Giovanni Tonon

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc High-resolution genomic profiles of human lung cancer
    Giovanni Tonon
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:9625-30. 2005
  2. ncbi request reprint Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myeloma
    Klaus Podar
    Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Cancer Res 67:1680-8. 2007
  3. doi request reprint From oncogene to network addiction: the new frontier of cancer genomics and therapeutics
    Giovanni Tonon
    Dana Farber Cancer Institute, Harvard Medical School Mayer Building, 44 Binney Street, Boston, MA 02115, USA
    Future Oncol 4:569-77. 2008
  4. ncbi request reprint Molecular pathogenesis of multiple myeloma
    Giovanni Tonon
    Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Mayer Building, Rm 417, 44 Binney Street, Boston, MA 02115, USA
    Hematol Oncol Clin North Am 21:985-1006, vii. 2007
  5. doi request reprint The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment: therapeutic implications
    Klaus Podar
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Br J Haematol 155:438-48. 2011
  6. pmc Targeting PKC: a novel role for beta-catenin in ER stress and apoptotic signaling
    Marc S Raab
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 113:1513-21. 2009
  7. doi request reprint Targeting angiogenesis via a c-Myc/hypoxia-inducible factor-1alpha-dependent pathway in multiple myeloma
    Jing Zhang
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Cancer Res 69:5082-90. 2009
  8. ncbi request reprint Common and distinct genomic events in sporadic colorectal cancer and diverse cancer types
    Eric S Martin
    Department of Medical Oncology, Belfer Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 67:10736-43. 2007
  9. pmc CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells
    Yu Tzu Tai
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:4309-18. 2009
  10. ncbi request reprint High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patients
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:313-25. 2006

Detail Information

Publications27

  1. pmc High-resolution genomic profiles of human lung cancer
    Giovanni Tonon
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 102:9625-30. 2005
    ..Integrated DNA-RNA analyses identified WHSC1L1 and TPX2 as two candidates likely targeted for amplification in both pancreatic ductal adenocarcinoma and non-small-cell lung cancer...
  2. ncbi request reprint Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myeloma
    Klaus Podar
    Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Cancer Res 67:1680-8. 2007
    ..Finally, our data suggest that this mechanism may not only be restricted to MM but may also be important in a broad range of malignancies including erythroleukemia and solid tumors...
  3. doi request reprint From oncogene to network addiction: the new frontier of cancer genomics and therapeutics
    Giovanni Tonon
    Dana Farber Cancer Institute, Harvard Medical School Mayer Building, 44 Binney Street, Boston, MA 02115, USA
    Future Oncol 4:569-77. 2008
    ..This new perspective, arising from genomic and systems biology studies, will likely provide a valuable frame for the design of the cancer drugs of the future...
  4. ncbi request reprint Molecular pathogenesis of multiple myeloma
    Giovanni Tonon
    Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Mayer Building, Rm 417, 44 Binney Street, Boston, MA 02115, USA
    Hematol Oncol Clin North Am 21:985-1006, vii. 2007
    ..Recent and ongoing high-resolution genomic studies are leading the way toward a more refined and conclusive understanding of this disease...
  5. doi request reprint The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment: therapeutic implications
    Klaus Podar
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Br J Haematol 155:438-48. 2011
    ..Our data therefore provide the rationale for the clinical evaluation of Natalizumab, preferably in combination with novel agents (e.g. bortezomib) to enhance MM cytotoxicity and improve patient outcome...
  6. pmc Targeting PKC: a novel role for beta-catenin in ER stress and apoptotic signaling
    Marc S Raab
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 113:1513-21. 2009
    ..Moreover, we identify p73 as a potential novel therapeutic target in MM. Based on these and previous data, enzastaurin is currently under clinical investigation in a variety of hematologic malignancies, including MM...
  7. doi request reprint Targeting angiogenesis via a c-Myc/hypoxia-inducible factor-1alpha-dependent pathway in multiple myeloma
    Jing Zhang
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
    Cancer Res 69:5082-90. 2009
    ..Our data, therefore, identify Hif-1alpha as a novel molecular target in MM and add another facet to anti-MM drug activity...
  8. ncbi request reprint Common and distinct genomic events in sporadic colorectal cancer and diverse cancer types
    Eric S Martin
    Department of Medical Oncology, Belfer Institute for Innovative Cancer Science, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 67:10736-43. 2007
    ....
  9. pmc CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells
    Yu Tzu Tai
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:4309-18. 2009
    ..These studies provide direct evidence of the role of CS1 in myeloma pathogenesis, define molecular mechanisms regulating its effects, and further support novel therapies targeting CS1 in MM...
  10. ncbi request reprint High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patients
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:313-25. 2006
    ....
  11. pmc The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, and Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Cancer Cell 11:349-60. 2007
    ..The similarities of this model with the human disease, coupled with documented frequent XBP-1s overexpression in human MM, serve to implicate XBP-1s dysregulation in MM pathogenesis...
  12. pmc Synthetic Lethal Approaches Exploiting DNA Damage in Aggressive Myeloma
    Francesca Cottini
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts Functional Genomics of Cancer Unit, Division of Experimental Oncology, Istituto di Ricovero e Cura a Carattere Scientifico IRCCS San Raffaele Scientific Institute, Milan, Italy
    Cancer Discov 5:972-87. 2015
    ..This synthetic lethal approach, enhancing oxidative stress while concomitantly blocking replicative stress response, provides a novel combination targeted therapy to address an unmet medical need in this subset of multiple myeloma...
  13. doi request reprint Moving toward individualized cancer therapies
    Giovanni Tonon
    Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Clin Cancer Res 14:4682-4. 2008
    ....
  14. pmc Pancreatic cancers require autophagy for tumor growth
    Shenghong Yang
    Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Genes Dev 25:717-29. 2011
    ....
  15. pmc p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation
    Hongwu Zheng
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 455:1129-33. 2008
    ....
  16. pmc The small-molecule VEGF receptor inhibitor pazopanib (GW786034B) targets both tumor and endothelial cells in multiple myeloma
    Klaus Podar
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 103:19478-83. 2006
    ....
  17. ncbi request reprint Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets
    Teru Hideshima
    Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Nat Rev Cancer 7:585-98. 2007
    ..Recent oncogenomic studies have further advanced our understanding of the molecular pathogenesis of multiple myeloma, providing the framework for new prognostic classification and identifying new therapeutic targets...
  18. pmc Telomere dysfunction induces metabolic and mitochondrial compromise
    Ergun Sahin
    Belfer Institute for Applied Cancer Science, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Nature 470:359-65. 2011
    ..We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction...
  19. pmc Rescue of Hippo coactivator YAP1 triggers DNA damage-induced apoptosis in hematological cancers
    Francesca Cottini
    1 Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA 2 Functional Genomics of Cancer Unit, Division of Molecular Oncology, Istituto di Ricovero e Cura a Carattere Scientifico IRCCS San Raffaele Scientific Institute, Milan, Italy
    Nat Med 20:599-606. 2014
    ..Our data therefore identify a new synthetic-lethal strategy to selectively target cancer cells presenting with endogenous DNA damage and low YAP1 levels. ..
  20. doi request reprint Disentangling the myeloma web
    Giovanni Tonon
    Functional Genomics of Cancer Unit, Division of Molecular Oncology, San Raffaele Scientific Institute, Milan, Italy
    Clin Cancer Res 17:7210-2. 2011
    ..Novel computational tools are now helping investigators integrate heterogeneous data sets to identify universal and robust classifiers...
  21. pmc Integrating data on DNA copy number with gene expression levels and drug sensitivities in the NCI-60 cell line panel
    Kimberly J Bussey
    Laboratory of Molecular Pharmacology, National Cancer Institute, Building 37, Room 5056, NIH, MSC 4255, 9000 Rockville Pike, Bethesda, MD 20892 4255, USA
    Mol Cancer Ther 5:853-67. 2006
    ..The DNA copy number database presented here will enable other investigators to explore DNA transcript-drug relationships in their own domains of research focus...
  22. ncbi request reprint t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway
    Giovanni Tonon
    Genetics Branch, Center for Cancer Research, National Cancer Institute and the National Naval Medical Center, Bethesda, Maryland 20889, USA
    Nat Genet 33:208-13. 2003
    ..These data suggest a new mechanism to disrupt the function of a Notch co-activator in a common type of malignant salivary gland tumor...
  23. ncbi request reprint Karyotypic complexity of the NCI-60 drug-screening panel
    Anna V Roschke
    Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20889 5105, USA
    Cancer Res 63:8634-47. 2003
    ....
  24. ncbi request reprint Multiple reciprocal translocations in salivary gland mucoepidermoid carcinomas
    Giovanni Tonon
    Genetics Branch, National Cancer Institute, NNMC, 8901 Wisconsin Avenue, Bldg 8, Room 5101, Bethesda, MD 20889 5105, USA
    Cancer Genet Cytogenet 152:15-22. 2004
    ..The presence of multiple reciprocal translocations in both benign and malignant salivary gland tumors may also suggest a particular mechanism within mucous or serous glands mediating chromosomal rearrangements...
  25. pmc Karyotypic "state" as a potential determinant for anticancer drug discovery
    Anna V Roschke
    Genetics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 102:2964-9. 2005
    ..Thus, we delineate an approach for the identification of "lead compounds" for anticancer drug discovery complementary to those that are focused at the outset on a given gene or pathway...
  26. pmc Somatic mutations affect key pathways in lung adenocarcinoma
    Li Ding
    The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA
    Nature 455:1069-75. 2008
    ..Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment...
  27. pmc Stable karyotypes in epithelial cancer cell lines despite high rates of ongoing structural and numerical chromosomal instability
    Anna V Roschke
    Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20889 5105, USA
    Neoplasia 4:19-31. 2002
    ..We did not observe a profound difference in the rates of numerical or structural instability in the cell lines with a replication error phenotype (RER+) versus the other cell lines...