Research Topics
| P ComoglioSummaryAffiliation: Institute for Cancer Research and Treatment Country: Italy Publications
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Detail Information
Publications
Invasive growth: a two-way street for semaphorin signallingPaolo M Comoglio
Nat Cell Biol 6:1155-7. 2004- p190 Rho-GTPase activating protein associates with plexins and it is required for semaphorin signallingDavide Barberis
Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Candiolo, Torino 10060, Italy
J Cell Sci 118:4689-700. 2005..We conclude that p190-RhoGAP is crucially involved in semaphorin signalling to the actin cytoskeleton, via interaction with plexins... - Cancer: the matrix is now in controlPaolo M Comoglio
Nat Med 11:1156-9. 2005 
Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibitionSimona Corso
Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo Torino, Italy
Mol Cancer 9:121. 2010..Perspective studies are thus mandatory to identify the molecular mechanisms that could cause resistance to these therapies...
Plexin-B1 plays a redundant role during mouse development and in tumour angiogenesisPietro Fazzari
Institute for Cancer Research and Treatment, University of Torino Medical School, Division of Molecular Oncology, Candiolo, Turin, Italy
BMC Dev Biol 7:55. 2007..In order to shed light on PlexinB1 function in vivo, we therefore undertook the genomic targeting of the mouse gene to obtain loss of function mutants...- Interactions between growth factor receptors and adhesion molecules: breaking the rulesPaolo M Comoglio
Institute for Cancer Research and Treatment, University of Torino School of Medicine, Strada Provinciale 142, 10060 Candiolo Torino, Italy
Curr Opin Cell Biol 15:565-71. 2003.... - Scatter factor-dependent branching morphogenesis: structural and histological featuresP Comoglio
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Candiolo, Torino, Italy
Eur J Histochem 51:79-92. 2007.... 
Drug development of MET inhibitors: targeting oncogene addiction and expediencePaolo M Comoglio
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Turin School of Medicine, Candiolo, Turin 10060, Italy
Nat Rev Drug Discov 7:504-16. 2008..Here we discuss recent progress in the development of molecules that inhibit MET function and consider their application in a subset of human tumours that are potentially responsive to MET-targeted therapies...- Truncated RON tyrosine kinase drives tumor cell progression and abrogates cell-cell adhesion through E-cadherin transcriptional repressionChiara Bardella
Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, University of Torino Medical School, 10060 Candiolo, Turin, Italy
Cancer Res 64:5154-61. 2004..Altogether, these data show that expression of a naturally occurring, constitutively active truncated RON kinase results in loss of epithelial phenotype and aggressive behavior and, thus, it might contribute to tumor progression... - An uncleavable form of pro-scatter factor suppresses tumor growth and dissemination in miceMassimiliano Mazzone
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
J Clin Invest 114:1418-32. 2004..These data show that proteolytic activation of pro-SF is a limiting step in tumor progression, thus suggesting a new strategy for the treatment or prevention of the malignant conversion of neoplastic lesions... - Invasive growth: from development to metastasisPaolo M Comoglio
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo (Torino, Italy
J Clin Invest 109:857-62. 2002 - "Active" cancer immunotherapy by anti-Met antibody gene transferElisa Vigna
Laboratory for Gene Transfer and Therapy, Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Turin, Italy
Cancer Res 68:9176-83. 2008..These data provide proof of concept both for targeting the Met receptor and for a gene transfer-based immunotherapy strategy... - Hypoxia promotes invasive growth by transcriptional activation of the met protooncogeneSelma Pennacchietti
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
Cancer Cell 3:347-61. 2003..These data show that hypoxia promotes tumor invasion by sensitizing cells to HGF stimulation, providing a molecular basis to explain Met overexpression in cancer... - Ab-induced ectodomain shedding mediates hepatocyte growth factor receptor down-regulation and hampers biological activityAnnalisa Petrelli
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, 10060 Candiolo, Italy
Proc Natl Acad Sci U S A 103:5090-5. 2006..Interestingly, the "decoy effect" generated by the shed ectodomain, acting as a dominant negative molecule, enhanced the inhibitory effect of the Ab... - A differentiation switch for genetically modified hepatocytesCarla Boccaccio
Institute for Cancer Research and Treatment, University of Torino Medical School, 10060 Candiolo Torino, Italy
FASEB J 16:120-2. 2002.... - Novel somatic mutations of the MET oncogene in human carcinoma metastases activating cell motility and invasionAnnalisa Lorenzato
Laboratory of Cancer Genetics, Institute for Cancer Research and Treatment, Torino, Italy
Cancer Res 62:7025-30. 2002..These data suggest that MET might be one of the long sought oncogenes controlling progression of primary cancers to metastasis... - Inhibition of Src impairs the growth of met-addicted gastric tumorsAndrea Bertotti
Division of Molecular Oncology and Laboratory of Functional Genomics, The Oncogenomics Center, Institute for Cancer Research and Treatment, University of Torino Medical School, Strada Provinciale 142, Candiolo, Turin, Italy
Clin Cancer Res 16:3933-43. 2010..We examined whether inhibition of Src tyrosine kinase, a downstream effector of the MET oncogene, can hinder the malignant properties of gastric tumors dependent on Met for growth and survival... - p38 MAPK turns hepatocyte growth factor to a death signal that commits ovarian cancer cells to chemotherapy-induced apoptosisNadia 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... - An HGF-MSP chimera disassociates the trophic properties of scatter factors from their pro-invasive activityPaolo Michieli
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, I 10060 Candiolo, Torino, Italy
Nat Biotechnol 20:488-95. 2002..In an in vivo murine model of drug-induced nephrotoxicity, intravenous injection of recombinant Metron factor 1 prevented renal damage and preserved tubular integrity... - The semaphorin 4D receptor controls invasive growth by coupling with MetSilvia Giordano
Institute for Cancer Research and Treatment, University of Torino School of Medicine, 10060 Candiolo, Torino, Italy
Nat Cell Biol 4:720-4. 2002..This work identifies a novel biological function of semaphorins and suggests the involvement of an unexpected signalling mechanism, namely, the coupling of a plexin to a tyrosine kinase receptor... - Scatter-factor and semaphorin receptors: cell signalling for invasive growthLivio Trusolino
Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo, Italy
Nat Rev Cancer 2:289-300. 2002..What are the differences between physiological and pathological activation of these signalling molecules, and can we exploit them therapeutically to prevent metastasis?.. - The RON and MET oncogenes are co-expressed in human ovarian carcinomas and cooperate in activating invasivenessPiera Maggiora
Laboratory of Cancer Genetics of the Institute for Cancer Research and Treatment, University of Torino School of Medicine, SP 142, Km 3 95, 10060 Candiolo Torino, Italy
Exp Cell Res 288:382-9. 2003..These data suggest that coexpression of the MET and RON receptors confer a selective advantage to ovarian cancer cells and might promote ovarian cancer progression... - Cancer therapy: can the challenge be MET?Simona Corso
IRCC, Institute for Cancer Research and Treatment, University of Turin School of Medicine, Division of Molecular Oncology, 10060 Candiolo, Turin, Italy
Trends Mol Med 11:284-92. 2005..Interfering with Met activation is thus a new and challenging approach to hamper tumorigenic and metastatic processes... - Prevention of hypoxia by myoglobin expression in human tumor cells promotes differentiation and inhibits metastasisMaria Galluzzo
Laboratory of Experimental Therapy, Institute for Cancer Research and Treatment, University of Turin Medical School, Turin, Italy
J Clin Invest 119:865-75. 2009..Although limited to xenograft models, these data provide experimental proof of the concept that hypoxia is not just a side effect of deregulated growth but a key factor on which the tumor relies in order to promote its own expansion... - The MET receptor tyrosine kinase in invasion and metastasisSilvia Benvenuti
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Candiolo Torino, Italy
J Cell Physiol 213:316-25. 2007..Among those soluble factors a major position is exerted by hepatocyte growth factor (HGF) together with its receptor MET and macrophage-stimulating protein (MSP) in cooperation with its receptor RON... - The tumor suppressor semaphorin 3B triggers a prometastatic program mediated by interleukin 8 and the tumor microenvironmentCharlotte Rolny
Institute for Cancer Research and Treatment IRCC, University of Turin, School of Medicine, 10060 Candiolo, Italy
J Exp Med 205:1155-71. 2008..In conclusion, we report that SEMA3B exerts unexpected functions in cancer progression by fostering a prometastatic environment through elevated IL-8 secretion and recruitment of macrophages coupled to the suppression of tumor growth... - A high affinity hepatocyte growth factor-binding site in the immunoglobulin-like region of MetCristina Basilico
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Turin Medical School, I 10060 Candiolo, Turin, Italy
J Biol Chem 283:21267-77. 2008..Although the IPT-HGF-alpha interaction provides binding strength, the Sema-HGF-beta contact confers selective sensitivity to the active form of the ligand... - Sema3E-Plexin D1 signaling drives human cancer cell invasiveness and metastatic spreading in miceAndrea Casazza
Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
J Clin Invest 120:2684-98. 2010..In sum, Sema3E-Plexin D1 signaling in cancer cells is crucially implicated in their metastatic behavior and may therefore be a promising target for strategies aimed at blocking tumor metastasis... - Mutations in the met oncogene unveil a "dual switch" mechanism controlling tyrosine kinase activityFederica Chiara
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, I 10060 Candiolo, Torino, Italy
J Biol Chem 278:29352-8. 2003..This explains why mutant met provides an oncogenic predisposition but needs a second activating "hit," provided by sustained ligand stimulation or receptor overexpression, to achieve a fully transformed phenotype... - MicroRNAs impair MET-mediated invasive growthCristina Migliore
Institute for Cancer Research and Treatment, University of Torino School of Medicine, Candiolo, Torino, Italy
Cancer Res 68:10128-36. 2008..In conclusion, we have identified miRNAs that behave as oncosuppressors by negatively targeting MET and might thus provide an additional option to inhibit this oncogene in tumors displaying its deregulation... - MET overexpression turns human primary osteoblasts into osteosarcomasSalvatore Patanè
Laboratory of Cancer Genetics, University of Turin School of Medicine, Candiolo Turin, Italy
Cancer Res 66:4750-7. 2006..These data show that MET overexpression is oncogenic and that it is essential for the maintenance of the cancer phenotype... - Induction of MET by ionizing radiation and its role in radioresistance and invasive growth of cancerFrancesca De Bacco
IRCC Institute for Cancer Research at Candiolo, University of Turin Medical School, Candiolo, Italy
J Natl Cancer Inst 103:645-61. 2011..The MET oncogene encodes the hepatocyte growth factor (HGF) receptor and is known to drive "invasive growth", a regenerative and prosurvival program unduly activated in metastasis... - Genetic link between cancer and thrombosisCarla Boccaccio
Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo, Torino, Italy
J Clin Oncol 27:4827-33. 2009..Targeting the tumor procoagulant activity can fight not only a dangerous tumor adverse effect, but also the core mechanisms of cancer onset and progression... - The Met pathway: master switch and drug target in cancer progressionMassimiliano Mazzone
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, Strada Provinciale 142, Km 3 95, I 10060 Candiolo Torino, Italy
FASEB J 20:1611-21. 2006..As we suggest possible directions for drug development, we propose the receptor for the hepatocyte growth factor, Met, as an ideal target for tackling cancer progression... - The Slit/Robo system suppresses hepatocyte growth factor-dependent invasion and morphogenesisMaria Cristina Stella
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino School of Medicine, 10060 Candiolo, Torino, Italy
Mol Biol Cell 20:642-57. 2009.... - MET signalling: principles and functions in development, organ regeneration and cancerLivio Trusolino
Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, 10060 Candiolo, Torino, Italy
Nat Rev Mol Cell Biol 11:834-48. 2010..Controlled activation of MET signalling can be exploited in regenerative medicine, whereas MET inhibition might slow down tumour progression... - Invasive growth: a MET-driven genetic programme for cancer and stem cellsCarla Boccaccio
Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Str Prov 142, 10060 Candiolo, Italy
Nat Rev Cancer 6:637-45. 2006.... - Plexin-B3 is a functional receptor for semaphorin 5AStefania Artigiani
Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, 10060 Candiolo To, Italy
EMBO Rep 5:710-4. 2004..We thus conclude that Sema5A is able to elicit multiple functional responses through its receptor plexin-B3... - Targeting the tumor and its microenvironment by a dual-function decoy Met receptorPaolo Michieli
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, I 10060 Candiolo Torino, Italy
Cancer Cell 6:61-73. 2004.... - The MET oncogene drives a genetic programme linking cancer to haemostasisCarla Boccaccio
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Turin Medical School, Str Prov 142, I 10060 Candiolo, Torino, Italy
Nature 434:396-400. 2005..In vivo analysis showed that both proteins support the thrombohaemorrhagic phenotype, thus providing direct genetic evidence for the long-sought-after link between oncogene activation and haemostasis... - To move or not to move? Semaphorin signalling in cell migrationLuca Tamagnone
Institute for Cancer Research and Treatment, University of Turin Medical School IRCC, SP 142, 10060 Candiolo, Turin, Italy
EMBO Rep 5:356-61. 2004..This review focuses on the mechanisms whereby semaphorins are thought to regulate cell migration... - Negative feedback regulation of Met-dependent invasive growth by NotchM Cristina Stella
Institute for Cancer Research and Treatment, University of Turin School of Medicine, Division of Molecular Oncology, IV Floor, Str Prov 142, km 3, 95, 10060 Candiolo, Torino, Italy
Mol Cell Biol 25:3982-96. 2005..These results unravel an in-built mechanism of negative feedback regulation in which Met activation leads to transcriptional induction of Notch function, which in turn limits HGF activity through repression of the Met oncogene... - A functional role for hemostasis in early cancer developmentCarla Boccaccio
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Turin Medical School, Turino, Italy
Cancer Res 65:8579-82. 2005..These findings reveal a long-sought mechanistic link between coagulation and cancer, highlighting a clinically important perspective on malignant invasion and metastasis... - Hepatocyte growth factor sensitizes human ovarian carcinoma cell lines to paclitaxel and cisplatinAndrea 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... - Invasive growth: a genetic programAlessandra Gentile
IRCC, Institute for Cancer Research and Treatment, University of Torino School of Medicine, 10060 Candiolo, Torino, Italy
Int J Dev Biol 48:451-6. 2004..Here we discuss the different biological facets of invasive growth and analyze the intracellular signals which lead to its execution... - Beta4 integrin is a transforming molecule that unleashes Met tyrosine kinase tumorigenesisAndrea Bertotti
Division of Molecular Oncology, Institute for Cancer Research and Treatment (IRCC, University of Torino School of Medicine, Candiolo (Torino, Italy
Cancer Res 65:10674-9. 2005.... - Only a subset of Met-activated pathways are required to sustain oncogene addictionAndrea Bertotti
Division of Molecular Oncology, Institute for Cancer Research and Treatment IRCC, University of Torino Medical School, 10060 Candiolo Torino, Italy
Sci Signal 2:ra80. 2009.... - Beta4 integrin activates a Shp2-Src signaling pathway that sustains HGF-induced anchorage-independent growthAndrea Bertotti
Division of Molecular Oncology, Institute for Cancer Research and Treatment, University of Torino School of Medicine, 10060 Candiolo, Torino, Italy
J Cell Biol 175:993-1003. 2006..These results unravel a novel pathway whereby beta4 directs tyrosine kinase-based signals toward adhesion-unrelated outcomes... - The Met tyrosine kinase receptor in development and cancerAlessandra Gentile
Division of Molecular Oncology, University of Turin Medical School, 10060, Candiolo Torino, Italy
Cancer Metastasis Rev 27:85-94. 2008..Several approaches have been recently developed to interfere with the tumorigenic and metastatic processes triggered by Met... - Functional regulation of semaphorin receptors by proprotein convertasesStefania Artigiani
Institute for Cancer Research and Treatment IRCC, University of Torino School of Medicine, 10060 Candiolo, Italy
J Biol Chem 278:10094-101. 2003..Thus, we conclude that cleavage by proprotein convertases is a novel regulatory step for semaphorin receptors localized at the cell surface... - Tyrosine kinase signal specificity: lessons from the HGF receptorAndrea Bertotti
IRCC, Institute for Cancer Research and Treatment, University of Torino School of Medicine, 10060, Candiolo (Torino, Italy
Trends Biochem Sci 28:527-33. 2003..This suggests that integration of cell-restricted expression of receptor partners that modulate kinase outputs with the intrinsic signalling features of receptors is required for specification of biological responses... - Molecular profiling of the "plexinome" in melanoma and pancreatic cancerAsha Balakrishnan
Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy
Hum Mutat 30:1167-74. 2009..5206C>T, p.H1736Y allele had lost this activity. Our study is the first systematic analysis of the "plexinome" in human tumors, and indicates that multiple mutated plexins may be involved in cancer progression... - Reactive oxygen species mediate Met receptor transactivation by G protein-coupled receptors and the epidermal growth factor receptor in human carcinoma cellsOliver M Fischer
Department of Molecular Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D 82152 Martinsried, Germany
J Biol Chem 279:28970-8. 2004.... - Hepatocyte growth factor and its receptor are required for malaria infectionMargarida Carrolo
, Rua da Quinta Grande 6, 2780-156 Oeiras, Portugal
Nat Med 9:1363-9. 2003..Our findings identify HGF and MET as potential targets for new approaches to malaria prevention... - Feline STK gene expression in mammary carcinomasRaffaella De Maria
Comparative Oncology Center, Institute for Cancer Research and Treatment, University of Torino, SP 142, Km 3 95, 10060 Candiolo Torino Italy
Oncogene 21:1785-90. 2002.... - The endophilin-CIN85-Cbl complex mediates ligand-dependent downregulation of c-MetAnnalisa Petrelli
CNR CIOS and Department of Genetics, Biology and Biochemistry, University of Torino, 10126 Torino, Italy
Nature 416:187-90. 2002..These data provide further evidence of a relationship between receptor-mediated signalling and endocytosis, and disclose a novel functional role for Cbl in HGF receptor signalling... - Metron factor-1 prevents liver injury without promoting tumor growth and metastasisTerumi Takahara
Third Department of Internal Medicine, Faculty of Medicine, University of Toyama, Toyama, Japan
Hepatology 47:2010-25. 2008..CONCLUSION: These data suggest that MF-1 is as effective as HGF at preventing liver injury and at promoting hepatocyte regeneration, but therapeutically safer than HGF because it lacks proangiogenic and prometastatic activity...