Sylvie Giuriato

Summary

Country: France

Publications

  1. ncbi request reprint Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy
    Sylvie Giuriato
    INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
    Cancer Biol Ther 6:1318-23. 2007
  2. doi request reprint ALK+ALCLs induce cutaneous, HMGB-1-dependent IL-8/CXCL8 production by keratinocytes through NF-κB activation
    Emilie Dejean
    Centre de Recherches en Cancérologie de Toulouse, Unite Mixte de Recherche, 1037 Inserm Université Toulouse III, Toulouse, France
    Blood 119:4698-707. 2012
  3. doi request reprint Conditional TPM3-ALK and NPM-ALK transgenic mice develop reversible ALK-positive early B-cell lymphoma/leukemia
    Sylvie Giuriato
    INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
    Blood 115:4061-70. 2010
  4. pmc Targeting autophagy enhances the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma
    Géraldine Mitou
    INSERM, UMR1037 CRCT, F 31000 Toulouse, France
    Oncotarget 6:30149-64. 2015
  5. ncbi request reprint Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations
    Asa Karlsson
    Division of Oncology, Department of Medicine, Stanford University, CA 94305, USA
    Blood 101:2797-803. 2003
  6. ncbi request reprint Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma model
    Sandrine Sander
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 24:6101-7. 2005
  7. pmc Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fates
    Emmanuelle Passegue
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 202:1599-611. 2005
  8. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008

Collaborators

  • Dean Felsher
  • Emmanuelle Passegue
  • Géraldine Mitou
  • Fabienne Meggetto
  • Laurence Lamant
  • Emilie Dejean
  • Asa Karlsson
  • Phuoc T Tran
  • Sandrine Sander
  • Isabelle Beau
  • Aurore Desquesnes
  • Estelle Espinos
  • Sophie Le Gonidec
  • Julie Frentzel
  • Pierre Brousset
  • Talal Alsaati
  • Patrice Codogno
  • Marianne Foisseau
  • Abdelghafour Marfak
  • Frédérique Gaits-Iacovoni
  • Georges Delsol
  • Frédéric Lagarrigue
  • Nais Prade
  • Kim Komatsubara
  • Craig S Wang
  • Alice C Fan
  • Pavan K Bendapudi
  • Shan Koh
  • Joy Chen
  • George Horng
  • David I Bellovin
  • Jeffrey A Whitsett
  • Jonathan R Pollack
  • Lars Bullinger
  • Tina Hernandez-Boussard
  • Göran Levan
  • Flora Tang
  • Jingly Fung-Weier

Detail Information

Publications8

  1. ncbi request reprint Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy
    Sylvie Giuriato
    INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
    Cancer Biol Ther 6:1318-23. 2007
    ....
  2. doi request reprint ALK+ALCLs induce cutaneous, HMGB-1-dependent IL-8/CXCL8 production by keratinocytes through NF-κB activation
    Emilie Dejean
    Centre de Recherches en Cancérologie de Toulouse, Unite Mixte de Recherche, 1037 Inserm Université Toulouse III, Toulouse, France
    Blood 119:4698-707. 2012
    ..We propose that these mediators create a premetastatic niche within the skin, thereby participating in ALK(+) lymphoma epidermotropism...
  3. doi request reprint Conditional TPM3-ALK and NPM-ALK transgenic mice develop reversible ALK-positive early B-cell lymphoma/leukemia
    Sylvie Giuriato
    INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
    Blood 115:4061-70. 2010
    ..Our models offer a new tool to investigate in vivo the molecular mechanisms associated with ALK-induced lymphoproliferative disorders...
  4. pmc Targeting autophagy enhances the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma
    Géraldine Mitou
    INSERM, UMR1037 CRCT, F 31000 Toulouse, France
    Oncotarget 6:30149-64. 2015
    ..Altogether, our results suggest that co-treatment with crizotinib and chloroquine (two drugs already used in clinics) could be beneficial for ALK-positive ALCL patients. ..
  5. ncbi request reprint Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations
    Asa Karlsson
    Division of Oncology, Department of Medicine, Stanford University, CA 94305, USA
    Blood 101:2797-803. 2003
    ..We conclude that even highly genetically complex cancers are reversible on the inactivation of MYC, unless they acquire novel genetic alterations that can sustain a neoplastic phenotype...
  6. ncbi request reprint Comparative genomic hybridization on mouse cDNA microarrays and its application to a murine lymphoma model
    Sandrine Sander
    Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
    Oncogene 24:6101-7. 2005
    ....
  7. pmc Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fates
    Emmanuelle Passegue
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 202:1599-611. 2005
    ....
  8. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008
    ..However, most cancers are caused by multiple genetic events making it difficult to determine which oncogenes or combination of oncogenes will be the most effective targets for their treatment...