Inhibition of PI3K-AKT-mTOR signaling sensitizes melanoma cells to cisplatin and temozolomide.
暂无分享,去创建一个
K. Flaherty | C. Garbe | B. Schittek | F. Meier | T. Sinnberg | H. Niessner | K. Lasithiotakis | D. Kulms | E. Maczey | M. Campos | J. Gogel | Jeannette Gogel
[1] K. Flaherty,et al. Combined inhibition of MAPK and mTOR signaling inhibits growth, induces cell death, and abrogates invasive growth of melanoma cells. , 2008, The Journal of investigative dermatology.
[2] P. Valent,et al. Comparison of a treatment strategy combining CCI-779 plus DTIC versus DTIC monotreatment in human melanoma in SCID mice. , 2007, The Journal of investigative dermatology.
[3] H. Bojar,et al. ERK1/2 is highly phosphorylated in melanoma metastases and protects melanoma cells from cisplatin-mediated apoptosis. , 2007, The Journal of investigative dermatology.
[4] P. Hersey,et al. Apoptosis Induction in Human Melanoma Cells by Inhibition of MEK Is Caspase-Independent and Mediated by the Bcl-2 Family Members PUMA, Bim, and Mcl-1 , 2007, Clinical Cancer Research.
[5] M. Soengas,et al. Therapeutic window for melanoma treatment provided by selective effects of the proteasome on Bcl-2 proteins , 2007, Cell Death and Differentiation.
[6] C. Garbe,et al. Combined targeting of MAPK and AKT signalling pathways is a promising strategy for melanoma treatment , 2007, The British journal of dermatology.
[7] M. Zvelebil,et al. Exploring the specificity of the PI3K family inhibitor LY294002. , 2007, The Biochemical journal.
[8] R. Scolyer,et al. Mcl-1, Bcl-XL and Stat3 expression are associated with progression of melanoma whereas Bcl-2, AP-2 and MITF levels decrease during progression of melanoma , 2007, Modern Pathology.
[9] P. Valent,et al. CCI-779 plus Cisplatin Is Highly Effective against Human Melanoma in a SCID Mouse Xenotranplantation Model , 2007, Pharmacology.
[10] L. Weber,et al. In vitro and in vivo synergy of MCP compounds with mitogen-activated protein kinase pathway– and microtubule-targeting inhibitors , 2007, Molecular Cancer Therapeutics.
[11] V. Sondak,et al. Chemotherapy for metastatic melanoma , 2007, Cancer.
[12] James T. Elder,et al. A novel BH3 mimetic reveals a mitogen-activated protein kinase-dependent mechanism of melanoma cell death controlled by p53 and reactive oxygen species. , 2006, Cancer research.
[13] S. Winograd-Katz,et al. Cisplatin induces PKB/Akt activation and p38MAPK phosphorylation of the EGF receptor , 2006, Oncogene.
[14] M. Ratain,et al. Sorafenib in advanced melanoma: a Phase II randomised discontinuation trial analysis , 2006, British Journal of Cancer.
[15] Kazuhiro Takahashi,et al. Inhibition of phosphatidylinositol 3-kinase increases efficacy of cisplatin in in vivo ovarian cancer models. , 2006, Endocrinology.
[16] K. Flaherty. Chemotherapy and Targeted Therapy Combinations in Advanced Melanoma , 2006, Clinical Cancer Research.
[17] Hong Zhang,et al. Bcl-xL and bcl-2 proteins in melanoma progression and UVB-induced apoptosis. , 2006, International journal of oncology.
[18] P. Hersey. Apoptosis and melanoma: how new insights are effecting the development of new therapies for melanoma , 2006, Current opinion in oncology.
[19] Gordon B Mills,et al. mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. , 2006, Cancer research.
[20] R. Stahel,et al. Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation , 2005, International journal of cancer.
[21] J. Gills,et al. Inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway but not the MEK/ERK pathway attenuates laminin-mediated small cell lung cancer cellular survival and resistance to imatinib mesylate or chemotherapy. , 2005, Cancer research.
[22] Gang Li,et al. The RAS/RAF/MEK/ERK and PI3K/AKT signaling pathways present molecular targets for the effective treatment of advanced melanoma. , 2005, Frontiers in bioscience : a journal and virtual library.
[23] Gerolama Condorelli,et al. PED mediates AKT-dependent chemoresistance in human breast cancer cells. , 2005, Cancer research.
[24] T. Kwon,et al. LY294002 inhibits LPS-induced NO production through a inhibition of NF-kappaB activation: independent mechanism of phosphatidylinositol 3-kinase. , 2005, Immunology letters.
[25] Mustafa Al-Chalabi,et al. LY-294002 [2-(4-Morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] Affects Calcium Signaling in Airway Smooth Muscle Cells Independently of Phosphoinositide 3-Kinase Inhibition , 2004, Journal of Pharmacology and Experimental Therapeutics.
[26] D. Auclair,et al. BAY 43-9006 Exhibits Broad Spectrum Oral Antitumor Activity and Targets the RAF/MEK/ERK Pathway and Receptor Tyrosine Kinases Involved in Tumor Progression and Angiogenesis , 2004, Cancer Research.
[27] C. Marshall,et al. B-RAF is a therapeutic target in melanoma , 2004, Oncogene.
[28] C. Springer,et al. V599EB-RAF is an Oncogene in Melanocytes , 2004, Cancer Research.
[29] H. Pehamberger,et al. Mcl-1 antisense therapy chemosensitizes human melanoma in a SCID mouse xenotransplantation model. , 2003, The Journal of investigative dermatology.
[30] R. Offringa,et al. Rapamycin specifically interferes with GM-CSF signaling in human dendritic cells, leading to apoptosis via increased p27KIP1 expression. , 2003, Blood.
[31] J. Litz,et al. Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy. , 2002, Molecular cancer therapeutics.
[32] C. Sawyers,et al. The phosphatidylinositol 3-Kinase–AKT pathway in human cancer , 2002, Nature Reviews Cancer.
[33] Walter Kolch,et al. Ras/Raf signalling and emerging pharmacotherapeutic targets , 2002, Expert opinion on pharmacotherapy.
[34] R. Craig. MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesis , 2002, Leukemia.
[35] P. Dennis,et al. Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. , 2001, Cancer research.
[36] R. Tallarida. Response Surface Analysis of Drug Combinations , 2000 .
[37] Min-Liang Kuo,et al. The Antiapoptotic Gene mcl-1 Is Up-Regulated by the Phosphatidylinositol 3-Kinase/Akt Signaling Pathway through a Transcription Factor Complex Containing CREB , 1999, Molecular and Cellular Biology.
[38] C. Garbe,et al. A fluorometric rapid microassay to identify anti‐proliferative compounds for human melanoma cells in vitro , 1991, Melanoma research.
[39] M. Pittelkow,et al. New techniques for the in vitro culture of human skin keratinocytes and perspectives on their use for grafting of patients with extensive burns. , 1986, Mayo Clinic proceedings.
[40] Gang Li,et al. The role of Bcl-2 family members in the progression of cutaneous melanoma , 2004, Clinical & Experimental Metastasis.
[41] D. Grossman,et al. Apoptosis regulators and responses in human melanocytic and keratinocytic cells. , 2003, The Journal of investigative dermatology.
[42] D. Elder,et al. Human melanoma progression in skin reconstructs : biological significance of bFGF. , 2000, The American journal of pathology.