New therapeutic perspectives in CCDC6 deficient lung cancer cells (462 views)
Int J Cancer (ISSN: 0020-7136), 2015; 136(9): 2146-2157.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 5.531, 5-year impact factor: 5.624
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84923212201&partnerID=40&md5=066c625f3467714bce439e2bb26ec1c3
Keywords: Candidate Biomarker, Ccdc6, Dna Damage And Homologousdirected Repair, Nsclc, Resistance To Platinum Salts And Parp-1 Inhibitor Sensitivity, Dna Damage And Homologous-Directed Repair, Cisplatin, Coiled Coil Domain Containing 6 Protein, Olaparib, Rad51 Protein, Tumor Suppressor Protein, Unclassified Drug, Adult, Article, Cancer Resistance, Disease Association, Disease Free Survival, Dna Repair, Drug Mechanism, Drug Potentiation, Drug Sensitization, Female, Homologous Recombination, Human, Human Cell, Human Tissue, Immunohistochemistry, Lung Cancer Cell Line, Lymph Node Metastasis, Non Small Cell Lung Cancer, Overall Survival, Priority Journal, Protein Deficiency, Protein Expression, Tissue Microarray,
Affiliations:
*** IBB - CNR ***
Istituto per l'Endocrinologia e l'Oncologia Sperimentale Gaetano Salvatore, CNR, IEOS, Via Pansini, 5Naples, Italy
Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Universitá Federico IINapoli, Italy
Dipartimento di Scienze Biomediche Avanzate, Universitá Federico IINapoli, Italy
UOC Chirurgia Toracica, Azienda Ospedaliera di Rilievo Nazionale A.CardarelliNapoli, Italy
CEINGE-Biotecnologie AvanzateNapoli, Italy
UOC Anatomia Patologica e Citopatologia, ISNT Fondazione G. PascaleNapoli, Italy
Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, 237 Fulham RoadLondon, United Kingdom
Department of Molecular Biology and Microbiology, College of Medicine, University of Central FloridaOrlando, FL, United States
References:
Jemal, A., Siegel, R., Ward, E., Cancer statistics 2009 (2009) CA Cancer J Clin, 59, pp. 225-24
Andre, F., McShane, L.M., Michiels, S., Biomarker studies: A call for a comprehensive biomarker study registry (2011) Nat Rev Clin Oncol, 8, pp. 171-176
Curtin, N.J., DNA repair dysregulation from cancer driver to therapeutic target (2012) Nat Rev Cancer, 12, pp. 801-817
Lynch, T.J., Bell, D.W., Sordella, R., Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib (2004) N Engl J Med, 350, pp. 2129-2139
Camidge, D.R., Bang, Y.J., Kwak, E.L., Activity and safety of crizotinib in patients with ALKpositive non-small-cell lung cancer: Up dated results from a phase 1 study (2012) Lancet Oncol, 13, pp. 1011-1019
Okamoto, K., Kodama, K., Takase, K., Antitumor activities of the targeted multi-Tyrosine kinase inhibitor lenvatinib (E7080) against RET gene fusion-driven tumor models (2013) Cancer Lett, 340, pp. 97-103
Zeng-Rong, N., Paterson, J., Alpert, L., Elevated DNA repair capacity is associated with intrinsic resistance of lung cancer to chemotherapy (1995) Cancer Res, 55, pp. 4760-4764
Bosken, C.H., Wei, Q., Amos, C.I., Spitz, M.R., An analysis of DNA repair as a determinant of survival in patients with non-small-cell lung cancer (2002) J Natl Cancer Inst, 94, pp. 1091-1099
Duchesne, G.M., Fundamental bases of combined therapy in lung cancer: Cell resistance to chemotherapy and radiotherapy (1994) Lung Cancer, 10, pp. S67-S72
Guo, W.F., Lin, R.X., Huang, J., Identification of differentially expressed genes contributing to radioresistance in lung cancer cells using microarray analysis (2005) Radiat Res, 164, pp. 27-35
De Lorenzo, S.B., Patel, A.G., Hurley, R.M., Kaufmann, S.H., The elephant and the blind men: Making sense of PARP inhibitors in homologous recombination deficient tumor cells (2013) Front Oncol, 3, p. 228
Ashworth, A., A synthetic lethal therapeutic approach: Poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair (2008) J Clin Oncol, 26, pp. 3785-3790
Tentori, L., Graziani, G., Chemopotentiation by PARP inhibitors in cancer therapy (2005) Pharmacol Res, 52, pp. 25-33
Oplustilova, L., Wolanin, K., Mistrik, M., Evaluation of candidate biomarkers to predict cancer cell sensitivity or resistance to PARP-1 inhibitor treatment (2012) Cell Cycle, 11, pp. 3837-3850
Postel-Vinay, S., Bajrami, I., Friboulet, L., A high-Throughput screen identifies PARP1/2 inhibitors as a potential therapy for ERCC1-deficient non-small cell lung cancer (2013) Oncogene, 32, pp. 5377-5387
Celetti, A., Cerrato, A., Merolla, F., H4(D10S170), a gene frequently rearranged with RET in papillary thyroid carcinomas: Functional characterization (2004) Oncogene, 23, pp. 109-121
Merolla, F., Pentimalli, F., Pacelli, R., Involvement of H4(D10S170) protein in ATMdependent response to DNA damage (2007) Oncogene, 26, pp. 6167-6175
Merolla, F., Luise, C., Muller, M.T., Loss of CCDC6, the first identified RET partner gene, affects pH2AX S139 levels and accelerates mitotic entry upon DNA damage (2012) PLos ONE, 7, p. e36177
Grieco, M., Santoro, M., Berlingieri, M.T., PTC is a novel rearranged form of the RET protooncogene and is frequently detected in vivo in human thyroid papillary carcinomas (1990) Cell, 60, pp. 557-563
Drechsler, M., Hildebrandt, B., Kündgen, A., Fusion of H4/D10S170 to PDGFRbeta in a patient with chronic myelomonocytic leukemia and long-Term responsiveness to imatinib (2007) Ann Hematol, 86, pp. 353-354
Takeuchi, K., Soda, M., Togashi, Y., RET, ROS1 and ALK fusions in lung cancer (2012) Nat Med, 18, pp. 378-381
Imielinski, M., Berger, A.H., Hammerman, P.S., Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing (2012) Cell, 150, pp. 1107-1120
Matsubara, D., Kanai, Y., Ishikawa, S., Identification of CCDC6-RET fusion in the human lung adenocarcinoma cell line, LC-2/ad (2012) J Thorac Oncol, 7, pp. 1872-1876
Chou, T.C., Talaly, P., A simple generalized equation for the analysis of multiple inhibitions of Michaelis-Menten kinetic systems (1977) J Biol Chem, 252, pp. 6438-6442
Jasin, M., Genetic manipulation of genomes with rare-cutting endonucleases (1996) Trends Genet, 12, pp. 224-228
Staibano, S., Ilardi, G., Leone, V., Critical role of CCDC6 in the neoplastic growth of testicular germ cell tumors (2013) BMC Cancer, 13, pp. 433-444
Tutt, A., Bertwistle, D., Valentine, J., Mutation in Brca2 stimulates error-prone homologydirected repair of DNA double-strand breaks occurring between repeated sequences (2001) EMBO J, 20, pp. 4704-4716
Mao, Z., Bozzella, M., Seluanov, A., Gorbunova, V., Comparison of nonhomologous end joining and homologous recombination in human cells (2008) DNA Repair (Amst), 10, pp. 1765-1771
Edge, S.B., Byrd, D.R., Compton, C.C., (2010) AJCC Cancer Staging Manual, pp. 253-270. , 7th ed. New York: Springer
Farmer, H., McCabe, N., Lord, C.J., Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy (2005) Nature, 434, pp. 917-921
Cuozzo, C., Porcellini, A., Angrisano, T., DNA damage, homology-directed repair, and DNA methylation (2007) PLoS Genet, 3, p. e110
Lee, B., Kim, J., Taylor, M., Muller, M.T., DNA methyltransferase 1-Associated protein (DMAP1) is a co-repressor that stimulates DNA methylation globally and locally at sites of double strand DNA break repair (2010) J Biol Chem, 285, pp. 37630-37640
Lee, B., Morano, A., Porcellini, A., Muller, M.T., GADD45a inhibition of DNMT1 dependent DNA methylation during homology directed DNA repair (2011) Nucleic Acids Res, 40, pp. 2481-2493
Morano, A., Angrisano, T., Russo, G., Targeted DNA methylation by homology-directed repair in mammalian cells. Transcription reshapes methylation of the repaired gene (2014) Nucleic Acids Res, 42, pp. 804-821
Rottenberg, S., Jaspers, J.E., Kersbergen, A., High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs (2008) Proc Natl Acad Sci USA, 105, pp. 17079-17084
Fong, P.C., Boss, D.S., Yap, T.A., Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers (2009) N Engl J Med, 361, pp. 123-134
Tutt, A., Robson, M., Garber, J.E., Oral poly(-ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: A proof-of-concept trial (2010) Lancet, 376, pp. 235-244
Chang, A., Chemotherapy, chemoresistance and the changing treatment landscape for NSCLC (2012) Lung Cancer, 71, pp. 3-10
Birkelbach, M., Ferraiolo, N., Gheorghiu, L., Detection of impaired homologous recombination repair in NSCLC cells and tissues (2013) J Thorac Oncol, 8, pp. 279-286
Cheng, H., Zhang, Z., Borczuk, A., PARP inhibition selectively increases sensitivity to cisplatin in ERCC1-low non-small cell lung cancer cells (2013) Carcinogenesis, 34, pp. 739-749
Gridelli, C., Rossi, A., Di Maio, M., Rationale and design of MILES-3 and MILES-4 studies: Two randomized phase 3 trials comparing singleagent chemotherapy versus cisplatin-based doublets in elderly patients with advanced Non-Small-Cell Lung Cancer (2014) Clin Lung Cancer, 15, pp. 166-170
Bowden, N.A., Nucleotide excision repair: Why is it not used to predict response to platinum-based chemotherapy? (2014) Cancer Lett, 346, pp. 163-171
Lord, C.J., McDonald, S., Swift, S., A highthroughput RNA interference screen for DNA repair determinants of PARP inhibitor sensitivity (2008) DNA Repair (Amst), 7, pp. 2010-2019
Sandhu, S.K., Schelman, W.R., Wilding, G., The poly(ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: A phase 1 doseescalation trial (2013) Lancet Oncol, 14, pp. 882-892
Zhao, J., Tang, J., Men, W., Ren, K., FBXW7-mediated degradation of CCDC6 is impaired by ATM during DNA damage response in lung cancer cells (2012) FEBS, 586, pp. 4257-4263
Sowa, M.E., Bennett, E.J., Gygi, S.P., Harper, J.W., Defining the human deubiquitinating enzyme interaction landscape (2009) Cell, 138, pp. 389-403
Leone, V., Mansueto, G., Pierantoni, G.M., CCDC6 represses CREB1 activity by recruiting histone deacetylase 1 and protein phosphatase 1 (2010) Oncogene, 29, pp. 4341-4351
Jeannot, V., Busser, B., Brambilla, E., The PI3K/AKT pathway promotes gefitinib resistance in mutant KRAS lung adenocarcinoma by a deacetylase-dependent mechanism (2014) Int J Cancer, 134, pp. 2560-2571
Ciardiello, F., Tortora, G., EGFR antagonists in cancer treatment (2008) N Engl J Med, 13, pp. 1160-1174
Gerlinger, M., Rowan, A.J., Horswell, S., Intratumor heterogeneity and branched evolution revealed by multiregion sequencing (2012) N Engl J Med., 366, pp. 883-892
Curtin, N. J., DNA repair dysregulation from cancer driver to therapeutic target (2012) Nat Rev Cancer, 12, pp. 801-817
Lynch, T. J., Bell, D. W., Sordella, R., Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib (2004) N Engl J Med, 350, pp. 2129-2139
Camidge, D. R., Bang, Y. J., Kwak, E. L., Activity and safety of crizotinib in patients with ALKpositive non-small-cell lung cancer: Up dated results from a phase 1 study (2012) Lancet Oncol, 13, pp. 1011-1019
Bosken, C. H., Wei, Q., Amos, C. I., Spitz, M. R., An analysis of DNA repair as a determinant of survival in patients with non-small-cell lung cancer (2002) J Natl Cancer Inst, 94, pp. 1091-1099
Duchesne, G. M., Fundamental bases of combined therapy in lung cancer: Cell resistance to chemotherapy and radiotherapy (1994) Lung Cancer, 10, pp. S67-S72
Guo, W. F., Lin, R. X., Huang, J., Identification of differentially expressed genes contributing to radioresistance in lung cancer cells using microarray analysis (2005) Radiat Res, 164, pp. 27-35
De Lorenzo, S. B., Patel, A. G., Hurley, R. M., Kaufmann, S. H., The elephant and the blind men: Making sense of PARP inhibitors in homologous recombination deficient tumor cells (2013) Front Oncol, 3, p. 228
Chou, T. C., Talaly, P., A simple generalized equation for the analysis of multiple inhibitions of Michaelis-Menten kinetic systems (1977) J Biol Chem, 252, pp. 6438-6442
Edge, S. B., Byrd, D. R., Compton, C. C., (2010) AJCC Cancer Staging Manual, pp. 253-270. , 7th ed. New York: Springer
Fong, P. C., Boss, D. S., Yap, T. A., Inhibition of poly (ADP-ribose) polymerase in tumors from BRCA mutation carriers (2009) N Engl J Med, 361, pp. 123-134
Bowden, N. A., Nucleotide excision repair: Why is it not used to predict response to platinum-based chemotherapy? (2014) Cancer Lett, 346, pp. 163-171
Lord, C. J., McDonald, S., Swift, S., A highthroughput RNA interference screen for DNA repair determinants of PARP inhibitor sensitivity (2008) DNA Repair (Amst), 7, pp. 2010-2019
Sandhu, S. K., Schelman, W. R., Wilding, G., The poly (ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: A phase 1 doseescalation trial (2013) Lancet Oncol, 14, pp. 882-892
Sowa, M. E., Bennett, E. J., Gygi, S. P., Harper, J. W., Defining the human deubiquitinating enzyme interaction landscape (2009) Cell, 138, pp. 389-403
Int J Cancer (ISSN: 0020-7136), 2015; 136(9): 2146-2157.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 5.531, 5-year impact factor: 5.624
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84923212201&partnerID=40&md5=066c625f3467714bce439e2bb26ec1c3
Keywords: Candidate Biomarker, Ccdc6, Dna Damage And Homologousdirected Repair, Nsclc, Resistance To Platinum Salts And Parp-1 Inhibitor Sensitivity, Dna Damage And Homologous-Directed Repair, Cisplatin, Coiled Coil Domain Containing 6 Protein, Olaparib, Rad51 Protein, Tumor Suppressor Protein, Unclassified Drug, Adult, Article, Cancer Resistance, Disease Association, Disease Free Survival, Dna Repair, Drug Mechanism, Drug Potentiation, Drug Sensitization, Female, Homologous Recombination, Human, Human Cell, Human Tissue, Immunohistochemistry, Lung Cancer Cell Line, Lymph Node Metastasis, Non Small Cell Lung Cancer, Overall Survival, Priority Journal, Protein Deficiency, Protein Expression, Tissue Microarray,
Affiliations:
*** IBB - CNR ***
Istituto per l'Endocrinologia e l'Oncologia Sperimentale Gaetano Salvatore, CNR, IEOS, Via Pansini, 5Naples, Italy
Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Universitá Federico IINapoli, Italy
Dipartimento di Scienze Biomediche Avanzate, Universitá Federico IINapoli, Italy
UOC Chirurgia Toracica, Azienda Ospedaliera di Rilievo Nazionale A.CardarelliNapoli, Italy
CEINGE-Biotecnologie AvanzateNapoli, Italy
UOC Anatomia Patologica e Citopatologia, ISNT Fondazione G. PascaleNapoli, Italy
Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, 237 Fulham RoadLondon, United Kingdom
Department of Molecular Biology and Microbiology, College of Medicine, University of Central FloridaOrlando, FL, United States
References:
Jemal, A., Siegel, R., Ward, E., Cancer statistics 2009 (2009) CA Cancer J Clin, 59, pp. 225-24
Andre, F., McShane, L.M., Michiels, S., Biomarker studies: A call for a comprehensive biomarker study registry (2011) Nat Rev Clin Oncol, 8, pp. 171-176
Curtin, N.J., DNA repair dysregulation from cancer driver to therapeutic target (2012) Nat Rev Cancer, 12, pp. 801-817
Lynch, T.J., Bell, D.W., Sordella, R., Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib (2004) N Engl J Med, 350, pp. 2129-2139
Camidge, D.R., Bang, Y.J., Kwak, E.L., Activity and safety of crizotinib in patients with ALKpositive non-small-cell lung cancer: Up dated results from a phase 1 study (2012) Lancet Oncol, 13, pp. 1011-1019
Okamoto, K., Kodama, K., Takase, K., Antitumor activities of the targeted multi-Tyrosine kinase inhibitor lenvatinib (E7080) against RET gene fusion-driven tumor models (2013) Cancer Lett, 340, pp. 97-103
Zeng-Rong, N., Paterson, J., Alpert, L., Elevated DNA repair capacity is associated with intrinsic resistance of lung cancer to chemotherapy (1995) Cancer Res, 55, pp. 4760-4764
Bosken, C.H., Wei, Q., Amos, C.I., Spitz, M.R., An analysis of DNA repair as a determinant of survival in patients with non-small-cell lung cancer (2002) J Natl Cancer Inst, 94, pp. 1091-1099
Duchesne, G.M., Fundamental bases of combined therapy in lung cancer: Cell resistance to chemotherapy and radiotherapy (1994) Lung Cancer, 10, pp. S67-S72
Guo, W.F., Lin, R.X., Huang, J., Identification of differentially expressed genes contributing to radioresistance in lung cancer cells using microarray analysis (2005) Radiat Res, 164, pp. 27-35
De Lorenzo, S.B., Patel, A.G., Hurley, R.M., Kaufmann, S.H., The elephant and the blind men: Making sense of PARP inhibitors in homologous recombination deficient tumor cells (2013) Front Oncol, 3, p. 228
Ashworth, A., A synthetic lethal therapeutic approach: Poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair (2008) J Clin Oncol, 26, pp. 3785-3790
Tentori, L., Graziani, G., Chemopotentiation by PARP inhibitors in cancer therapy (2005) Pharmacol Res, 52, pp. 25-33
Oplustilova, L., Wolanin, K., Mistrik, M., Evaluation of candidate biomarkers to predict cancer cell sensitivity or resistance to PARP-1 inhibitor treatment (2012) Cell Cycle, 11, pp. 3837-3850
Postel-Vinay, S., Bajrami, I., Friboulet, L., A high-Throughput screen identifies PARP1/2 inhibitors as a potential therapy for ERCC1-deficient non-small cell lung cancer (2013) Oncogene, 32, pp. 5377-5387
Celetti, A., Cerrato, A., Merolla, F., H4(D10S170), a gene frequently rearranged with RET in papillary thyroid carcinomas: Functional characterization (2004) Oncogene, 23, pp. 109-121
Merolla, F., Pentimalli, F., Pacelli, R., Involvement of H4(D10S170) protein in ATMdependent response to DNA damage (2007) Oncogene, 26, pp. 6167-6175
Merolla, F., Luise, C., Muller, M.T., Loss of CCDC6, the first identified RET partner gene, affects pH2AX S139 levels and accelerates mitotic entry upon DNA damage (2012) PLos ONE, 7, p. e36177
Grieco, M., Santoro, M., Berlingieri, M.T., PTC is a novel rearranged form of the RET protooncogene and is frequently detected in vivo in human thyroid papillary carcinomas (1990) Cell, 60, pp. 557-563
Drechsler, M., Hildebrandt, B., Kündgen, A., Fusion of H4/D10S170 to PDGFRbeta in a patient with chronic myelomonocytic leukemia and long-Term responsiveness to imatinib (2007) Ann Hematol, 86, pp. 353-354
Takeuchi, K., Soda, M., Togashi, Y., RET, ROS1 and ALK fusions in lung cancer (2012) Nat Med, 18, pp. 378-381
Imielinski, M., Berger, A.H., Hammerman, P.S., Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing (2012) Cell, 150, pp. 1107-1120
Matsubara, D., Kanai, Y., Ishikawa, S., Identification of CCDC6-RET fusion in the human lung adenocarcinoma cell line, LC-2/ad (2012) J Thorac Oncol, 7, pp. 1872-1876
Chou, T.C., Talaly, P., A simple generalized equation for the analysis of multiple inhibitions of Michaelis-Menten kinetic systems (1977) J Biol Chem, 252, pp. 6438-6442
Jasin, M., Genetic manipulation of genomes with rare-cutting endonucleases (1996) Trends Genet, 12, pp. 224-228
Staibano, S., Ilardi, G., Leone, V., Critical role of CCDC6 in the neoplastic growth of testicular germ cell tumors (2013) BMC Cancer, 13, pp. 433-444
Tutt, A., Bertwistle, D., Valentine, J., Mutation in Brca2 stimulates error-prone homologydirected repair of DNA double-strand breaks occurring between repeated sequences (2001) EMBO J, 20, pp. 4704-4716
Mao, Z., Bozzella, M., Seluanov, A., Gorbunova, V., Comparison of nonhomologous end joining and homologous recombination in human cells (2008) DNA Repair (Amst), 10, pp. 1765-1771
Edge, S.B., Byrd, D.R., Compton, C.C., (2010) AJCC Cancer Staging Manual, pp. 253-270. , 7th ed. New York: Springer
Farmer, H., McCabe, N., Lord, C.J., Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy (2005) Nature, 434, pp. 917-921
Cuozzo, C., Porcellini, A., Angrisano, T., DNA damage, homology-directed repair, and DNA methylation (2007) PLoS Genet, 3, p. e110
Lee, B., Kim, J., Taylor, M., Muller, M.T., DNA methyltransferase 1-Associated protein (DMAP1) is a co-repressor that stimulates DNA methylation globally and locally at sites of double strand DNA break repair (2010) J Biol Chem, 285, pp. 37630-37640
Lee, B., Morano, A., Porcellini, A., Muller, M.T., GADD45a inhibition of DNMT1 dependent DNA methylation during homology directed DNA repair (2011) Nucleic Acids Res, 40, pp. 2481-2493
Morano, A., Angrisano, T., Russo, G., Targeted DNA methylation by homology-directed repair in mammalian cells. Transcription reshapes methylation of the repaired gene (2014) Nucleic Acids Res, 42, pp. 804-821
Rottenberg, S., Jaspers, J.E., Kersbergen, A., High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs (2008) Proc Natl Acad Sci USA, 105, pp. 17079-17084
Fong, P.C., Boss, D.S., Yap, T.A., Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers (2009) N Engl J Med, 361, pp. 123-134
Tutt, A., Robson, M., Garber, J.E., Oral poly(-ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: A proof-of-concept trial (2010) Lancet, 376, pp. 235-244
Chang, A., Chemotherapy, chemoresistance and the changing treatment landscape for NSCLC (2012) Lung Cancer, 71, pp. 3-10
Birkelbach, M., Ferraiolo, N., Gheorghiu, L., Detection of impaired homologous recombination repair in NSCLC cells and tissues (2013) J Thorac Oncol, 8, pp. 279-286
Cheng, H., Zhang, Z., Borczuk, A., PARP inhibition selectively increases sensitivity to cisplatin in ERCC1-low non-small cell lung cancer cells (2013) Carcinogenesis, 34, pp. 739-749
Gridelli, C., Rossi, A., Di Maio, M., Rationale and design of MILES-3 and MILES-4 studies: Two randomized phase 3 trials comparing singleagent chemotherapy versus cisplatin-based doublets in elderly patients with advanced Non-Small-Cell Lung Cancer (2014) Clin Lung Cancer, 15, pp. 166-170
Bowden, N.A., Nucleotide excision repair: Why is it not used to predict response to platinum-based chemotherapy? (2014) Cancer Lett, 346, pp. 163-171
Lord, C.J., McDonald, S., Swift, S., A highthroughput RNA interference screen for DNA repair determinants of PARP inhibitor sensitivity (2008) DNA Repair (Amst), 7, pp. 2010-2019
Sandhu, S.K., Schelman, W.R., Wilding, G., The poly(ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: A phase 1 doseescalation trial (2013) Lancet Oncol, 14, pp. 882-892
Zhao, J., Tang, J., Men, W., Ren, K., FBXW7-mediated degradation of CCDC6 is impaired by ATM during DNA damage response in lung cancer cells (2012) FEBS, 586, pp. 4257-4263
Sowa, M.E., Bennett, E.J., Gygi, S.P., Harper, J.W., Defining the human deubiquitinating enzyme interaction landscape (2009) Cell, 138, pp. 389-403
Leone, V., Mansueto, G., Pierantoni, G.M., CCDC6 represses CREB1 activity by recruiting histone deacetylase 1 and protein phosphatase 1 (2010) Oncogene, 29, pp. 4341-4351
Jeannot, V., Busser, B., Brambilla, E., The PI3K/AKT pathway promotes gefitinib resistance in mutant KRAS lung adenocarcinoma by a deacetylase-dependent mechanism (2014) Int J Cancer, 134, pp. 2560-2571
Ciardiello, F., Tortora, G., EGFR antagonists in cancer treatment (2008) N Engl J Med, 13, pp. 1160-1174
Gerlinger, M., Rowan, A.J., Horswell, S., Intratumor heterogeneity and branched evolution revealed by multiregion sequencing (2012) N Engl J Med., 366, pp. 883-892
Curtin, N. J., DNA repair dysregulation from cancer driver to therapeutic target (2012) Nat Rev Cancer, 12, pp. 801-817
Lynch, T. J., Bell, D. W., Sordella, R., Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib (2004) N Engl J Med, 350, pp. 2129-2139
Camidge, D. R., Bang, Y. J., Kwak, E. L., Activity and safety of crizotinib in patients with ALKpositive non-small-cell lung cancer: Up dated results from a phase 1 study (2012) Lancet Oncol, 13, pp. 1011-1019
Bosken, C. H., Wei, Q., Amos, C. I., Spitz, M. R., An analysis of DNA repair as a determinant of survival in patients with non-small-cell lung cancer (2002) J Natl Cancer Inst, 94, pp. 1091-1099
Duchesne, G. M., Fundamental bases of combined therapy in lung cancer: Cell resistance to chemotherapy and radiotherapy (1994) Lung Cancer, 10, pp. S67-S72
Guo, W. F., Lin, R. X., Huang, J., Identification of differentially expressed genes contributing to radioresistance in lung cancer cells using microarray analysis (2005) Radiat Res, 164, pp. 27-35
De Lorenzo, S. B., Patel, A. G., Hurley, R. M., Kaufmann, S. H., The elephant and the blind men: Making sense of PARP inhibitors in homologous recombination deficient tumor cells (2013) Front Oncol, 3, p. 228
Chou, T. C., Talaly, P., A simple generalized equation for the analysis of multiple inhibitions of Michaelis-Menten kinetic systems (1977) J Biol Chem, 252, pp. 6438-6442
Edge, S. B., Byrd, D. R., Compton, C. C., (2010) AJCC Cancer Staging Manual, pp. 253-270. , 7th ed. New York: Springer
Fong, P. C., Boss, D. S., Yap, T. A., Inhibition of poly (ADP-ribose) polymerase in tumors from BRCA mutation carriers (2009) N Engl J Med, 361, pp. 123-134
Bowden, N. A., Nucleotide excision repair: Why is it not used to predict response to platinum-based chemotherapy? (2014) Cancer Lett, 346, pp. 163-171
Lord, C. J., McDonald, S., Swift, S., A highthroughput RNA interference screen for DNA repair determinants of PARP inhibitor sensitivity (2008) DNA Repair (Amst), 7, pp. 2010-2019
Sandhu, S. K., Schelman, W. R., Wilding, G., The poly (ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: A phase 1 doseescalation trial (2013) Lancet Oncol, 14, pp. 882-892
Sowa, M. E., Bennett, E. J., Gygi, S. P., Harper, J. W., Defining the human deubiquitinating enzyme interaction landscape (2009) Cell, 138, pp. 389-403
New therapeutic perspectives in CCDC6 deficient lung cancer cells
Non-small cell lung cancer (NSCLC) is the main cause of cancer-related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled-coildomain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index <1. Finally, CCDC6 is expressed at low levels in about 30% of the NSCL tumors we analyzed by TMA immunostaining. The weak CCDC6 protein staining is significatively correlated with the presence of lymph node metastasis (p≤0.02) and negatively correlated to the disease free survival (p≤0.01) and the overall survival (p≤0.05). Collectively, the data indicate that CCDC6 levels provide valuable insight for OS. CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC. © 2014 UICC.
Non-small cell lung cancer (NSCLC) is the main cause of cancer-related death worldwide and new therapeutic strategies are urgently needed. In this study, we have characterized a panel of NSC lung cancer cell lines for the expression of coiled-coildomain containing 6 (CCDC6), a tumor suppressor gene involved in apoptosis and DNA damage response. We show that low CCDC6 protein levels are associated with a weak response to DNA damage and a low number of Rad51 positive foci. Moreover, CCDC6 deficient lung cancer cells show defects in DNA repair via homologous recombination. In accordance with its role in the DNA damage response, CCDC6 attenuation confers resistance to cisplatinum, the current treatment of choice for NSCLC, but sensitizes the cells to olaparib, a small molecule inhibitor of the repair enzymes PARP1/2. Remarkably, the combination of the two drugs is more effective than each agent individually, as demonstrated by a combination index <1. Finally, CCDC6 is expressed at low levels in about 30% of the NSCL tumors we analyzed by TMA immunostaining. The weak CCDC6 protein staining is significatively correlated with the presence of lymph node metastasis (p≤0.02) and negatively correlated to the disease free survival (p≤0.01) and the overall survival (p≤0.05). Collectively, the data indicate that CCDC6 levels provide valuable insight for OS. CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC. © 2014 UICC.
New therapeutic perspectives in CCDC6 deficient lung cancer cells
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