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399 results on '"Cuffe, S."'

54. OA 17.06 Updated Analysis of KEYNOTE-024: Pembrolizumab vs Platinum-Based Chemotherapy for Advanced NSCLC With PD-L1 TPS ≥50%

Author

Brahmer, J., primary, Rodríguez-Abreu, D., additional, Robinson, A., additional, Hui, R., additional, Csőszi, T., additional, Fülöp, A., additional, Gottfried, M., additional, Peled, N., additional, Tafreshi, A., additional, Cuffe, S., additional, O'Brien, M., additional, Rao, S., additional, Hotta, K., additional, Riccio, A., additional, Yang, J., additional, Pietanza, M.C., additional, and Reck, M., additional

Published
2017
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55. MA 04.10 An Assessment of the Willingness to Provide Serial Bio-Specimens: Experience from an Irish Tertiary Cancer Centre

Author

Baird, A., primary, Keegan, N., additional, Barr, M., additional, Fishleder, S., additional, Idris, A., additional, Harrold, E., additional, O'Kelly, P., additional, Duff, E., additional, Lim, S., additional, O'Donnell, M., additional, Gallagher, D., additional, Grant, C., additional, Kennedy, J., additional, O'Donnell, D., additional, Sukor, S., additional, O'Brien, C., additional, Finn, S., additional, and Cuffe, S., additional

Published
2017
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57. P2.02-064 A Novel 5-miR Signature Shows Potential as a Diagnostic Tool and as a Predictive Biomarker of Cisplatin Response in NSCLC

Author

Donagh, L. Mac, primary, Gray, S., additional, Gallagher, M., additional, Ffrench, B., additional, Gasch, C., additional, Young, V., additional, Ryan, R., additional, Nicholson, S., additional, Leonard, N., additional, Finn, S., additional, Cuffe, S., additional, O’Byrne, K., additional, and Barr, M., additional

Published
2017
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58. P1.09-007 Targeting MET/TAM Receptors in Mesothelioma: Are Multi-TKIs Superior to Specific TKI?

Author

Gray, S., primary, Baird, A., additional, Easty, D., additional, Jarzabek, M., additional, Shiels, L., additional, Wu, C., additional, Soltermann, A., additional, Raeppel, S., additional, Macdonagh, L., additional, Melovic, M., additional, Lambkin, H., additional, Stanfill, B., additional, Nonaka, D., additional, Goparju, C., additional, Murer, B., additional, O'Donnell, D., additional, Mutti, L., additional, Barr, M., additional, Finn, S., additional, Cuffe, S., additional, Pass, H., additional, O’Byrne, K., additional, Schmitt-Opitz, I., additional, and Byrne, A., additional

Published
2017
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59. P2.02-069 Targeting Neuropilin-1 in NSCLC

Author

Barr, M., primary, Pidgeon, G., additional, Gray, S., additional, Gately, K., additional, Hams, E., additional, Fallon, P., additional, Cuffe, S., additional, Finn, S., additional, and O’Byrne, K., additional

Published
2017
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64. P1.09-006 JMJ and BRD Domain Family Members in Malignant Pleural Mesothelioma: Potential Therapeutic Targets or Not?

Author

Gray, S., primary, Breslin, M., additional, Cregan, S., additional, Quinn, L., additional, Wennstedt, S., additional, Singh, A., additional, Macdonagh, L., additional, Roche, G., additional, Gao, Y., additional, Albadri, C., additional, Griggs, K., additional, Kirschner, M., additional, O’Byrne, K., additional, Klebe, S., additional, Reid, G., additional, Finn, S., additional, and Cuffe, S., additional

Published
2017
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65. ICORG 10-14: NEOadjuvant trial in Adenocarcinoma of the oEsophagus and oesophagoGastric junction International Study (Neo-AEGIS)

Author

Reynolds, JV, primary, Preston, SR, additional, O’Neill, B, additional, Baeksgaard, L, additional, Griffin, SM, additional, Mariette, C, additional, Cuffe, S, additional, Cunningham, M, additional, Crosby, T, additional, Parker, I, additional, Hofland, K, additional, Hanna, G, additional, Svendsen, LB, additional, Donohoe, CL, additional, Muldoon, C, additional, O’Toole, D, additional, Johnson, C, additional, Ravi, N, additional, Jones, G, additional, Corkhill, AK, additional, Illsley, M, additional, Mellor, J, additional, Lee, K, additional, Dib, M, additional, Marchesin, V, additional, Cunnane, M, additional, Scott, K, additional, Lawner, P, additional, Warren, S, additional, O’Reilly, S, additional, O’Dowd, G, additional, Leonard, G, additional, Hennessy, B, additional, and Dermott, R Mc, additional

Published
2017
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67. Clinical utility of portable electrophysiology to measure fatigue in treatment-naïve non-small cell lung cancer.

Author

O'Connor, B., Walsh, D., Markicevic, M., Newman, L., Poduval, R. K., Reilly, R. B., Tiernan, E., Hanrahan, E., and Cuffe, S.

Subjects
NON-small-cell lung carcinoma, CANCER fatigue, FATIGUE (Physiology), MOTOR cortex
Abstract

Purpose: Cancer-related fatigue (CRF) biology remains poorly understood. Responsible mechanisms may be central or peripheral and originate anywhere from the brain to muscle fiber. Objective measurement is complex and previously limited to specialized laboratories. Portable electroencephalography (EEG) and electromyography (EMG) may enhance objective measurement. This study evaluated the feasibility and acceptability of portable EMG-EEG in CRF assessment.Methods: A prospective observational feasibility study compared ten outpatients with inoperable, treatment-naïve non-small cell lung cancer and CRF to ten healthy volunteers. All completed a sustained isometric hand-grip contraction at 30% maximal level until self-perceived exhaustion. 128-channel EEG and 2-channel EMG signals of forearm muscles were recorded. Device acceptability was evaluated by questionnaire.Results: The task was evaluated in two stages; first and last 20 s. CRF cohort perceived exhaustion earlier than volunteers (mean 137 ± 76 s vs 208 ± 51 s). As fatigue progressed, EMG amplitude increased significantly (CRF p = 0.02; volunteers: p = 0.04) in both groups as did EMG beta band power (CRF p = 0.008; volunteers: p = 0.006). The increase was significantly less in CRF (amplitude p = 0.032; beta power: p = 0.014). EEG beta band power in the contralateral motor cortex increased significantly (CRF p = 0.03; volunteers: p = 0.019) in both cohorts but to greater extent (p = 0.024) in CRF. One hundred percent device acceptability was reported.Conclusions: A laboratory-based evaluation was successfully adapted to the outpatient setting during routine visits. High acceptability supports clinical utility. In CRF, a higher degree of cortical activation was required to drive a much lower level of muscle performance. This suggests impairment of both central and peripheral mechanisms in CRF. [ABSTRACT FROM AUTHOR]

Published
2019
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68. 2: XRCC6BP1: A key player in cisplatin resistance and lung cancer stem cells

Author

Barr, M.P., Singh, S., Foley, E., He, Y., Young, V., Ryan, R., Nicholson, S., Leonard, N., O'Byrne, K.J., Cuffe, S., Finn, S., Barr, M.P., Singh, S., Foley, E., He, Y., Young, V., Ryan, R., Nicholson, S., Leonard, N., O'Byrne, K.J., Cuffe, S., and Finn, S.

Abstract

Alterations in the DNA repair capacity of damaged cells is now recognised as an important factor in mediating resistance to chemotherapeutic agents.

Published
2017

69. Multiple RTK targeting as a therapeutic option in malignant pleural mesothelioma

Author

Baird, A., Easty, D., Mohamed, B.M., Jarzabek, M., Shiels, L., Soltermann, A., Raeppel, S., McDonagh, L., Clarke, G., Crosbie-Staunton, K., Stanfill, B., Nonaka, D., Goparju, C.M., Prina-Mello, A., Volkov, Y., Murer, B., Fennell, D.A., O'Donnell, D.M., Mutti, L., Barr, M.P., Finn, S., Cuffe, S., Pass, H.I., Schmitt-Opitz, I., Byrne, A., O'Byrne, K.J., Gray, S.G., Baird, A., Easty, D., Mohamed, B.M., Jarzabek, M., Shiels, L., Soltermann, A., Raeppel, S., McDonagh, L., Clarke, G., Crosbie-Staunton, K., Stanfill, B., Nonaka, D., Goparju, C.M., Prina-Mello, A., Volkov, Y., Murer, B., Fennell, D.A., O'Donnell, D.M., Mutti, L., Barr, M.P., Finn, S., Cuffe, S., Pass, H.I., Schmitt-Opitz, I., Byrne, A., O'Byrne, K.J., and Gray, S.G.

Abstract

Malignant pleural mesothelioma (MPM) is an aggressive inflammatory cancer associated with exposure to asbestos. Untreated, MPM has a median survival time of 6 months,and most patients die within two years of diagnosis. There is an urgent need to identify new therapies for treating MPM patients.

Published
2017

70. ICORG 10-14:NEOadjuvant trial in Adenocarcinoma of the oEsophagus and oesophagoGastric junction International Study (Neo-AEGIS)

Author

Reynolds, J V, Preston, S R, O'Neill, B, Baeksgaard, L, Griffin, S M, Mariette, C, Cuffe, S, Cunningham, M, Crosby, T, Parker, I, Hofland, K, Hanna, G, Svendsen, L B, Donohoe, C L, Muldoon, C, O'Toole, D, Johnson, C, Ravi, N, Jones, G, Corkhill, A K, Illsley, M, Mellor, J, Lee, K, Dib, M, Marchesin, V, Cunnane, M, Scott, K, Lawner, P, Warren, S, O'Reilly, S, O'Dowd, G, Leonard, G, Hennessy, B, Dermott, R Mc, Reynolds, J V, Preston, S R, O'Neill, B, Baeksgaard, L, Griffin, S M, Mariette, C, Cuffe, S, Cunningham, M, Crosby, T, Parker, I, Hofland, K, Hanna, G, Svendsen, L B, Donohoe, C L, Muldoon, C, O'Toole, D, Johnson, C, Ravi, N, Jones, G, Corkhill, A K, Illsley, M, Mellor, J, Lee, K, Dib, M, Marchesin, V, Cunnane, M, Scott, K, Lawner, P, Warren, S, O'Reilly, S, O'Dowd, G, Leonard, G, Hennessy, B, and Dermott, R Mc

Abstract

BACKGROUND: Neoadjuvant therapy is increasingly the standard of care in the management of locally advanced adenocarcinoma of the oesophagus and junction (AEG). In randomised controlled trials (RCTs), the MAGIC regimen of pre- and postoperative chemotherapy, and the CROSS regimen of preoperative chemotherapy combined with radiation, were superior to surgery only in RCTs that included AEG but were not powered on this cohort. No completed RCT has directly compared neoadjuvant or perioperative chemotherapy and neoadjuvant chemoradiation. The Neo-AEGIS trial, uniquely powered on AEG, and including comprehensive modern staging, compares both these regimens.METHODS: This open label, multicentre, phase III RCT randomises patients (cT2-3, N0-3, M0) in a 1:1 fashion to receive CROSS protocol (Carboplatin and Paclitaxel with concurrent radiotherapy, 41.4Gy/23Fr, over 5 weeks). The power calculation is a 10% difference in favour of CROSS, powered at 80%, two-sided alpha level of 0.05, requiring 540 patients to be evaluable, 594 to be recruited if a 10% dropout is included (297 in each group). The primary endpoint is overall survival, with a minimum 3-year follow up. Secondary endpoints include: disease free survival, recurrence rates, clinical and pathological response rates, toxicities of induction regimens, post-operative pathology and tumour regression grade, operative in-hospital complications, and health-related quality of life. The trial also affords opportunities for establishing a bio-resource of pre-treatment and resected tumour, and translational research.DISCUSSION: This RCT directly compares two established treatment regimens, and addresses whether radiation therapy positively impacts on overall survival compared with a standard perioperative chemotherapy regimen Sponsor: Irish Clinical Research Group (ICORG).TRIAL REGISTRATION: NCT01726452 . Protocol 10-14. Date of registration 06/11/2012.

Published
2017

71. A phase II trial of erlotinib (E) and bevacizumab (B) in patients with advanced non-small-cell lung cancer (NSCLC) with activating epidermal growth factor receptor (EGFR) mutations with and without T790M mutation. The Spanish Lung Cancer Group (SLCG) and the European Thoracic Oncology Platform (ETOP) BELIEF trial

Author

Stahel, R. A. Dafni, U. Gautschi, O. Felip, E. and Curioni-Fontecedro, A. Peters, S. Massuti, B. Cardenal, F. and Aix, S. P. Frueh, M. Pless, M. Popat, S. Kotsakis, A. Cuffe, S. Bidoli, P. Favaretto, A. Carcereny, E. and Sanchez Ronco, M. Molina, M. A. Rosell, R.

Published
2015

72. 56: Multiple RTK targeting as a therapeutic option in malignant pleural mesothelioma

Author

Baird, A., primary, Easty, D., additional, Mohamed, B.M., additional, Jarzabek, M., additional, Shiels, L., additional, Soltermann, A., additional, Raeppel, S., additional, McDonagh, L., additional, Clarke, G., additional, Crosbie-Staunton, K., additional, Stanfill, B., additional, Nonaka, D., additional, Goparju, C.M., additional, Prina-Mello, A., additional, Volkov, Y., additional, Murer, B., additional, Fennell, D.A., additional, O'Donnell, D.M., additional, Mutti, L., additional, Barr, M.P., additional, Finn, S., additional, Cuffe, S., additional, Pass, H.I., additional, Schmitt-Opitz, I., additional, Byrne, A., additional, O'Byrne, K.J., additional, and Gray, S.G., additional

Published
2017
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77. 70P Identification of a novel microRNA signature: Potential diagnostic biomarkers and predictors of cisplatin response?

Author

Barr, M.P., MacDonagh, L., Gray, S.G., Reidy, M., Sui, J. Sze Yin, Nicholson, S., Leonard, N., O'Byrne, K., Cuffe, S., Finn, S., Barr, M.P., MacDonagh, L., Gray, S.G., Reidy, M., Sui, J. Sze Yin, Nicholson, S., Leonard, N., O'Byrne, K., Cuffe, S., and Finn, S.

Abstract

Background In addition to their involvement in mechanisms underlying cancer initiation and progression, emerging evidence has highlighted a key role for microRNAs in resistance to a number of anti-cancer therapies. Methods MicroRNA profiling and validation was carried out on a panel of age-matched parent (PT) and cisplatin resistant (CisR) NSCLC cell lines using 7th generation miRCURY LNA™ arrays (Exiqon). Transient transfections were used to either inhibit or over-express these microRNAs using antagomirs or pre-miRs, respectively. The effects of modulating these miRNAs on cell proliferation, apoptosis and clonogenic survival were examined in response to cisplatin. The translational relevance of these miRNAs in lung cancer was confirmed in a cohort of chemo-naïve matched normal and tumour lung tissues and sera from NSCLC patients. MicroRNAs were also assessed in mouse xenograft FFPE tissues from H460 CisR-derived ALDH1+ and ALDH1– cancer stem cell subpopulations. Results A 5-miRNA signature consisting of members of the miR-30 family, miR-34a and miR-4286 was identified and validated. MicroRNAs were significantly up-regulated in all CisR cell lines relative to their parental counterparts, in contrast to miR-4286 which was significantly down-regulated. Inhibition of the miR-30 family and miR-34a and forced over-expression of miR-4286 significantly reduced the clonogenic survival ability of CisR cells in response to cisplatin. The miR-30 family was significantly decreased in AD and SCC tissues. MiR-34a expression was significantly lower in SCC tissues while miR-4286 levels were significantly increased in AD tissues only. A significant-fold increase in miR-4286 was found in sera from SCC lung cancer patients. Similar to that found at the in vitro level, the miR-30 family and miR-34a were up-regulated in mouse xenograft FFPE tissues derived from CisR and PT cell lines in vivo. Conclusions In this study, a 5-microRNA signature was identified using an in vitro model of cis

Published
2016

78. 75P inhibition and exploitation of aldehyde dehydrogenase 1 (ALDH1) as a cancer stem cell marker in cisplatin resistant NSCLC

Author

Barr, M.P., MacDonagh, L., Gray, S.G., O'Byrne, K., Cuffe, S., Finn, S., Barr, M.P., MacDonagh, L., Gray, S.G., O'Byrne, K., Cuffe, S., and Finn, S.

Abstract

Background The root of therapeutic resistance is hypothesized to be due to the presence of a rare CSC population within the tumour population. When challenged with chemotherapy, this tumour cell subset survives the insult and has the potential to recapitulate a heterogenic tumour. Aldehyde dehydrogenase 1 (ALDH1) is involved in the catalytic conversion of vitamin A (retinol) to retinoic acid and has been identified as a CSC marker in a number of solid malignancies. Methods FACS analysis of an isogenic panel of matched parent (PT) and cisplatin resistant (CisR) NSCLC cell lines of different histologies was used to examine ALDH1 activity. The H460 CisR subline was FACS-sorted (MoFlo®) into ALDH1-positive and ALDH1-negative fractions and subcutaneously injected into NOD/SCID mice to assess tumour initiation and growth. The effects of inhibiting ALDH1 on cell proliferation (BrdU), apoptosis (Annexin-V/propidium iodide) and colony formation (crystal violet) in PT and CisR cell lines was assessed in vitro using two ALDH1 inhibitors, DEAB (N,N-diethylaminobenzaldehyde) and disulfiram (Antabuse), alone and in combination with cisplatin. Lung cancer cells were treated with retinol and All-trans retinoic acid (ATRA) to exploit the role of ALDH1 in the vitamin A/retinoic acid axis in NSCLC. Results ALDH1 activity was significantly increased in all CisR cell lines relative to their parental counterparts in which little or no ALDH1 expression was detected. Xenograft studies using ALDH1+ and ALDH1– fractions from H460 CisR cells showed no significant difference in tumour growth in mice. ALDH1 inhibition, in combination with cisplatin, significantly decreased cell viability, proliferation and clonogenic survival of CisR sublines only and increased apoptotic cell death compared to cells treated with cisplatin alone. Similarly, treatment of cells with retinol or ATRA, in combination with cisplatin, showed similar re-sensitizing effects.

Published
2016

79. 437O KEYNOTE-024: Pembrolizumab (pembro) vs platinum-based chemotherapy (chemo) as first-line therapy for advanced NSCLC with a PD-L1 tumor proportion score (TPS) ≥50%

Author

Reck, M., primary, Rodríguez-Abreu, D., additional, Robinson, A., additional, Hui, R., additional, Csoszi, T., additional, Fülöp, A., additional, Gottfried, M., additional, Peled, N., additional, Tafreshi, A., additional, Cuffe, S., additional, O'Brien, M.E., additional, Rao, S., additional, Hotta, K., additional, Leiby, M., additional, Lubiniecki, G., additional, Shentu, Y., additional, Rangwala, R., additional, and Brahmer, J., additional

Published
2016
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80. Insomnia prevalence in an oncology patient population: an Irish tertiary referral centre experience

Author

Harrold, E.C., primary, Idris, A.F., additional, Keegan, N.M., additional, Corrigan, L., additional, Teo, M.Y., additional, Lim, S.T., additional, Duff, E., additional, Donnell, M.O., additional, Kennedy, J., additional, O'Donnell, D., additional, Sukor, S., additional, Grant, C., additional, Gallagher, D., additional, Collier, S., additional, Kingston, T., additional, O'Dwyer, A.M., additional, and Cuffe, S., additional

Published
2016
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81. KEYNOTE-024: Pembrolizumab (pembro) vs platinum-based chemotherapy (chemo) as first-line therapy for advanced NSCLC with a PD-L1 tumor proportion score (TPS) ≥50%

Author

Reck, M., primary, Rodríguez-Abreu, D., additional, Robinson, A.G., additional, Hui, R., additional, Csoszi, T., additional, Fülöp, A., additional, Gottfried, M., additional, Peled, N., additional, Tafreshi, A., additional, Cuffe, S., additional, O'Brien, M., additional, Rao, S., additional, Hotta, K., additional, Leiby, M., additional, Lubiniecki, G.M., additional, Shentu, Y., additional, Rangwala, R., additional, and Brahmer, J.R., additional

Published
2016
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99. 86 When RON MET TAM: potential interventions for mesothelioma therapy

Author

Baird, A., primary, Easty, D., additional, Mohamed, B.M., additional, Jarzabek, M.A., additional, Sheils, L., additional, Soltermann, A., additional, Raeppel, S., additional, Mcdonagh, L., additional, Clarke, G., additional, Crosbie-Staunton, K., additional, Stanfill, B., additional, Nonaka, D., additional, Goparju, C.M., additional, Prina-Mello, A., additional, Volkov, Y., additional, Murer, B., additional, Fennell, D., additional, O'Donnell, D.M., additional, Mutti, L., additional, Barr, M.P., additional, Finn, S.P., additional, Cuffe, S., additional, Pass, H.I., additional, Schmitt-Opitz, J., additional, Byrne, A.T., additional, O'Byrne, K.J., additional, and Gray, S.G., additional

Published
2016
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