Prevalence of the Hippo Effectors YAP1/TAZ in Tumors of Soft Tissue and Bone

[1]  S. Fröhling,et al.  Requirement for YAP1 signaling in myxoid liposarcoma , 2019, EMBO molecular medicine.

[2]  O. Larsson,et al.  SS18-SSX–Dependent YAP/TAZ Signaling in Synovial Sarcoma , 2019, Clinical Cancer Research.

[3]  E. Wardelmann,et al.  Phosphatidylinositol-3-kinase (PI3K)/Akt Signaling is Functionally Essential in Myxoid Liposarcoma , 2019, Molecular Cancer Therapeutics.

[4]  H. Arakawa,et al.  Survivin: A novel marker and potential therapeutic target for human angiosarcoma , 2017, Cancer science.

[5]  S. Fröhling,et al.  FUS–DDIT3 Fusion Protein-Driven IGF-IR Signaling is a Therapeutic Target in Myxoid Liposarcoma , 2017, Clinical Cancer Research.

[6]  M. Milhem,et al.  TAZ and YAP are frequently activated oncoproteins in sarcomas , 2016, Oncotarget.

[7]  G. Huet,et al.  Non-Photoinduced Biological Properties of Verteporfin. , 2016, Current medicinal chemistry.

[8]  B. Győrffy,et al.  Tumor-selective proteotoxicity of verteporfin inhibits colon cancer progression independently of YAP1 , 2015, Science Signaling.

[9]  Sharon Gerecht,et al.  Deregulation of the Hippo pathway in soft-tissue sarcoma promotes FOXM1 expression and tumorigenesis , 2015, Proceedings of the National Academy of Sciences.

[10]  D. Ribatti.  The chick embryo chorioallantoic membrane as a model for tumor biology. , 2014, Experimental cell research.

[11]  O. Larsson,et al.  SS18-SSX fusion protein-induced Wnt/β-catenin signaling is a therapeutic target in synovial sarcoma , 2014, Oncogene.

[12]  G. G. Galli,et al.  The Hippo transducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation. , 2014, Cancer cell.

[13]  Joan W. Miller,et al.  The clinically used photosensitizer Verteporfin (VP) inhibits YAP-TEAD and human retinoblastoma cell growth in vitro without light activation. , 2014, Experimental eye research.

[14]  R. Bentley,et al.  Alveolar rhabdomyosarcoma-associated PAX3-FOXO1 promotes tumorigenesis via Hippo pathway suppression. , 2014, The Journal of clinical investigation.

[15]  M. Rubin,et al.  Novel YAP1‐TFE3 fusion defines a distinct subset of epithelioid hemangioendothelioma , 2013, Genes, chromosomes & cancer.

[16]  O. Larsson,et al.  SRC signaling is crucial in the growth of synovial sarcoma cells. , 2013, Cancer research.

[17]  David M. Thomas,et al.  The Hippo pathway and human cancer , 2013, Nature Reviews Cancer.

[18]  Satoshi O. Suzuki,et al.  Cancer susceptibility and embryonic lethality in Mob1a/1b double-mutant mice. , 2012, The Journal of clinical investigation.

[19]  Jun O. Liu,et al.  Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP. , 2012, Genes & development.

[20]  M. Gerstein,et al.  Identification of a Disease-Defining Gene Fusion in Epithelioid Hemangioendothelioma , 2011, Science Translational Medicine.

[21]  C. Antonescu,et al.  A novel WWTR1‐CAMTA1 gene fusion is a consistent abnormality in epithelioid hemangioendothelioma of different anatomic sites , 2011, Genes, chromosomes & cancer.

[22]  Nicola Elvassore,et al.  Role of YAP/TAZ in mechanotransduction , 2011, Nature.

[23]  F. Chibon,et al.  YAP1 and VGLL3, encoding two cofactors of TEAD transcription factors, are amplified and overexpressed in a subset of soft tissue sarcomas , 2010, Genes, chromosomes & cancer.

[24]  D. Pan,et al.  The hippo signaling pathway in development and cancer. , 2010, Developmental cell.

[25]  S. Fulda,et al.  Targeting XIAP bypasses Bcl-2-mediated resistance to TRAIL and cooperates with TRAIL to suppress pancreatic cancer growth in vitro and in vivo. , 2008, Cancer research.

[26]  Li Li,et al.  Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control. , 2007, Genes & development.

[27]  Steffen Hauptmann,et al.  Frequent hypermethylation of MST1 and MST2 in soft tissue sarcoma , 2007, Molecular carcinogenesis.

[28]  Felicitas Genze,et al.  Inhibition of IκB Kinase Activity by Acetyl-boswellic Acids Promotes Apoptosis in Androgen-independent PC-3 Prostate Cancer Cells in Vitro and in Vivo* , 2005, Journal of Biological Chemistry.

[29]  W. Tao,et al.  Mice deficient of Lats1 develop soft-tissue sarcomas, ovarian tumours and pituitary dysfunction , 1999, Nature Genetics.

[30]  J. Fletcher,et al.  Molecular characterization of a 17q11.2 translocation in a malignant schwannoma cell line , 1992, Human Genetics.

[31]  F. Mitelman,et al.  Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11) , 1992, Genes, chromosomes & cancer.

[32]  G. Mills,et al.  Verteporfin inhibits YAP function through up-regulating 14-3-3σ sequestering YAP in the cytoplasm. , 2016, American journal of cancer research.

[33]  C. Fletcher,et al.  WHO classification of tumours of soft tissue and bone , 2013 .

[34]  K. Guan,et al.  A coordinated phosphorylation by Lats and CK1 regulates YAP stability through SCF(beta-TRCP). , 2010, Genes & development.