Carlo Gambacorti-Passerini

Summary

Affiliation: University of Milano-Bicocca
Country: Italy

Publications

  1. doi request reprint Part I: Milestones in personalised medicine--imatinib
    Carlo Gambacorti-Passerini
    Clinical Research Unit, University of Milano Bicocca, San Gerardo Hospital, Monza, Italy
    Lancet Oncol 9:600. 2008
  2. ncbi request reprint Constitutive activation of Jak2 contributes to proliferation and resistance to apoptosis in NPM/ALK-transformed cells
    Holger Ruchatz
    The National Cancer Institute, Oncogenic Fusion Proteins Unit, Department of Experimental Oncology, Milan, Italy
    Exp Hematol 31:309-15. 2003
  3. doi request reprint Bosutinib : a review of preclinical and clinical studies in chronic myelogenous leukemia
    Francesca Rusconi
    University of Milano Bicocca, Department of Health Sciences, Via Cadore 48, 20900 Monza, Italy
    Expert Opin Pharmacother 15:701-10. 2014
  4. ncbi request reprint Gene expression analysis fails to identify patients with chronic myeloid leukemia who will achieve cytogenetic response to imatinib
    Carlo Gambacorti-Passerini
    Professor of Internal Medicine and OncologyNCI University of Milano Bicocca, Italy and JGH, McGill University, Montreal, Canada
    Haematologica 90:434. 2005
  5. doi request reprint Multicenter independent assessment of outcomes in chronic myeloid leukemia patients treated with imatinib
    Carlo Gambacorti-Passerini
    Hematology and Clinical Research Unit, San Gerardo Hospital, Italy
    J Natl Cancer Inst 103:553-61. 2011
  6. ncbi request reprint The ALK gene, an attractive target for inhibitor development
    Carmen J Tartari
    Department of Clinical Medicine, University of Milano Bicocca, Italy
    Curr Top Med Chem 11:1406-19. 2011
  7. ncbi request reprint Prognostic variables in patients with chronic myeloid leukemia treated with imatinib
    Carlo Gambacorti-Passerini
    University of Milano Bicocca, Monza, Italy
    Haematologica 91:145a. 2006
  8. pmc Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation
    Addolorata Maria Luce Coluccia
    Department of Clinical Medicine, University of Milano Bicocca, Monza, Milan, Italy
    EMBO J 26:1456-66. 2007
  9. doi request reprint Valproic acid enhances bosutinib cytotoxicity in colon cancer cells
    Luca Mologni
    Department of Clinical Medicine and Prevention, University of Milano Bicocca, Monza, Italy
    Int J Cancer 124:1990-6. 2009
  10. ncbi request reprint In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells
    Miriam Puttini
    Department of Clinical Medicine, S Gerardo Hospital University of Milano Bicocca, Monza, Italy
    Cancer Res 66:11314-22. 2006

Detail Information

Publications63

  1. doi request reprint Part I: Milestones in personalised medicine--imatinib
    Carlo Gambacorti-Passerini
    Clinical Research Unit, University of Milano Bicocca, San Gerardo Hospital, Monza, Italy
    Lancet Oncol 9:600. 2008
  2. ncbi request reprint Constitutive activation of Jak2 contributes to proliferation and resistance to apoptosis in NPM/ALK-transformed cells
    Holger Ruchatz
    The National Cancer Institute, Oncogenic Fusion Proteins Unit, Department of Experimental Oncology, Milan, Italy
    Exp Hematol 31:309-15. 2003
    ..Jak/Stat signaling is aberrantly activated in several human hematopoietic malignancies. We investigated the role of Jak2 in the context of NPM/ALK-mediated oncogenesis...
  3. doi request reprint Bosutinib : a review of preclinical and clinical studies in chronic myelogenous leukemia
    Francesca Rusconi
    University of Milano Bicocca, Department of Health Sciences, Via Cadore 48, 20900 Monza, Italy
    Expert Opin Pharmacother 15:701-10. 2014
    ..Bosutinib shows a good therapeutic activity with a benign safety profile, no cardiovascular toxicity, and offers an important therapeutic addition to the armamentarium that physicians can use against resistant CML. ..
  4. ncbi request reprint Gene expression analysis fails to identify patients with chronic myeloid leukemia who will achieve cytogenetic response to imatinib
    Carlo Gambacorti-Passerini
    Professor of Internal Medicine and OncologyNCI University of Milano Bicocca, Italy and JGH, McGill University, Montreal, Canada
    Haematologica 90:434. 2005
  5. doi request reprint Multicenter independent assessment of outcomes in chronic myeloid leukemia patients treated with imatinib
    Carlo Gambacorti-Passerini
    Hematology and Clinical Research Unit, San Gerardo Hospital, Italy
    J Natl Cancer Inst 103:553-61. 2011
    ..Imatinib slows development of chronic myeloid leukemia (CML). However, available information on morbidity and mortality is largely based on sponsored trials, whereas independent long-term field studies are lacking...
  6. ncbi request reprint The ALK gene, an attractive target for inhibitor development
    Carmen J Tartari
    Department of Clinical Medicine, University of Milano Bicocca, Italy
    Curr Top Med Chem 11:1406-19. 2011
    ..Here, we described normal function of the ALK receptor and its role in tumors; formation of the constitutively activated ALK fusion proteins and we reported an update of developed small molecule inhibitors of the ALK kinase activity...
  7. ncbi request reprint Prognostic variables in patients with chronic myeloid leukemia treated with imatinib
    Carlo Gambacorti-Passerini
    University of Milano Bicocca, Monza, Italy
    Haematologica 91:145a. 2006
  8. pmc Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation
    Addolorata Maria Luce Coluccia
    Department of Clinical Medicine, University of Milano Bicocca, Monza, Milan, Italy
    EMBO J 26:1456-66. 2007
    ..These findings indicate the Bcr-Abl triggered Y phosphorylation of beta-catenin as a new mechanism responsible for its protein stabilization and nuclear signalling activation in CML...
  9. doi request reprint Valproic acid enhances bosutinib cytotoxicity in colon cancer cells
    Luca Mologni
    Department of Clinical Medicine and Prevention, University of Milano Bicocca, Monza, Italy
    Int J Cancer 124:1990-6. 2009
    ..These results suggest that VPA may be employed as a positive modulator of bosutinib antitumor activity in colorectal cancer...
  10. ncbi request reprint In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells
    Miriam Puttini
    Department of Clinical Medicine, S Gerardo Hospital University of Milano Bicocca, Monza, Italy
    Cancer Res 66:11314-22. 2006
    ..Modeling considerations attribute the superior activity of SKI-606 to its ability to bind a conformation of Bcr-Abl different from imatinib...
  11. ncbi request reprint Expression, purification, and inhibition of human RET tyrosine kinase
    Luca Mologni
    Department of Clinical Medicine, University of Milano Bicocca, Monza, Italy
    Protein Expr Purif 41:177-85. 2005
    ..These reagents were used to develop a rapid ELISA-based kinase assay for screening potential inhibitors. Novel RET inhibitors were identified using this assay...
  12. ncbi request reprint Peripheral blood progenitor cell collection in chronic myeloid leukemia patients with complete cytogenetic response after treatment with imatinib mesylate
    Paolo Perseghin
    Department of Clinical Pathology Immunohematology and Transfusion Service, Therapeutic Apheresis Unit, San Gerardo de Tintori Hospital, Monza, Italy
    Transfusion 45:1214-20. 2005
    ..Nevertheless, some concerns exist about the duration of response to treatment and the onset of resistance to IM...
  13. doi request reprint Three novel patient-derived BCR/ABL mutants show different sensitivity to second and third generation tyrosine kinase inhibitors
    Sara Redaelli
    Department of Clinical Medicine and Prevention, University of Milano Bicocca, S Gerardo Hospital, Monza, Milan, Italy
    Am J Hematol 87:E125-8. 2012
    ..The availability of drugs activity profiles may become a useful tool for clinicians dealing with the treatment of drug-resistant CML patients...
  14. ncbi request reprint Inhibition of RET tyrosine kinase by SU5416
    Luca Mologni
    Department of Clinical Medicine, Prevention and Biotechnology, University of Milan Bicocca, Monza, Italy
    J Mol Endocrinol 37:199-212. 2006
    ..We provide a possible explanation to these results by using molecular docking. Finally, SU5416 was also assessed against an array of 52 tyrosine and serine/threonine kinases...
  15. pmc Epigenetic silencing of the proapoptotic gene BIM in anaplastic large cell lymphoma through an MeCP2/SIN3a deacetylating complex
    Rocco Piazza
    Department of Health Sciences, University of Milano, Bicocca, Monza, Italy
    Neoplasia 15:511-22. 2013
    ....
  16. pmc Recurrent SETBP1 mutations in atypical chronic myeloid leukemia
    Rocco Piazza
    Department of Health Sciences, University of Milano Bicocca, Monza, Italy
    Nat Genet 45:18-24. 2013
    ..In summary, mutated SETBP1 represents a newly discovered oncogene present in aCML and closely related diseases...
  17. ncbi request reprint Characterization of some molecular mechanisms governing autoactivation of the catalytic domain of the anaplastic lymphoma kinase
    Carmen J Tartari
    Department of Clinical and Prevention Medicine, University of Milano Bicocca, Via Cadore 48, Monza 20052, Italy
    J Biol Chem 283:3743-50. 2008
    ..Together, our findings indicate that phosphorylation of the first tyrosine of the YXXXYY motif is necessary for the autoactivation of the ALK kinase domain and the transforming activity of NPM/ALK...
  18. pmc CEQer: a graphical tool for copy number and allelic imbalance detection from whole-exome sequencing data
    Rocco Piazza
    Department of Health Sciences, University of Milano Bicocca, Monza, Italy
    PLoS ONE 8:e74825. 2013
    ..Therefore, we propose CEQer as an efficient, robust and user-friendly graphical tool for the identification of CNA/AI in the context of whole-exome sequencing data. ..
  19. ncbi request reprint Oncogenic fusion tyrosine kinases as molecular targets for anti-cancer therapy
    Rosalind H Gunby
    Department of Clinical Medicine, University of Milano Bicocca, Monz, Italy
    Anticancer Agents Med Chem 7:594-611. 2007
    ..Here we review the PTKs known to be expressed as FTKs in cancer and the strategies for molecularly targeting these FTKs in anti-cancer therapy...
  20. pmc ERG deregulation induces PIM1 over-expression and aneuploidy in prostate epithelial cells
    Vera Magistroni
    Department of Clinical Medicine, University of Milano Bicocca, Monza, Italy
    PLoS ONE 6:e28162. 2011
    ..Here we provide the first evidence for an ERG-mediated PIM1 up-regulation in prostate cells in vitro and in vivo, suggesting a direct effect of ERG transcriptional activity in the alteration of genetic stability...
  21. doi request reprint Crizotinib-resistant NPM-ALK mutants confer differential sensitivity to unrelated Alk inhibitors
    Monica Ceccon
    Department of Health Sciences, University of Milano Bicocca, Via Cadore 48, Monza 20900, Italy
    Mol Cancer Res 11:122-32. 2013
    ..This study provides potentially relevant information for the management of patients with ALCL that may relapse after crizotinib treatment...
  22. pmc Synergistic effects of combined Wnt/KRAS inhibition in colorectal cancer cells
    Luca Mologni
    Department of Health Sciences, University of Milano Bicocca, Monza, Italy
    PLoS ONE 7:e51449. 2012
    ..Expression analysis of selected cancer-relevant genes revealed down-regulation of CD44 as a common response to the combined treatments. These data provide a proof of principle for a combination therapeutic strategy in colorectal cancer...
  23. ncbi request reprint Structural insights into the ATP binding pocket of the anaplastic lymphoma kinase by site-directed mutagenesis, inhibitor binding analysis, and homology modeling
    Rosalind H Gunby
    Department of Clinical Medicine, University of Milano Bicocca, Monza, 20052, Italy
    J Med Chem 49:5759-68. 2006
    ..In addition, 4-phenylamino-quinoline compounds may have potential as templates for ALK inhibitors...
  24. ncbi request reprint The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years
    Rocco G Piazza
    University of Milano Bicocca, S Gerardo Hospital, Monza, Italy
    Blood Cells Mol Dis 37:111-5. 2006
    ..0001). This 6-year follow-up of the efficacy of Imatinib therapy in CML patients who obtained a durable CCyR indicates that the relapses rate is low over this period of observation and that the rate of relapse does not increase over time...
  25. pmc NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma
    Annamaria Galietta
    Department of Clinical Medicine, University of Milano Bicocca, Monza, Italy
    Blood 110:2600-9. 2007
    ..These results identify PSF as a novel NPM/ALK-binding protein and substrate, and suggest that PSF function may be perturbed in NPM/ALK-transformed cells...
  26. doi request reprint Ponatinib is a potent inhibitor of wild-type and drug-resistant gatekeeper mutant RET kinase
    Luca Mologni
    Dept of Health Sciences, University of Milano Bicocca, Via Cadore 48, 20900 Monza, Italy
    Mol Cell Endocrinol 377:1-6. 2013
    ..We suggest that ponatinib should be considered for the treatment of RET+ tumors, in particular those expressing vandetanib-resistant V804M/L mutations...
  27. doi request reprint BRAF silencing by short hairpin RNA or chemical blockade by PLX4032 leads to different responses in melanoma and thyroid carcinoma cells
    Elisa Sala
    University of Milano Bicocca, Via Cadore 48, Monza, 20052 Italy
    Mol Cancer Res 6:751-9. 2008
    ..Furthermore, we suggest that a BRAF-independent mechanism of cell survival exists in anaplastic thyroid cancer cells...
  28. doi request reprint Synthesis, structure-activity relationship and crystallographic studies of 3-substituted indolin-2-one RET inhibitors
    Luca Mologni
    Department of Clinical Medicine and Prevention, University of Milano Bicocca, Monza, Italy
    Bioorg Med Chem 18:1482-96. 2010
    ..Crystallographic analysis confirmed predictions from molecular modelling and helped refine SAR results. These data provide important information for the development of indolinone inhibitors for the treatment of RET-driven cancers...
  29. ncbi request reprint A rapid method for the purification of wild-type and V804M mutant ret catalytic domain: A tool to study thyroid cancer
    Elisa Sala
    Department of Experimental Oncology, National Cancer Institute, Milan, Italy
    Int J Biol Macromol 39:60-5. 2006
    ....
  30. pmc FusionAnalyser: a new graphical, event-driven tool for fusion rearrangements discovery
    Rocco Piazza
    Department of Clinical Medicine, University of Milano Bicocca, Monza, 20900, Italy
    Nucleic Acids Res 40:e123. 2012
    ..Therefore, we propose FusionAnalyser as an efficient and robust graphical tool for the identification of functional rearrangements in the context of high-throughput transcriptome sequencing data...
  31. ncbi request reprint Imatinib failed to eradicate chronic myeloid leukemia in a patient with minimal residual disease
    Anna Franceschino
    University of Milano Bicocca, Section of Hematology, Ospedale S Gerardo, Via Cadore 48, 20052 Monza, Italy
    Haematologica 91:ECR14. 2006
  32. ncbi request reprint The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells
    Michael W N Deininger
    Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute, Portland, Oregon 97239, USA
    Cancer 110:1509-19. 2007
    ..In some patients, CCA/Ph-negative status was associated with myelodysplasia or acute myeloid leukemia. The objective of the current study was to determine the prognostic impact of CCA/Ph-negative cells...
  33. ncbi request reprint Decrease of resistance to imatinib in leukaemia
    Carlo Gambacorti-Passerini
    Lancet 359:1777. 2002
  34. doi request reprint Alterations in creatine kinase, phosphate and lipid values in patients with chronic myeloid leukemia during treatment with imatinib
    Anna Franceschino
    Haematologica 93:317-8. 2008
    ..We present here data from a retrospective analysis on metabolic abnormalities occurring during therapy which show increased creatine kinase, inverse creatine kinase-phosphate correlation, cholesterol and triglyceride values...
  35. pmc A mechanistic design principle for protein tyrosine kinase sensors: application to a validated cancer target
    Aya Wakata
    Department of Biochemistry, The Albert Einstein College of Medicine of Yeshiva University, 1300 Morris Park Avenue, Bronx, New York 10461, USA
    Org Lett 10:301-4. 2008
    ....
  36. doi request reprint Characterization of compound 584, an Abl kinase inhibitor with lasting effects
    Miriam Puttini
    School of Pharmaceutical Sciences, University of Geneva, Quai Ernest Ansermet 30, 1211 Geneve 4, Switzerland
    Haematologica 93:653-61. 2008
    ..In the current study we describe the design, synthesis and biological properties of an imatinib analog with a chlorine-substituted benzamide, namely compound 584 (cmp-584)...
  37. doi request reprint Validation of PDGFRbeta and c-Src tyrosine kinases as tumor/vessel targets in patients with multiple myeloma: preclinical efficacy of the novel, orally available inhibitor dasatinib
    Addolorata Maria Luce Coluccia
    Department of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy
    Blood 112:1346-56. 2008
    ..Overall data highlight the biologic and therapeutic relevance of the combined targeting of PDGFRbeta/c-Src TKs in MM, providing a framework for future clinical trials...
  38. ncbi request reprint Bcr-Abl mutations, resistance to imatinib, and imatinib plasma levels
    Carlo Gambacorti-Passerini
    Blood 102:1933-4; author reply 1934-5. 2003
  39. ncbi request reprint Development of c-Kit-expressing small-cell lung cancer in a chronic myeloid leukemia patient during imatinib treatment
    Carlo Gambacorti-Passerini
    J Natl Cancer Inst 96:1723-4. 2004
  40. ncbi request reprint Bcl-XL down-regulation suppresses the tumorigenic potential of NPM/ALK in vitro and in vivo
    Addolorata Maria Luce Coluccia
    Department of Experimental Oncology, National Cancer Institute, Milan, Italy
    Blood 103:2787-94. 2004
    ..Bcl-XL deserves further investigation as a possible therapeutic target in ALK+ ALCLs...
  41. ncbi request reprint Gynaecomastia in men with chronic myeloid leukaemia after imatinib
    Carlo Gambacorti-Passerini
    National Cancer Institute, Milan, Italy
    Lancet 361:1954-6. 2003
    ..36 pmol/L (-1.02 to 13.74). In most men with chronic myeloid leukaemia studied here, imatinib was associated with a reduction in the production of testicular hormones and in some, with the development of gynaecomastia...
  42. ncbi request reprint Sensitivity to imatinib but low frequency of the TEL/PDGFRbeta fusion protein in chronic myelomonocytic leukemia
    Rosalind Helen Gunby
    Oncogenic Fusion Protein Unit, Department of Experimental Oncology, Istituto Nazionale Tumori, 20133 Milan, Italy
    Haematologica 88:408-15. 2003
    ..The expression of PDGFRbeta fusions in CMML could have therapeutic relevance, as PDGFRb is inhibited by the selective tyrosine kinase inhibitor, imatinib. Here, we investigated the possibility of employing imatinib to treat CMML...
  43. ncbi request reprint Alpha1 acid glycoprotein binds to imatinib (STI571) and substantially alters its pharmacokinetics in chronic myeloid leukemia patients
    Carlo Gambacorti-Passerini
    Department of Experimental Oncology, Istituto Nazionale Tumori, Milano, Italy
    Clin Cancer Res 9:625-32. 2003
    ..alpha1 acid glycoprotein (AGP) binds to imatinib with high affinity and inhibits imatinib activity in vitro and in vivo in an animal model. A pharmacokinetics analysis of imatinib was undertaken in CML patients...
  44. ncbi request reprint Molecular cytogenetics of the acute promyelocytic leukemia-derived cell line NB4 and of four all-trans retinoic acid-resistant subclones
    Marie Joelle Mozziconacci
    Institut Paoli Calmettes and INSERM U119, Marseille, France
    Genes Chromosomes Cancer 35:261-70. 2002
    ..These data could focus further research for a better understanding of the molecular mechanisms underlying response or resistance to differentiating and/or apoptotic reagents...
  45. ncbi request reprint Binding of imatinib by alpha(1)-acid glycoprotein
    Carlo Gambacorti-Passerini
    Blood 100:367-8; author reply 368-9. 2002
  46. ncbi request reprint Unique substrate specificity of anaplastic lymphoma kinase (ALK): development of phosphoacceptor peptides for the assay of ALK activity
    Arianna Donella-Deana
    Department of Biochemistry, University of Padova, Viale G Colombo 3, 35121 Padova, Italy
    Biochemistry 44:8533-42. 2005
    ..Such a peculiar substrate specificity allows the specific monitoring of ALK activity in crude extracts of NPM-ALK positive cells, using the YFF peptide, which is only marginally phosphorylated by a number of other tyrosine kinases...
  47. ncbi request reprint An enzyme-linked immunosorbent assay to screen for inhibitors of the oncogenic anaplastic lymphoma kinase
    Rosalind Helen Gunby
    Haematologica 90:988-90. 2005
    ..To this aim we have developed and optimized an ALK-specific enzyme-linked immunosorbent assay that employs a novel ALK peptide substrate and purified ALK kinase domain...
  48. ncbi request reprint In reply to 'Cardiotoxicity of the cancer therapeutic agent imatinib mesylate'
    Carlo Gambacorti-Passerini
    Nat Med 13:13-4; author reply 15-6. 2007
  49. ncbi request reprint Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia
    Hagop Kantarjian
    M D Anderson Cancer Center, Houston, TX 77030, USA
    N Engl J Med 346:645-52. 2002
    ..Chronic myelogenous leukemia (CML) is caused by the BCR-ABL tyrosine kinase, the product of the Philadelphia chromosome. Imatinib mesylate, formerly STI571, is a selective inhibitor of this kinase...
  50. pmc FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia
    Paolo Neviani
    Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio, USA
    J Clin Invest 117:2408-21. 2007
    ..Altogether, these results highlight the therapeutic relevance of rescuing PP2A tumor suppressor activity in Ph1 leukemias and strongly support the introduction of the PP2A activator FTY720 in the treatment of CML-BC and Ph1 ALL patients...
  51. ncbi request reprint Simultaneous development of Philadelphia chromosome-positive and -negative leukemias in the same patient
    Sarit Assouline
    Am J Hematol 81:646. 2006
  52. ncbi request reprint Panniculitis during dasatinib therapy for imatinib-resistant chronic myelogenous leukemia
    Sarit Assouline
    N Engl J Med 354:2623-4. 2006
  53. ncbi request reprint Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study
    Moshe Talpaz
    M D Anderson Cancer Center, Houston, Texas, USA
    Blood 99:1928-37. 2002
    ..Orally administered imatinib is an effective and well-tolerated treatment for patients with CML in accelerated phase. A daily dose of 600 mg is more effective than 400 mg, with similar toxicity...
  54. ncbi request reprint BCR-ABL nuclear entrapment kills human CML cells: ex vivo study on 35 patients with the combination of imatinib mesylate and leptomycin B
    Alessandra Aloisi
    Department of Biomedical Sciences, Section of General Pathology, University of Catania, Via Androne, 83 95124 Catania, Italy
    Blood 107:1591-8. 2006
    ....
  55. ncbi request reprint Determination of alpha-1 acid glycoprotein in patients with Ph+ chronic myeloid leukemia during the first 13 weeks of therapy with STI571
    Philipp Le Coutre
    Abteilung für Hämatologie und Onkologie, Campus Virchow, Charite, Humboldt Universitat, Berlin, Germany
    Blood Cells Mol Dis 28:75-85. 2002
    ....
  56. ncbi request reprint ALK as a novel lymphoma-associated tumor antigen: identification of 2 HLA-A2.1-restricted CD8+ T-cell epitopes
    Lorena Passoni
    Oncogenic Fusion Genes and Proteins Unit, Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133 Milan, Italy
    Blood 99:2100-6. 2002
    ....
  57. ncbi request reprint BCR-ABL suppresses C/EBPalpha expression through inhibitory action of hnRNP E2
    Danilo Perrotti
    Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    Nat Genet 30:48-58. 2002
    ..Our results indicate that BCR-ABL regulates the expression of C/EBPalpha by inducing hnRNP E2-which inhibits the translation of CEBPA mRNA...
  58. pmc hnRNP A1 nucleocytoplasmic shuttling activity is required for normal myelopoiesis and BCR/ABL leukemogenesis
    Angela Iervolino
    Department of Microbiology and Immunology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    Mol Cell Biol 22:2255-66. 2002
    ..Together, these results suggest that the shuttling activity of hnRNP A1 is important for the nucleocytoplasmic trafficking of mRNAs that encode proteins influencing the phenotype of normal and BCR/ABL-transformed myeloid progenitors...
  59. ncbi request reprint Selective cytotoxicity of betulinic acid on tumor cell lines, but not on normal cells
    Valentina Zuco
    Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133, Milan, Italy
    Cancer Lett 175:17-25. 2002
    ..These data support further preclinical studies of betulinic acid not confined to melanoma and neuroectodermal tumors independently of p53 status...
  60. ncbi request reprint ErbB-2 receptor cooperates with E6/E7 oncoproteins of HPV type 16 in breast tumorigenesis
    Amber Yasmeen
    Montreal Center for Experimental Therapeutics in Cancer, Lady Davis Institute for Medical Research, Sir Mortimer B Davis Jewish General Hospital, Montreal, Quebec H3T 1E2 Canada
    Cell Cycle 6:2939-43. 2007
    ..These findings provide evidence that the ErbB-2 receptor cooperates with high-risk HPVs in breast tumorigenesis via beta-catenin activation...
  61. pmc Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis
    Anna M Eiring
    Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics and Comprehensive Cancer Center, Ohio State University, Columbus, USA
    Blood 111:816-28. 2008
    ..Thus, the complexity of the mRNA/RBP network, together with the discovery of E2F3 as an hnRNP-A1-regulated factor, outlines the relevant role played by RBPs in posttranscriptional regulation of CML development and progression...
  62. ncbi request reprint SKI-606 decreases growth and motility of colorectal cancer cells by preventing pp60(c-Src)-dependent tyrosine phosphorylation of beta-catenin and its nuclear signaling
    Addolorata Maria Luce Coluccia
    Department of Experimental Oncology, National Cancer Institute, Milan, Italy
    Cancer Res 66:2279-86. 2006
    ....
  63. ncbi request reprint Sorafenib functions to potently suppress RET tyrosine kinase activity by direct enzymatic inhibition and promoting RET lysosomal degradation independent of proteasomal targeting
    Ivan Plaza-Menacho
    Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, SW3 6JB London, United Kingdom
    J Biol Chem 282:29230-40. 2007
    ..In addition, because inhibition of RET is not impaired by mutation of the Val(804) gatekeeper residue, MEN2 tumors may be less susceptible to acquired Sorafenib resistance...