Research Topics
| M M MoasserSummaryAffiliation: University of California Country: USA Publications
Research Grants
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Detail Information
Publications
Phase II study of celecoxib and trastuzumab in metastatic breast cancer patients who have progressed after prior trastuzumab-based treatmentsChau T Dang
Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York, USA
Clin Cancer Res 10:4062-7. 2004..CONCLUSIONS: Celecoxib combined with trastuzumab is well tolerated. However, this combination in patients with HER2/neu-overexpressing, trastuzumab-refractory disease, was not active...
Targeting the function of the HER2 oncogene in human cancer therapeuticsM 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...- Improved tumor vascular function following high-dose epidermal growth factor receptor tyrosine kinase inhibitor therapyMark 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... - The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesisM 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... - The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cellsM 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... - Inhibition of Src kinases by a selective tyrosine kinase inhibitor causes mitotic arrestM 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... 
MRI methods for evaluating the effects of tyrosine kinase inhibitor administration used to enhance chemotherapy efficiency in a breast tumor xenograft modelS 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...- Targeting HER proteins in cancer therapy and the role of the non-target HER3A 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... - Phosphorylation of Trask by Src kinases inhibits integrin clustering and functions in exclusion with focal adhesion signalingDanislav 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... - Inhibition of heat shock protein 90 function by ansamycins causes the morphological and functional differentiation of breast cancer cellsP 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... - The epidermal growth factor receptor family: biology driving targeted therapeuticsM 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... - Oral gossypol in the treatment of patients with refractory metastatic breast cancer: a phase I/II clinical trialC 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... - A tumor-suppressing function in the epithelial adhesion protein TraskD 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... - The use of molecular markers in farnesyltransferase inhibitor (FTI) therapy of breast cancerM 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... - Cellular mechanisms of resistance to anthracyclines and taxanes in cancer: intrinsic and acquiredA 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... - Resiliency and vulnerability in the HER2-HER3 tumorigenic driverDhara 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... - A phase I study of a 2-day lapatinib chemosensitization pulse preceding nanoparticle albumin-bound Paclitaxel for advanced solid malignanciesAmy 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... - The transmembrane src substrate Trask is an epithelial protein that signals during anchorage deprivationDanislav 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... - Phosphorylation of the SRC epithelial substrate Trask is tightly regulated in normal epithelia but widespread in many human epithelial cancersChing Hang Wong
Department of Medicine, University of California, San Francisco, San Francisco, California 94143 0875, USA
Clin Cancer Res 15:2311-22. 2009.... - Adhesion signaling by a novel mitotic substrate of src kinasesAmi 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... - Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3Natalia 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... - 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 mutantsDavid 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... - 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 signalingQing-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..These data have important predictive and therapeutic clinical implications... - The HER family and cancer: emerging molecular mechanisms and therapeutic targetsNatalia 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... - A phase II trial of gemcitabine in patients with metastatic breast cancer previously treated with an anthracycline and taxaneShanu Modi
Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
Clin Breast Cancer 6:55-60. 2005..The activity and safety reported in this trial are consistent with previous reports in similar patients... - S-phase inhibition of cell cycle progression by a novel class of pyridopyrimidine tyrosine kinase inhibitorsOlga 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 Grants
- Pilot studies to develop probes for in vivo imaging of P13K/Akt pathway activityMark Moasser; Fiscal Year: 2007..If successful, this modality could potentially lead to a ground-breaking predictive clinical monitoring tool. ..
- Adhesion signaling by a novel mitotic substrate of srcMark Moasser; Fiscal Year: 2009..abstract_text> ..
- Understanding resistance to HER family tyrosine kinase inhibitorsMark Moasser; Fiscal Year: 2007....
- Understanding resistance to HER family tyrosine kinase inhibitorsMark Moasser; Fiscal Year: 2009....