in breast tumors, they highlight the potential roles of FPTase activity and p53 function for further analysis...
  16. doi request reprint Cellular mechanisms of resistance to anthracyclines and taxanes in cancer: intrinsic and acquired
    A Jo Chien
    Department of Medicine, Division of Hematology Oncology, University of California San Francisco, San Francisco, CA, USA
    Semin Oncol 35:S1-S14; quiz S39. 2008
    ..Potential mechanisms behind these differences and their potential role in the treatment of both taxane- and anthracycline-refractory patients are discussed...
  17. pmc Resiliency and vulnerability in the HER2-HER3 tumorigenic driver
    Dhara N Amin
    Department of Medicine, University of California, San Francisco, CA 94143, USA
    Sci Transl Med 2:16ra7. 2010
    ..This strategy for inactivation of HER2-HER3 tumorigenic activity is proposed for clinical testing...
  18. pmc Adhesion signaling by a novel mitotic substrate of src kinases
    Ami S Bhatt
    School of Medicine, University of California, San Francisco, CA 94143, USA
    Oncogene 24:5333-43. 2005
    ..This suggests a potential pathway by which hyperactive src kinases in tumors can deregulate adhesion signaling and mediate the metastatic phenotype...
  19. pmc Phosphorylation of the SRC epithelial substrate Trask is tightly regulated in normal epithelia but widespread in many human epithelial cancers
    Ching Hang Wong
    Department of Medicine, University of California, San Francisco, San Francisco, California 94143 0875, USA
    Clin Cancer Res 15:2311-22. 2009
    ....
  20. pmc The transmembrane src substrate Trask is an epithelial protein that signals during anchorage deprivation
    Danislav S Spassov
    Department of Medicine, University of California, San Francisco, San Francisco, California 94143 0875, USA
    Am J Pathol 174:1756-65. 2009
    ..Trask is a novel epithelial membrane protein that is phosphorylated by src kinases when epithelial cells disengage from their tissue framework, identifying an important new regulator of epithelial tissue dynamics...
  21. ncbi request reprint A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants
    David R Huron
    Department of Medicine, Memorial Sloan Kettering Cancer Center and Program in Pharmacology, New York, New York 10021, USA
    Clin Cancer Res 9:1267-73. 2003
    ..PD166326 is a prototype of a new generation of anti-Bcr-abl compounds with picomolar potency and substantial activity against STI571-resistant mutants...
  22. pmc A phase I study of a 2-day lapatinib chemosensitization pulse preceding nanoparticle albumin-bound Paclitaxel for advanced solid malignancies
    Amy J Chien
    Department of Medicine, University of California San Francisco, San Francisco, California 94143 0875, USA
    Clin Cancer Res 15:5569-75. 2009
    ..This study investigates the clinical relevance of this approach...
  23. ncbi request reprint Resistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt pathway signaling
    Qing Bai She
    Department of Medicine and Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Clin Cancer Res 9:4340-6. 2003
    ..However, EGFR-overexpressing MDA-468 cells, which lack PTEN function, are resistant to ZD1839, and ZD1839 is unable to down-regulate Akt activity in these cells...
  24. pmc The HER family and cancer: emerging molecular mechanisms and therapeutic targets
    Natalia V Sergina
    University of California, San Francisco, San Francisco, CA 94143, USA
    Trends Mol Med 13:527-34. 2007
    ..Here, we review recent advances in our understanding of HER signaling and targeting in cancer...
  25. ncbi request reprint A phase II trial of gemcitabine in patients with metastatic breast cancer previously treated with an anthracycline and taxane
    Shanu Modi
    Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Clin Breast Cancer 6:55-60. 2005
    ..Gemcitabine was delivered at a dose of 800 mg/m2 on days 1, 8, and 15 of a 28-day cycle until evidence of disease progression...
  26. ncbi request reprint S-phase inhibition of cell cycle progression by a novel class of pyridopyrimidine tyrosine kinase inhibitors
    Olga A Mizenina
    Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    Cell Cycle 3:796-803. 2004
    ..These data identify a novel subset of pyridopyrimidine compounds which are inhibitors of src and Wee1 kinases and which inhibit tumor cell growth through cell cycle arrest in mid S-phase...

Research Grants10

  1. Pilot studies to develop probes for in vivo imaging of P13K/Akt pathway activity
    Mark Moasser; Fiscal Year: 2007
    ..If successful, this modality could potentially lead to a ground-breaking predictive clinical monitoring tool. ..
  2. Understanding resistance to HER family tyrosine kinase inhibitors
    Mark Moasser; Fiscal Year: 2009
    ....
  3. Adhesion signaling by a novel mitotic substrate of src
    Mark Moasser; Fiscal Year: 2009
    ..abstract_text> ..
  4. Understanding resistance to HER family tyrosine kinase inhibitors
    Mark Moasser; Fiscal Year: 2007
    ....
  5. Adhesion signaling by a novel mitotic substrate of src
    Mark Moasser; Fiscal Year: 2007
    ..abstract_text> ..
  6. Adhesion signaling by a novel mitotic substrate of src
    Mark Moasser; Fiscal Year: 2006
    ..abstract_text> ..
  7. Adhesion signaling by a novel mitotic substrate of src
    Mark Moasser; Fiscal Year: 2005
    ..abstract_text> ..