The Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma

Friedegund Meier, Birgit Schittek, Silke Busch, Claus Garbe, Keiran Smalley, Kapaettu Satyamoorthy, Gang Li, Meenhard Herlyn

    Research output: Contribution to journalReview article

    190 Citations (Scopus)

    Abstract

    Malignant melanoma is a highly aggressive tumor of the pigment-producing cells in the skin with a rapidly increasing incidence and a poor prognosis for patients with advanced disease that is resistant to current therapeutic concepts. Therefore, the development of novel strategies for treating melanoma are of utmost importance. In melanoma, both the Ras-Raf-MEK-ERK (MAPK) and the PI3K-AKT (AKT) signaling pathways are constitutively activated through multiple mechanisms, and thus exert several key functions in melanoma development and progression. Conversely, several molecules known to play key roles in melanoma development and progression such as the adhesion molecules E-/N-cadherin, MelCAM and alphavbeta3 integral are regulated by these pathways and/or activate the same. The results of the research to date indicate that in melanoma both the MAPK and the AKT signaling pathways may represent promising therapeutic targets.

    Original languageEnglish
    Pages (from-to)2986-3001
    Number of pages16
    JournalFrontiers in Bioscience
    Volume10
    Issue numberSUPPL. 3
    Publication statusPublished - 2005

    Fingerprint

    Mitogen-Activated Protein Kinase Kinases
    Phosphatidylinositol 3-Kinases
    Melanoma
    Molecules
    Cadherins
    Pigments
    Tumors
    Skin
    Adhesion
    Therapeutics
    Incidence
    Research
    Neoplasms

    All Science Journal Classification (ASJC) codes

    • Biochemistry, Genetics and Molecular Biology(all)
    • Biochemistry
    • Cell Biology

    Cite this

    Meier, F., Schittek, B., Busch, S., Garbe, C., Smalley, K., Satyamoorthy, K., ... Herlyn, M. (2005). The Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma. Frontiers in Bioscience, 10(SUPPL. 3), 2986-3001.
    Meier, Friedegund ; Schittek, Birgit ; Busch, Silke ; Garbe, Claus ; Smalley, Keiran ; Satyamoorthy, Kapaettu ; Li, Gang ; Herlyn, Meenhard. / The Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma. In: Frontiers in Bioscience. 2005 ; Vol. 10, No. SUPPL. 3. pp. 2986-3001.
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    abstract = "Malignant melanoma is a highly aggressive tumor of the pigment-producing cells in the skin with a rapidly increasing incidence and a poor prognosis for patients with advanced disease that is resistant to current therapeutic concepts. Therefore, the development of novel strategies for treating melanoma are of utmost importance. In melanoma, both the Ras-Raf-MEK-ERK (MAPK) and the PI3K-AKT (AKT) signaling pathways are constitutively activated through multiple mechanisms, and thus exert several key functions in melanoma development and progression. Conversely, several molecules known to play key roles in melanoma development and progression such as the adhesion molecules E-/N-cadherin, MelCAM and alphavbeta3 integral are regulated by these pathways and/or activate the same. The results of the research to date indicate that in melanoma both the MAPK and the AKT signaling pathways may represent promising therapeutic targets.",
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    Meier, F, Schittek, B, Busch, S, Garbe, C, Smalley, K, Satyamoorthy, K, Li, G & Herlyn, M 2005, 'The Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma', Frontiers in Bioscience, vol. 10, no. SUPPL. 3, pp. 2986-3001.

    The Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma. / Meier, Friedegund; Schittek, Birgit; Busch, Silke; Garbe, Claus; Smalley, Keiran; Satyamoorthy, Kapaettu; Li, Gang; Herlyn, Meenhard.

    In: Frontiers in Bioscience, Vol. 10, No. SUPPL. 3, 2005, p. 2986-3001.

    Research output: Contribution to journalReview article

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