Andrea Rasola

Summary

Affiliation: Institute for Cancer Research and Treatment
Country: Italy

Publications

  1. ncbi request reprint Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X(L)- and PKB/AKT-independent fashion
    D Gramaglia
    Division of Molecular Oncology, Institute for Cancer Research, University of Torino Medical School, Candiolo, Italy
    Cell Death Differ 11:342-53. 2004
  2. ncbi request reprint Hepatocyte growth factor sensitizes human ovarian carcinoma cell lines to paclitaxel and cisplatin
    Andrea Rasola
    Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
    Cancer Res 64:1744-50. 2004
  3. ncbi request reprint Genes regulated by hepatocyte growth factor as targets to sensitize ovarian cancer cells to cisplatin
    Martina Olivero
    Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, University of Torino School of Medicine, SP 142, Km 3 95, 10060, Candiolo Torino, Italy
    Mol Cancer Ther 5:1126-35. 2006
  4. ncbi request reprint p38 MAPK turns hepatocyte growth factor to a death signal that commits ovarian cancer cells to chemotherapy-induced apoptosis
    Nadia Coltella
    Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo, Italy
    Int J Cancer 118:2981-90. 2006
  5. ncbi request reprint Hepatocyte growth factor installs a survival platform for colorectal cancer cell invasive growth and overcomes p38 MAPK-mediated apoptosis
    Michela Fassetta
    Division of Molecular Oncology, University of Torino Medical School, Candiolo, Italy
    Cell Signal 18:1967-76. 2006
  6. ncbi request reprint A gain of function mutation in the activation loop of platelet-derived growth factor beta-receptor deregulates its kinase activity
    Federica Chiara
    Ludwig Institute for Cancer Research, Box 595, Uppsala S 751 24, Sweden
    J Biol Chem 279:42516-27. 2004
  7. ncbi request reprint The mitochondrial permeability transition pore and its involvement in cell death and in disease pathogenesis
    Andrea Rasola
    CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, I 35121 Padua, Italy
    Apoptosis 12:815-33. 2007
  8. pmc Cholesterol loss enhances TrkB signaling in hippocampal neurons aging in vitro
    Mauricio G Martin
    VIB and Department of Human Genetics, Catholic University of Leuven, B 3000 Leuven, Belgium
    Mol Biol Cell 19:2101-12. 2008
  9. pmc Hexokinase II detachment from mitochondria triggers apoptosis through the permeability transition pore independent of voltage-dependent anion channels
    Federica Chiara
    CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Padova, Italy
    PLoS ONE 3:e1852. 2008

Collaborators

  • Maria Flavia Di Renzo
  • Ferdinando Di Cunto
  • Nicoletta Filigheddu
  • P Bernardi
  • Michael Forte
  • P M Comoglio
  • Tibor Harkany
  • Pontus Aspenstrom
  • Federica Chiara
  • Nadia Coltella
  • Michela Fassetta
  • Mauricio G Martin
  • Martina Olivero
  • D Gramaglia
  • Oriano Marin
  • Pontus Holm
  • Magdalena Juhaszova
  • Tomi Rantamäki
  • WILLIAM S BRUSILOW
  • Eero Castren
  • Steven J Sollott
  • Valeria Petronilli
  • Diego Castellaro
  • Laura Trovò
  • Carlos G Dotti
  • Simona Perga
  • Elisa Nano
  • Andrea Graziani
  • Chiara Bardella
  • Stefania Crispi
  • Silvia Saviozzi
  • Tina Ruggiero
  • Raffaele Calogero
  • Lorenza D'Alessandro
  • Henrik Forsberg
  • Carl Henrik Heldin
  • M Fassetta
  • Aive Ahgren
  • Rainer Heuchel
  • V Petronilli
  • Carina Hellberg
  • Marie Jose Goumans
  • M Battaglia
  • L Ranzato
  • Christer Wernstedt
  • A Gentile

Detail Information

Publications9

  1. ncbi request reprint Apoptosis to necrosis switching downstream of apoptosome formation requires inhibition of both glycolysis and oxidative phosphorylation in a BCL-X(L)- and PKB/AKT-independent fashion
    D Gramaglia
    Division of Molecular Oncology, Institute for Cancer Research, University of Torino Medical School, Candiolo, Italy
    Cell Death Differ 11:342-53. 2004
    ..Apoptosis is not blocked per se by ATP depletion, as engagement of the Fas receptor directly activates caspases, thus bypassing ddFSK inhibition...
  2. ncbi request reprint Hepatocyte growth factor sensitizes human ovarian carcinoma cell lines to paclitaxel and cisplatin
    Andrea Rasola
    Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
    Cancer Res 64:1744-50. 2004
    ..This suggests that HGF may be used to improve response to chemotherapy in a set of human ovarian carcinomas molecularly classified based on the MET oncogene expression...
  3. ncbi request reprint Genes regulated by hepatocyte growth factor as targets to sensitize ovarian cancer cells to cisplatin
    Martina Olivero
    Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, University of Torino School of Medicine, SP 142, Km 3 95, 10060, Candiolo Torino, Italy
    Mol Cancer Ther 5:1126-35. 2006
    ..We also provide the proof-of-concept that the identified genes might be targeted to either increase the efficacy of chemotherapeutics or revert chemotherapy resistance...
  4. ncbi request reprint p38 MAPK turns hepatocyte growth factor to a death signal that commits ovarian cancer cells to chemotherapy-induced apoptosis
    Nadia Coltella
    Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo, Italy
    Int J Cancer 118:2981-90. 2006
    ..Therefore, the p38 MAPK pathway might be a suitable target to improve response to conventional chemotherapy in human ovarian cancer...
  5. ncbi request reprint Hepatocyte growth factor installs a survival platform for colorectal cancer cell invasive growth and overcomes p38 MAPK-mediated apoptosis
    Michela Fassetta
    Division of Molecular Oncology, University of Torino Medical School, Candiolo, Italy
    Cell Signal 18:1967-76. 2006
    ..Both p38 MAPK and HGF/HGFR signaling constitute potential molecular targets for inhibiting colorectal carcinogenesis...
  6. ncbi request reprint A gain of function mutation in the activation loop of platelet-derived growth factor beta-receptor deregulates its kinase activity
    Federica Chiara
    Ludwig Institute for Cancer Research, Box 595, Uppsala S 751 24, Sweden
    J Biol Chem 279:42516-27. 2004
    ..Our findings support a model whereby an activating point mutation results in a deregulated PDGFRbeta with oncogenic predisposition...
  7. ncbi request reprint The mitochondrial permeability transition pore and its involvement in cell death and in disease pathogenesis
    Andrea Rasola
    CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Viale Giuseppe Colombo 3, I 35121 Padua, Italy
    Apoptosis 12:815-33. 2007
    ..Here we review basic concepts about PTP structure, function and regulation within the framework of intracellular death signalling, and its role in disease pathogenesis...
  8. pmc Cholesterol loss enhances TrkB signaling in hippocampal neurons aging in vitro
    Mauricio G Martin
    VIB and Department of Human Genetics, Catholic University of Leuven, B 3000 Leuven, Belgium
    Mol Biol Cell 19:2101-12. 2008
    ....
  9. pmc Hexokinase II detachment from mitochondria triggers apoptosis through the permeability transition pore independent of voltage-dependent anion channels
    Federica Chiara
    CNR Institute of Neuroscience and Department of Biomedical Sciences, University of Padova, Padova, Italy
    PLoS ONE 3:e1852. 2008
    ..These findings have profound implications for our understanding of the pathways of outer mitochondrial membrane permeabilization and their inactivation in tumors...