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    • Plusieurs versions

    Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic

    Cerrato, Aniello, Morra, Francesco, Celetti, Angela, Cerrato, Aniello, Morra, Francesco, Celetti, Angela
    Journal of Experimental and Clinical Cancer Research, 2016, Vol.35 [Revue évaluée par les pairs]

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    Wirkungsorientiertes Krankenhausmanagement

    Morra, Francesco
    Bern ; Stuttgart [etc.] : P. Haupt
    1996
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    Titre: Wirkungsorientiertes Krankenhausmanagement / Francesco Morra
    Auteur: Morra, Francesco
    Editeur: Bern ; Stuttgart [etc.] : P. Haupt
    Date: 1996
    Collation: XX, 381 S. : Fig. ; 23 cm
    Note: Diss. Wirtsch.-wiss. St. Gallen, 1996 ; Nr. 1788
    No RERO: 2198078
    Permalien:
    http://data.rero.ch/01-2198078/html?view=FR_V1

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    Wirkungsorientiertes Krankenhausmanagement : ein Führungshandbuch

    Morra, Francesco
    Bern [etc.] : P. Haupt
    1996
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    Titre: Wirkungsorientiertes Krankenhausmanagement : ein Führungshandbuch / Francesco Morra
    Auteur: Morra, Francesco
    Editeur: Bern [etc.] : P. Haupt
    Date: 1996
    Collation: XX, 381 S. : Fig. ; 23 cm
    Sujet RERO: hôpital - administration
    Note: Diss. Wirtsch.-wiss. St. Gallen, 1996
    Classification: dr-sys CA/CH 58 h
    FSES M160
    Identifiant: 3258053324 (ISBN)
    No RERO: R229083860
    Permalien:
    http://data.rero.ch/01-R229083860/html?view=FR_V1

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    New therapeutic perspectives in CCDC6 deficient lung cancer cells

    Morra, Francesco, Luise, Chiara, Visconti, Roberta, Staibano, Stefania, Merolla, Francesco, Ilardi, Gennaro, Guggino, Gianluca, Paladino, Simona, Sarnataro, Daniela, Franco, Renato, Monaco, Roberto, Zitomarino, Federica, Pacelli, Roberto, Monaco, Guglielmo, Rocco, Gaetano, Cerrato, Aniello, Linardopoulos, Spiros, Muller, Mark T., Celetti, Angela
    International Journal of Cancer, 01 May 2015, Vol.136(9), pp.2146-2157 [Revue évaluée par les pairs]

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    The effect of body cooling on respiratory system mechanics and hysteresis in rats

    Rubini, Alessandro, El-Mazloum, Dania, Morra, Francesco, Bosco, Gerardo
    Respiratory physiology & neurobiology, 01 October 2013, Vol.189(1), pp.52-58 [Revue évaluée par les pairs]

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    Use of poly ADP-ribose polymerase PARP inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic

    Cerrato, Aniello, Morra, Francesco, Celetti, Angela
    Journal of experimental & clinical cancer research : CR, 24 November 2016, Vol.35(1), pp.179 [Revue évaluée par les pairs]
    MEDLINE/PubMed (U.S. National Library of Medicine)
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    Titre: Use of poly ADP-ribose polymerase PARP inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic
    Auteur: Cerrato, Aniello; Morra, Francesco; Celetti, Angela
    Sujet: Assays ; Brca1/2 and Brcaness ; Cancer ; Clinical Trials ; DNA Damage Response ; Hr Proficiency and Parp Activity ; Parp Enzymes ; Parp Inhibitors ; Brca1 Protein -- Genetics ; Brca2 Protein -- Genetics ; Neoplasms -- Drug Therapy ; Poly(Adp-Ribose) Polymerase Inhibitors -- Therapeutic Use
    Description: DNA damage response (DDR) defects imply genomic instability and favor tumor progression but make the cells vulnerable to the pharmacological inhibition of the DNA repairing enzymes. Targeting cellular proteins like PARPs, which cooperate and complement molecular defects of the DDR process, induces a specific lethality in DDR defective cancer cells and represents an anti-cancer strategy. Normal cells can tolerate the DNA damage generated by PARP inhibition because of an efficient homologous recombination mechanism (HR); in contrast, cancer cells with a deficient HR are unable to manage the DSBs and appear especially sensitive to the PARP inhibitors (PARPi) effects. In this review we discuss the proof of concept for the use of PARPi in different cancer types and the success and failure of their inclusion in clinical trials. The PARP inhibitor Olaparib [AZD2281] has been approved by the FDA for use in pretreated ovarian cancer patients with defective BRCA1/2 genes, and by the EMEA for maintenance therapy in platinum sensitive ovarian cancer patients with defective BRCA1/2 genes. BRCA mutations are now recognised as the molecular targets for PARPi sensitivity in several tumors. However, it is noteworthy that the use of PARPi has shown its efficacy also in non-BRCA related tumors. Several trials are ongoing to test different PARPi in different cancer types. Here we review the concept of BRCAness and the functional loss of proteins involved in DDR/HR mechanisms in cancer, including additional molecules that can influence the cancer cells sensitivity to PARPi. Given the complexity of the existing crosstalk between different DNA repair pathways, it is likely... PARP inhibition is a potentially important strategy for managing a significant subset of tumors. The discovery of both germline and somatic DNA repair deficiencies in different cancer patients, together with the development of new PARP inhibitors that can kill selectively cancer cells is a potent example of targeting therapy to molecularly defined tumor subtypes.
    Fait partie de: Journal of experimental & clinical cancer research : CR, 24 November 2016, Vol.35(1), pp.179
    Identifiant: 1756-9966 (E-ISSN); 27884198 Version (PMID)

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    The between Now and Then of Lung Cancer Chemotherapy and Immunotherapy

    Visconti, Roberta, Morra, Francesco, Guggino, Gianluca, Celetti, Angela
    International journal of molecular sciences, 27 June 2017, Vol.18(7) [Revue évaluée par les pairs]

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    The combined effect of USP7 inhibitors and PARP inhibitors in hormone-sensitive and castration-resistant prostate cancer cells

    Morra, Francesco, Merolla, Francesco, Napolitano, Virginia, Ilardi, Gennaro, Miro, Caterina, Paladino, Simona, Staibano, Stefania, Cerrato, Aniello, Celetti, Angela
    Oncotarget, 09 May 2017, Vol.8(19), pp.31815-31829 [Revue évaluée par les pairs]

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    Critical role of CCDC6 in the neoplastic growth of testicular germ cell tumors

    Staibano, Stefania, Ilardi, Gennaro, Leone, Vincenza, Luise, Chiara, Merolla, Francesco, Esposito, Francesco, Morra, Francesco, Siano, Maria, Franco, Renato, Fusco, Alfredo, Chieffi, Paolo, Celetti, Angela
    BMC Cancer, 2013, Vol.13, p.433 [Revue évaluée par les pairs]

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    FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC

    Morra, Francesco, Luise, Chiara, Merolla, Francesco, Poser, Ina, Visconti, Roberta, Ilardi, Gennaro, Paladino, Simona, Inuzuka, Hiroyuki, Guggino, Gianluca, Monaco, Roberto, Colecchia, David, Monaco, Guglielmo, Cerrato, Aniello, Chiariello, Mario, Denning, Krista, Claudio, Pier Paolo, Staibano, Stefania, Celetti, Angela
    Morra, F., C. Luise, F. Merolla, I. Poser, R. Visconti, G. Ilardi, S. Paladino, et al. 2015. “FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC.” Oncotarget 6 (14): 12697-12709. [Revue évaluée par les pairs]
    Harvard University Library
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    Titre: FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC
    Auteur: Morra, Francesco; Luise, Chiara; Merolla, Francesco; Poser, Ina; Visconti, Roberta; Ilardi, Gennaro; Paladino, Simona; Inuzuka, Hiroyuki; Guggino, Gianluca; Monaco, Roberto; Colecchia, David; Monaco, Guglielmo; Cerrato, Aniello; Chiariello, Mario; Denning, Krista; Claudio, Pier Paolo; Staibano, Stefania; Celetti, Angela
    Sujet: Ccdc6 ; Fbxw7 ; Usp7 ; Mitotic Kinases ; Cisplatinum
    Description: CCDC6 gene product is a pro-apoptotic protein substrate of ATM, whose loss or inactivation enhances tumour progression. In primary tumours, the impaired function of CCDC6 protein has been ascribed to CCDC6 rearrangements and to somatic mutations in several neoplasia. Recently, low levels of CCDC6 protein, in NSCLC, have been correlated with tumor prognosis. However, the mechanisms responsible for the variable levels of CCDC6 in primary tumors have not been described yet. We show that CCDC6 turnover is regulated in a cell cycle dependent manner. CCDC6 undergoes a cyclic variation in the phosphorylated status and in protein levels that peak at G2 and decrease in mitosis. The reduced stability of CCDC6 in the M phase is dependent on mitotic kinases and on degron motifs that are present in CCDC6 and direct the recruitment of CCDC6 to the FBXW7 E3 Ubl. The de-ubiquitinase enzyme USP7 appears responsible of the fine tuning of the CCDC6 stability, affecting cells behaviour and drug response. Thus, we propose that the amount of CCDC6 protein in primary tumors, as reported in lung, may depend on the impairment of the CCDC6 turnover due to altered protein-protein interaction and post-translational modifications and may be critical in optimizing personalized therapy.
    Fait partie de: Morra, F., C. Luise, F. Merolla, I. Poser, R. Visconti, G. Ilardi, S. Paladino, et al. 2015. “FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC.” Oncotarget 6 (14): 12697-12709.
    Identifiant: 1949-2553 (ISSN)