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Mark M Moasser

  1. "Human Oncology and Pathogenesis Program"
Formats
  1. Meeting Abstract (6)
  2. Journal Article (1)
Groups
  1. Department of Medicine (7)
  2. GSK Faculty (7)
  3. Genitourinary Oncology Service (7)
  4. Human Oncology and Pathogenesis Program (7)
  5. Solid Tumor Oncology Division (7)
  6. Breast Medicine Service (6)

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People
  1. David Solit (7)
  2. Neal Rosen (6)
  3. Qing-Bai She (4)
  4. Andrea Basso (3)
  5. Clifford Hudis (2)
  6. Francis Sirotnak (2)

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Years
  1. 2004 (1)
  2. 2003 (5)
  3. 2002 (1)
Publications
  1. Clinical Cancer Research (3)
  2. Proceedings of the American Association for Cancer Research Annual Meeting (3)
  3. Cancer Research (1)
Publishers
  1. American Association for Cancer Research (7)

Results (7)

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  • Restoration of PTEN-expression in tumor cells causes them to depend on EGFR for suppression
    Meeting Abstract

    She, Q.; Moasser, M. M.; Ye, Q.; O'reilly, K.; Solit, D.; Rosen, N.
    Cancer Research (2004)

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  • Pulsatile administration of the EGF receptor inhibitor Iressa (ZD1839) is significantly more effective than continuous dosing for sensitizing tumors to taxol
    Meeting Abstract

    Solit, D. B.; She, Y.; Moasser, M. M.; Hudis, C. A.; Kris, M. G.; Scher, H. I.; Rosen, N.; Sirotnak, F. M.
    Proceedings of the American Association for Cancer Research Annual Meeting (2003)

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  • Response and resistance to gefitinib (ZD1839, Iressa) in HER overexpressing tumor cells is mediated through the PI3K/Akt pathway
    Meeting Abstract

    She, Q. B.; Solit, D.; Basso, A.; Rosen, N.; Moasser, M. M.
    Proceedings of the American Association for Cancer Research Annual Meeting (2003)

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  • Pulsatile administration of the EGF receptor inhibitor gefitinib (Iressa, ZD 1839) is significantly more effective than continuous dosing for sensitizing tumors to Taxol
    Meeting Abstract

    Solit, D. B.; She, Y.; Moasser, M.; Hudis, C.; Kris, M.; Scher, H.; Rosen, N.; Sirotnak, F. M.
    Clinical Cancer Research (2003)

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  • Cyclin D expression and G1 progression are dependent on MEK-MAP kinase activity in tumor cells with B-Raf mutation but not in breast cancer cells with wild type Ras
    Meeting Abstract

    Sawai, A.; Basso, A. D.; Solit, D. B.; She, Q. B.; Grbovic, O.; Pratilas, C.; Chapman, P.; Moasser, M. M.; Rosen, N.
    Clinical Cancer Research (2003)

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  • 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
    Journal Article

    She, Q. B.; Solit, D.; Basso, A.; Moasser, M. M.
    Clinical Cancer Research (2003)

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  • Ras signaling is not required for transformed growth but does mediate the angiogenic properties of MCF-7 cells
    Meeting Abstract

    Moasser, M. M.; Solit, D.; Costa, C.; Rafii, S.; Rosen, N.
    Proceedings of the American Association for Cancer Research Annual Meeting (2002)

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