Activated growth signaling pathway expression in Ewing sarcoma and clinical outcome

In Ewing sarcoma (EWS) most of the research on signaling pathways has been performed on cell lines or animal models. The objective of the current study was to determine the relation between clinical outcome and the expression of proteins involved in active growth signaling pathways.

[1]  J. Mora,et al.  Treatment of Ewing sarcoma family of tumors with a modified P6 protocol in children and adolescents , 2011, Pediatric Blood & Cancer.

[2]  N. Pellegata,et al.  Levels of p27 Sensitize to Dual PI3K/mTOR Inhibition , 2011, Molecular Cancer Therapeutics.

[3]  Krishna R. Kalari,et al.  FKBP51 affects cancer cell response to chemotherapy by negatively regulating Akt. , 2009, Cancer cell.

[4]  Ludger Hengst,et al.  The Cdk inhibitor p27 in human cancer: prognostic potential and relevance to anticancer therapy , 2008, Nature Reviews Cancer.

[5]  David M Sabatini,et al.  Defining the role of mTOR in cancer. , 2007, Cancer cell.

[6]  D. Sabatini mTOR and cancer: insights into a complex relationship , 2006, Nature Reviews Cancer.

[7]  O. Delattre,et al.  EWS/FLI-1 Silencing and Gene Profiling of Ewing Cells Reveal Downstream Oncogenic Pathways and a Crucial Role for Repression of Insulin-Like Growth Factor Binding Protein 3 , 2004, Molecular and Cellular Biology.

[8]  S. Lowe,et al.  Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy , 2004, Nature.

[9]  Y. Iwamoto,et al.  The Prognostic and Therapeutic Relevance of p27kip1 in Ewing’s Family Tumors , 2004, Clinical Cancer Research.

[10]  E. Andreu,et al.  Imatinib Inhibits Proliferation of Ewing Tumor Cells Mediated by the Stem Cell Factor/KIT Receptor Pathway, and Sensitizes Cells to Vincristine and Doxorubicin-Induced Apoptosis , 2004, Clinical Cancer Research.

[11]  V. Notario,et al.  Rapamycin induces the fusion-type independent downregulation of the EWS/FLI-1 proteins and inhibits Ewing's sarcoma cell proliferation , 2003, Oncogene.

[12]  S. Chua,et al.  RESPONSE: Re: Insulin Resistance and Prostate Cancer Risk , 2003 .

[13]  C. Thiele,et al.  Potential use of imatinib in Ewing's Sarcoma: evidence for in vitro and in vivo activity. , 2003, Journal of the National Cancer Institute.

[14]  P. Lollini,et al.  C-kit receptor expression in Ewing's sarcoma: lack of prognostic value but therapeutic targeting opportunities in appropriate conditions. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[15]  P. Lollini,et al.  Expression of an IGF‐I receptor dominant negative mutant induces apoptosis, inhibits tumorigenesis and enhances chemosensitivity in Ewing's sarcoma cells , 2002, International journal of cancer.

[16]  H. Jürgens,et al.  c-KIT-expressing Ewing tumour cells are insensitive to imatinib mesylate (STI571) , 2002, Cancer Chemotherapy and Pharmacology.

[17]  P. Lollini,et al.  Effectiveness of insulin-like growth factor I receptor antisense strategy against Ewing's sarcoma cells , 2002, Cancer Gene Therapy.

[18]  S. Steinberg,et al.  Insulin‐like growth factor type 1 (IGF–1) and IGF binding protein–3 in patients with Ewing sarcoma family of tumors , 2001, Cancer.

[19]  K. Tanaka,et al.  Downregulation and forced expression of EWS-Fli1 fusion gene results in changes in the expression of G 1 regulatory genes , 2001, British Journal of Cancer.

[20]  P. Lollini,et al.  The metastatic ability of Ewing's sarcoma cells is modulated by stem cell factor and by its receptor c-kit. , 2000, The American journal of pathology.

[21]  S. Welford,et al.  EWS-FLI1, EWS-ERG, and EWS-ETV1 oncoproteins of Ewing tumor family all suppress transcription of transforming growth factor beta type II receptor gene. , 2000, Cancer research.

[22]  M. Ladanyi,et al.  Association of EWS-FLI1 type 1 fusion with lower proliferative rate in Ewing's sarcoma. , 2000, The American journal of pathology.

[23]  J. Toretsky,et al.  Phosphoinositide 3-hydroxide kinase blockade enhances apoptosis in the Ewing's sarcoma family of tumors. , 1999, Cancer research.

[24]  T. Hunter,et al.  The Kit receptor promotes cell survival via activation of PI 3-kinase and subsequent Akt-mediated phosphorylation of Bad on Ser136 , 1998, Current Biology.

[25]  G. Basso,et al.  c-kit is expressed in soft tissue sarcoma of neuroectodermic origin and its ligand prevents apoptosis of neoplastic cells. , 1998, Blood.

[26]  D. Leroith,et al.  The Insulin-like Growth Factor-I Receptor Is Required for EWS/FLI-1 Transformation of Fibroblasts* , 1997, The Journal of Biological Chemistry.

[27]  P. Lollini,et al.  Insulin-like growth factor I receptor-mediated circuit in Ewing's sarcoma/peripheral neuroectodermal tumor: a possible therapeutic target. , 1996, Cancer research.

[28]  D. Yee,et al.  Insulin-like growth factor I expression by tumors of neuroectodermal origin with the t(11;22) chromosomal translocation. A potential autocrine growth factor. , 1990, The Journal of clinical investigation.