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351 results on '"Cuffe, Sinead"'

105. P2.01-031 CCL Chemokines May Play an Important Role in Cisplatin Resistance

Author

Ryan, Sarah-Louise, primary, Godwin, Peter, additional, Heavey, Susan, additional, Umezawa, Kazuo, additional, Barr, Martin, additional, Gray, Steven, additional, Stanfill, Bryan, additional, Davies, Anthony, additional, Cuffe, Sinead, additional, Finn, Stephen, additional, Richard, Derek, additional, Gately, Kathy, additional, O’Byrne, Kenneth, additional, and Baird, Anne-Marie, additional

Published
2017
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106. P3.02c-030 Use of a 200-Mg Fixed Dose of Pembrolizumab for the Treatment of Advanced Non–Small Cell Lung Cancer (NSCLC)

Author

Garon, Edward, primary, Reck, Martin, additional, Rodríguez-Abreu, Delvys, additional, Robinson, Andrew, additional, Hui, Rina, additional, Tibor, Csőszi, additional, Fülöp, Andrea, additional, Gottfried, Maya, additional, Peled, Nir, additional, Tafreshi, Ali, additional, Cuffe, Sinead, additional, O'Brien, Mary, additional, Rao, Suman, additional, Hotta, Katsuyuki, additional, Turner, David, additional, Stone, Julie, additional, Rangwala, Reshma, additional, and Brahmer, Julie, additional

Published
2017
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107. P3.03-021 When RON MET TAM in Mesothelioma: All Druggable for One, and One Drug for All?

Author

Baird, Anne-Marie, primary, Easty, David, additional, Jarzabek, Monika, additional, Shiels, Liam, additional, Soltermann, Alex, additional, Raeppel, Stéphane, additional, Mcdonagh, Lauren, additional, Wu, Chengguang, additional, Goparju, Chandra, additional, Stanfill, Bryan, additional, Barr, Martin, additional, Nonaka, Daisuke, additional, Murer, Bruno, additional, Fennell, Dean, additional, O’Donnell, Dearbhaile, additional, Mutti, Luciano, additional, Finn, Stephen, additional, Cuffe, Sinead, additional, Pass, Harvey, additional, Schmitt-Opitz, Isabelle, additional, Byrne, Annette, additional, O’Byrne, Kenneth, additional, and Gray, Steven, additional

Published
2017
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108. PL04a.01: Health-Related Quality of Life for Pembrolizumab vs Chemotherapy in Advanced NSCLC with PD-L1 TPS ≥50%: Data from KEYNOTE-024

Author

Brahmer, Julie R., primary, Rodríguez-Abreu, Delvys, additional, Robinson, Andrew G., additional, Hui, Rina, additional, Csőszi, Tibor, additional, Fülöp, Andrea, additional, Gottfried, Maya, additional, Peled, Nir, additional, Tafreshi, Ali, additional, Cuffe, Sinead, additional, O’Brien, Mary, additional, Rao, Suman, additional, Hotta, Katsuyuki, additional, Deitz, Anne C., additional, Lubiniecki, Gregory M., additional, Zhang, Jin, additional, Rangwala, Reshma, additional, and Reck, Martin, additional

Published
2017
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111. In pursuit of synergy: An investigation of the PI3K/mTOR/MEK co-targeted inhibition strategy in NSCLC

Author

Heavey, Susan, Cuffe, Sinead, Finn, Stephen, Young, Vincent, Ryan, Ronan, Nicholson, Siobhan, Leonard, Niamh, McVeigh, Niall, Barr, Martin, O'Byrne, Ken, Gately, Kathy, Heavey, Susan, Cuffe, Sinead, Finn, Stephen, Young, Vincent, Ryan, Ronan, Nicholson, Siobhan, Leonard, Niamh, McVeigh, Niall, Barr, Martin, O'Byrne, Ken, and Gately, Kathy

Abstract

Clinical PI3K inhibition has been somewhat disappointing, due to both inadequate patient stratification and compensatory cell signalling through bypass mechanisms. As such, investigation of PI3K-MEK co-targeted inhibition has been recommended. With high mortality rates and a clear need for new therapeutic intervention strategies, non-small cell lung cancer (NSCLC) is an important setting to investigate the effectiveness of this approach. Here, 174 NSCLC tumours were screened for 150 mutations by Fluidigm technology, with 15 patients being profiled for phosphoprotein expression. The effects of GDC-0941 (a pan PI3K inhibitor), GDC-0980 (a dual PI3K/mTOR inhibitor) and GDC-0973 (a MEK inhibitor) alone and in combination were assessed in 3 NSCLC cell lines. PIK3CA was mutated in 5.17% of NSCLC patients. GDC-0941 and GDC-0980 treatment induced anti-proliferative and pro-apoptotic responses across all NSCLC cell lines, while GDC-0973 treatment induced only anti-proliferative responses. GDC-0980 and GDC-0973 combined treatment led to significant increases in apoptosis and synergistic reductions in proliferation across the panel of cell lines. This study found that the PI3K/MEK co-targeted inhibition strategy is synergistic in all 3 molecular subtypes of NSCLC investigated. Consequently, we would advocate clinical trials for NSCLC patients combining GDC-0980 and GDC-0973, each of which are separately under clinical investigation currently.

Published
2016

112. KAT5 (Tip60) is a potential therapeutic target in malignant pleural mesothelioma

Author

Cregan, Sian, McDonagh, Laura, Gao, Yun, Barr, Martin, O'Byrne, Ken, Finn, Stephen, Cuffe, Sinead, Gray, Steven, Cregan, Sian, McDonagh, Laura, Gao, Yun, Barr, Martin, O'Byrne, Ken, Finn, Stephen, Cuffe, Sinead, and Gray, Steven

Abstract

Malignant pleural mesothelioma (MPM) is a rare aggressive cancer of the pleura. Asbestos exposure (through inhalation) is the most well established risk factor for mesothelioma. The current standard of care for patients suffering from MPM is a combination of cisplatin and pemetrexed (or alternatively cisplatin and raltitrexed). Most patients, however, die within 24 months of diagnosis. New therapies are therefore urgently required for this disease. Lysine acetyltransferases (KATs) including KAT5 have been linked with the development of cisplatin resistance. This gene may therefore be altered in MPM and could represent a novel candidate target for intervention. Using RT-PCR screening the expression of all known KAT5 variants was found to be markedly increased in malignant tumors compared to benign pleura. When separated according to histological subtype, KAT5 was significantly overexpressed in both the sarcomatoid and biphasic subgroups for all transcript variants. A panel of MPM cell lines including the normal pleural cells LP9 and Met5A was screened for expression of KAT5 variants. Treatment of cells with a small molecule inhibitor of KAT5 (MG-149) caused significant inhibition of cellular proliferation (p<0.0001), induction of apoptosis and was accompanied by significant induction of pro-inflammatory cytokines/chemokines.

Published
2016

113. Pembrolizumab versus Chemotherapy for PD-L1–Positive Non–Small-Cell Lung Cancer

Author

Reck, Martin, primary, Rodríguez-Abreu, Delvys, additional, Robinson, Andrew G., additional, Hui, Rina, additional, Csőszi, Tibor, additional, Fülöp, Andrea, additional, Gottfried, Maya, additional, Peled, Nir, additional, Tafreshi, Ali, additional, Cuffe, Sinead, additional, O’Brien, Mary, additional, Rao, Suman, additional, Hotta, Katsuyuki, additional, Leiby, Melanie A., additional, Lubiniecki, Gregory M., additional, Shentu, Yue, additional, Rangwala, Reshma, additional, and Brahmer, Julie R., additional

Published
2016
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115. Abstract 269: The role of BRCA1 and AEG1 mRNA expression in advanced non-small-cell lung cancer (NSCLC) patients (p) with EGFR activating and pretreatment T790M mutations receiving the combination of erlotinib plus bevacizumab (E+B) in the BELIEF trial

Author

Rosell, Rafael, primary, Karachaliou, Niki, additional, Giménez-Capitán, Ana, additional, Codony-Servat, Carles, additional, Gautschi, Oliver, additional, Felip, Enriqueta, additional, Curioni-Fontecedro, Alessandra, additional, Peters, Solange, additional, Ponce-Aix, Santiago, additional, Früh, Martin, additional, Pless, Miklos, additional, Popat, Sanjay, additional, Cuffe, Sinead, additional, Bidoli, Paolo, additional, Favaretto, Adolfo, additional, Kammler, Roswitha, additional, Dafni, Urania, additional, Tsourti, Zoi, additional, Molina-Vila, Miguel Angel, additional, and Stahel, Rolf A., additional

Published
2016
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119. Identifying driver mutations in squamous cell lung cancer (SCC): The Lung Cancer Genomics Ireland (LCGI) study.

Author

Rafee, Shereen, primary, Toomey, Sinead, additional, Elamin, Yasir, additional, Carr, Aoife, additional, Gately, Kathy, additional, Finn, Stephen, additional, Nicholson, Siobhan, additional, Cuffe, Sinead, additional, Crown, John, additional, Morris, Patrick G., additional, Grogan, William, additional, Breathnach, Oscar S., additional, Kay, Elaine, additional, O'Grady, Anthony, additional, Hennessy, Bryan, additional, and O'Byrne, Kenneth, additional

Published
2015
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120. Cancer patients’ acceptability of incorporating an epidemiology questionnaire within a clinical trial

Author

Cuffe, Sinead, primary, Hon, Henrique, additional, Tobros, Kimberly, additional, Espin-Garcia, Osvaldo, additional, Brhane, Yonathan, additional, Harland, Luke, additional, Fadhel, Ehab, additional, Eng, Lawson, additional, LaDelfa, Anthony, additional, Waldron, John, additional, Siu, Lillian L, additional, Chen, Bingshu E, additional, Xu, Wei, additional, Simmons, Christine, additional, Kassam, Zahra, additional, Montenegro, Alexander, additional, Parulekar, Wendy R, additional, and Liu, Geoffrey, additional

Published
2015
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121. The role of DNA repair pathways in cisplatin resistant lung cancer

Author

O'Grady, Shane, Finn, Stephen, Cuffe, Sinead, Richard, Derek, O'Byrne, Ken, Barr, Martin, O'Grady, Shane, Finn, Stephen, Cuffe, Sinead, Richard, Derek, O'Byrne, Ken, and Barr, Martin

Abstract

Platinum chemotherapeutic agents such as cisplatin are currently used in the treatment of various malignancies such as lung cancer. However, their efficacy is significantly hindered by the development of resistance during treatment. While a number of factors have been reported that contribute to the onset of this resistance phenotype, alterations in the DNA repair capacity of damaged cells is now recognised as an important factor in mediating this phenomenon. The mode of action of cisplatin has been linked to its ability to crosslink purine bases on the DNA, thereby interfering with DNA repair mechanisms and inducing DNA damage. Following DNA damage, cells respond by activating a DNA-damage response that either leads to repair of the lesion by the cell thereby promoting resistance to the drug, or cell death via activation of the apoptotic response. Therefore, DNA repair is a vital target to improving cancer therapy and reduce the resistance of tumour cells to DNA damaging agents currently used in the treatment of cancer patients. To date, despite the numerous findings that differential expression of components of the various DNA repair pathways correlate with response to cisplatin, translation of such findings in the clinical setting are still warranted. The identification of alterations in specific proteins and pathways that contribute to these unique DNA repair pathways in cisplatin resistant cancer cells may potentially lead to a renewed interest in the development of rational novel therapies for cisplatin resistant cancers, in particular, lung cancer.

Published
2014

122. Cancer patients’ acceptance, understanding, and willingness-to-pay for pharmacogenomic testing

Author

Cuffe, Sinead, primary, Hon, Henrique, additional, Qiu, Xin, additional, Tobros, Kimberly, additional, Wong, Chung-Kwun Amy, additional, De Souza, Bradley, additional, McFarlane, Graham, additional, Masroor, Sohaib, additional, Azad, Abul K., additional, Hasani, Ekta, additional, Rozanec, Natalie, additional, Leighl, Natasha, additional, Alibhai, Shabbir, additional, Xu, Wei, additional, Issa, Amalia M., additional, and Liu, Geoffrey, additional

Published
2014
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123. Cancer patients’ acceptability of incorporating an epidemiology questionnaire within a clinical trial: A patient preference study and subanalysis of the NCIC clinical trials group HN.6 clinical trial.

Author

Cuffe, Sinead, primary, Hon, Henrique, additional, Tobros, Kimberly, additional, Espin-Garcia, Osvaldo, additional, Brhane, Yonathan, additional, Harland, Luke, additional, Fadhel, Ehab, additional, Eng, Lawson, additional, LaDelfa, Anthony, additional, Waldron, John N., additional, Chen, Bingshu E., additional, Xu, Wei, additional, Simmons, Christine E., additional, Kassam, Zahra, additional, Siu, Lillian L., additional, Montenegro, Alexander, additional, Parulekar, Wendy R., additional, and Liu, Geoffrey, additional

Published
2014
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125. Second-Hand Smoke As a Predictor of Smoking Cessation Among Lung Cancer Survivors

Author

Eng, Lawson, primary, Su, Jie, additional, Qiu, Xin, additional, Palepu, Prakruthi R., additional, Hon, Henrique, additional, Fadhel, Ehab, additional, Harland, Luke, additional, La Delfa, Anthony, additional, Habbous, Steven, additional, Kashigar, Aidin, additional, Cuffe, Sinead, additional, Shepherd, Frances A., additional, Leighl, Natasha B., additional, Pierre, Andrew F., additional, Selby, Peter, additional, Goldstein, David P., additional, Xu, Wei, additional, and Liu, Geoffrey, additional

Published
2014
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126. Brief Report on the Detection of the EGFRT790M Mutation in Exhaled Breath Condensate from Lung Cancer Patients

Author

Smyth, Robert J., Toomey, Sinead M., Sartori, Alexander, O'Hanrahan, Emer, Cuffe, Sinead D., Breathnach, Oscar S., Morgan, Ross K., and Hennessy, Bryan T.

Abstract

The EGFRT790M somatic mutation is the most common mechanism of resistance to tyrosine kinase inhibitors in NSCLC. Patients with advanced disease are not always amenable to repeat biopsy for further molecular analysis. Developing noninvasive methods to detect T790M in cell-free DNA in the absence of tissue is being actively investigated. Unfortunately, the low sensitivity of plasma for detection of T790M has limited its clinical use. Exhaled breath condensate (EBC) is an easily collected sample that is known to harbor cell-free DNA, including lung cancer mutations. This report details the potential utility of exhaled breath condensate in the detection of the EGFRT790M mutation.

Published
2018
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127. Overexpression of the mammalian target of rapamycin (mTOR) and angioinvasion are poor prognostic factors in early stage NSCLC: A verification study

Author

Gately, Kathy, Al-Alao, Bassel, Dhillon, Tony, Mauri, Francesco, Cuffe, Sinead, Seckl, Michael, O'Byrne, Kenneth, Gately, Kathy, Al-Alao, Bassel, Dhillon, Tony, Mauri, Francesco, Cuffe, Sinead, Seckl, Michael, and O'Byrne, Kenneth

Abstract

Background: A recent study by Dhillon et al. [12], identified both angioinvasion and mTOR as prognostic biomarkers for poor survival in early stage NSCLC. The aim of this study was to verify the above study by examining the angioinvasion and mTOR expression profile in a cohort of early stage NSCLC patients and correlate the results to patient clinico-pathological data and survival. Methods: Angioinvasion was routinely recorded by the pathologist at the initial assessment of the tumor following resection. mTOR was evaluated in 141 early stage (IA-IIB) NSCLC patients (67 - squamous; 60 - adenocarcinoma; 14 - others) using immunohistochemistry (IHC) analysis with an immunohistochemical score (IHS) calculated (% positive cells × staining intensity). Intensity was scored as follows: 0 (negative); 1+ (weak); 2+ (moderate); 3+ (strong). The range of scores was 0-300. Based on the previous study a cut-off score of 30 was used to define positive versus negative patients. The impact of angioinvasion and mTOR expression on prognosis was then evaluated. Results: 101 of the 141 tumors studied expressed mTOR. There was no difference in mTOR expression between squamous cell carcinoma and adenocarcinoma. Angioinvasion (p= 0.024) and mTOR staining (p= 0.048) were significant univariate predictors of poor survival. Both remained significant after multivariate analysis (p= 0.037 and p= 0.020, respectively). Conclusions: Our findings verify angioinvasion and mTOR expression as new biomarkers for poor outcome in patients with early stage NSCLC. mTOR expressing patients may benefit from novel therapies targeting the mTOR survival pathway. © 2011 Elsevier Ireland Ltd.

Published
2012

128. Cisplatin and gemcitabine in the management of metastatic penile cancer

Author

Power, D., Galvin, David, Cuffe, Sinead, McVey, Gerald, Mulholland, Paul, Farrelly, Cormac, Delaney, David, O'Byrne, Kenneth, Power, D., Galvin, David, Cuffe, Sinead, McVey, Gerald, Mulholland, Paul, Farrelly, Cormac, Delaney, David, and O'Byrne, Kenneth

Abstract

Penile cancer is rare and receives little public attention. There are few treatment options for advanced disease. The most active regimen to date is a combination of bleomycin, methotrexate, and cisplatin. However the treatment-related mortality is 11% and hence this combination has not been adapted as a standard of care. We report two cases of advanced penile cancer where a sustained palliative response was observed with combination chemotherapy using cisplatin and gemcitabine. Our experience demonstrates that this is a well tolerated regimen active in this setting. © 2009 Elsevier Inc. All rights reserved.

Published
2009

129. Assessment of accuracy of data obtained from patient-reported questionnaire (PRQ) compared to electronic patient records (EPR) in patients with lung cancer.

Author

Palepu, Prakruthi R., primary, Brown, Catherine, additional, Joshi, Gautam, additional, Epsin-Garcia, Osvaldo, additional, Eng, Lawson, additional, Ramanna, Jayalakshmi, additional, Hon, Henrique, additional, Momin, Salma, additional, Pringle, Dan, additional, Cuffe, Sinead, additional, Waddell, Thomas K., additional, Keshavjee, Shaf, additional, Darling, Gail Elizabeth, additional, Yasufuku, Kazuhiro, additional, de Perrot, Marc, additional, Pierre, Andrew, additional, Cypel, Marcelo, additional, Xu, Wei, additional, and Liu, Geoffrey, additional

Published
2013
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130. Willingness of patients to provide biologic samples for pharmacogenomic testing.

Author

Loo, Tenneille T., primary, Cuffe, Sinead, additional, Hon, Henrique, additional, Martin, Petra, additional, Brown, M Catherine, additional, Alibhai, Shabbir M.H., additional, Leighl, Natasha B., additional, Mascaux, Celine, additional, Tsao, Ming-Sound, additional, Shepherd, Frances A., additional, Qiu, Xin, additional, Xu, Wei, additional, and Liu, Geoffrey, additional

Published
2013
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131. Promoter polymorphisms of the SWI/SNF chromatin remodeling complex molecule, BRM, and esophageal adenocarcinoma outcome.

Author

Korpanty, Grzegorz, primary, Qiu, Xin, additional, Eng, Lawson, additional, Faluyi, Olusola Olusesan, additional, Cheng, Dangxiao, additional, Renouf, Daniel John, additional, Knox, Jennifer J., additional, Wong, Rebecca, additional, Darling, Gail, additional, Xu, Wei, additional, Dodbiba, Lorin, additional, Azad, Abul Kalam, additional, Reisman, David, additional, Cuffe, Sinead, additional, and Liu, Geoffrey, additional

Published
2013
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133. Effect of BRM promoter variants on survival outcomes of stage III-IV non-small cell lung cancer (NSCLC) patients.

Author

Cuffe, Sinead, primary, Cheng, Lu, additional, Azad, Abul Kalam, additional, Brhane, Yonathan, additional, Cheng, Dangxiao, additional, Chen, Zhuo, additional, Qiu, Xin, additional, Boyd, Kevin, additional, Emami, Marjan, additional, Leighl, Natasha B., additional, Der, Sandy, additional, Xu, Wei, additional, Shepherd, Frances A., additional, Tsao, Ming Sound, additional, Reisman, David, additional, and Liu, Geoffrey, additional

Published
2013
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135. Developing a comprehensive smoking cessation program in patients with lung cancer: The role of social smoking environments.

Author

Eng, Lawson, primary, Su, Jie, additional, Qiu, Xin, additional, Palepu, Prakruthi R., additional, Hon, Henrique, additional, Fadhel, Ehab, additional, Harland, Luke, additional, La Delfa, Anthony, additional, Habbous, Steven, additional, Kashigar, Aidin, additional, Cuffe, Sinead, additional, Leighl, Natasha B., additional, Pierre, Andrew, additional, Selby, Peter, additional, Goldstein, David P., additional, Liu, Geoffrey, additional, and Xu, Wei, additional

Published
2012
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136. Cancer patients’ and physicians’ preferences for decision making regarding pharmacogenomic testing (PGT).

Author

Cuffe, Sinead, primary, Hon, Henrique, additional, Qiu, Xin, additional, Masroor, Sohaib, additional, De Souza, Bradley, additional, McFarlane, Graham, additional, Wong, Chung-Kwun Amy, additional, Tobros, Kimberly, additional, Azad, Abul Kalam, additional, Hasani, Ekta, additional, Rozanec, Natalie, additional, Leighl, Natasha B., additional, Atehortua, Nelson A., additional, Alibhai, Shabbir M. H., additional, Xu, Wei, additional, Issa, Amalia M., additional, and Liu, Geoffrey, additional

Published
2012
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137. Use of iPad technology to determine cancer patient-reported preferences for and understanding of pharmacogenetic testing (PGT).

Author

Martin, Petra, primary, Brown, Catherine, additional, Cuffe, Sinead, additional, Pringle, Dan, additional, Mahler, Mary, additional, Villeneuve, Jodie, additional, Niu, Chongya, additional, Charow, Rebecca, additional, Lam, Christine, additional, Shani, Ravi M., additional, Hon, Henrique, additional, Otsuka, Memori, additional, Epsin-Garcia, Osvaldo, additional, Xu, Wei, additional, Alibbhai, Shabbir, additional, Jenkinson, Jodie, additional, and Liu, Geoffrey, additional

Published
2012
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138. Genetic sequence variant (GSV) in TERT-CLPTM1L (5p15.33 locus) and survival in platinum-treated stage-IV non-small cell lung cancer (NSCLC).

Author

Azad, Abul Kalam, primary, Qiu, Xiaoping, additional, Cuffe, Sinead, additional, Qiu, Xin, additional, Boyd, Kevin, additional, Kuang, Qin, additional, Emami, Marjan, additional, Perera, Nicole, additional, Palepu, Prakruthi R., additional, Patel, Devalben, additional, Chen, Zhuo, additional, Cheng, Dangxiao, additional, Feld, Ronald, additional, Leighl, Natasha B., additional, Shepherd, Frances A., additional, Tsao, Ming Sound, additional, Xu, Wei, additional, and Liu, Geoffrey, additional

Published
2012
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139. Cancer patient acceptance, understanding, and willingness to pay for pharmacogenetic testing (PGT).

Author

Hon, Henrique, primary, Qiu, Xin, additional, Tobros, Kimberly, additional, Wong, Chung-Kwun Amy, additional, De Souza, Bradley, additional, McFarlane, Graham, additional, Masroor, Sohaib, additional, Azad, Abul Kalam, additional, Hasani, Ekta, additional, Rozanec, Natalie, additional, Leighl, Natasha B., additional, Alibhai, Shabbir M.H., additional, Xu, Wei, additional, Issa, Amalia M., additional, Liu, Geoffrey, additional, and Cuffe, Sinead, additional

Published
2012
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140. Single nucleotide polymorphisms (SNPs) of the platinum pharmacogenetic and VEGF pathways: Association with survival of platinum-treated stage IV non-small cell lung cancer (NSCLC) patients.

Author

Cuffe, Sinead, primary, Qiu, Xiaoping, additional, Azad, Abul Kalam, additional, Qiu, Xin, additional, Boyd, Kevin, additional, Kuang, Qin, additional, Marsh, Sharon, additional, Savas, Sevtap, additional, Emami, Marjan, additional, Perera, Nicole, additional, Palepu, Prakruthi R., additional, Chen, Zhuo, additional, Patel, Devalben, additional, Cheng, Dangxiao, additional, Feld, Ronald, additional, Leighl, Natasha B., additional, Shepherd, Frances A., additional, Tsao, Ming Sound, additional, Xu, Wei, additional, and Liu, Geoffrey, additional

Published
2012
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141. Social environment as a predictor of smoking cessation and recidivism in lung cancer survivors.

Author

Eng, Lawson, primary, Su, Jie, additional, Palepu, Prakruthi R., additional, Hon, Henrique, additional, Fadhel, Ehab, additional, Harland, Luke, additional, La Delfa, Anthony, additional, Habbous, Steven, additional, Kashigar, Aidin, additional, Cuffe, Sinead, additional, Leighl, Natasha B., additional, Pierre, Andrew, additional, Goldstein, David P., additional, Liu, Geoffrey, additional, and Xu, Wei, additional

Published
2012
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143. Erlotinib and bevacizumab in patients with advanced non-small-cell lung cancer and activating EGFRmutations (BELIEF): an international, multicentre, single-arm, phase 2 trial

Author

Rosell, Rafael, Dafni, Urania, Felip, Enriqueta, Curioni-Fontecedro, Alessandra, Gautschi, Oliver, Peters, Solange, Massutí, Bartomeu, Palmero, Ramon, Aix, Santiago Ponce, Carcereny, Enric, Früh, Martin, Pless, Miklos, Popat, Sanjay, Kotsakis, Athanasios, Cuffe, Sinead, Bidoli, Paolo, Favaretto, Adolfo, Froesch, Patrizia, Reguart, Noemí, Puente, Javier, Coate, Linda, Barlesi, Fabrice, Rauch, Daniel, Thomas, Michael, Camps, Carlos, Gómez-Codina, Jose, Majem, Margarita, Porta, Rut, Shah, Riyaz, Hanrahan, Emer, Kammler, Roswitha, Ruepp, Barbara, Rabaglio, Manuela, Kassapian, Marie, Karachaliou, Niki, Tam, Rachel, Shames, David S, Molina-Vila, Miguel A, and Stahel, Rolf A

Abstract

The tyrosine kinase inhibitor erlotinib improves the outcomes of patients with advanced non-small-cell lung carcinoma (NSCLC) harbouring epidermal growth factor receptor (EGFR) mutations. The coexistence of the T790M resistance mutation with another EGFRmutation in treatment-naive patients has been associated with a shorter progression-free survival to EGFR inhibition than in the absence of the T790M mutation. To test this hypothesis clinically, we developed a proof-of-concept study, in which patients with EGFR-mutant NSCLC were treated with the combination of erlotinib and bevacizumab, stratified by the presence of the pretreatment T790M mutation.

Published
2017
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148. D7-06: Open Non-randomised Phase II Pilot Study of Neoadjuvant Cetuximab in combination with Cisplatin and Gemcitabine in patients with resectable Non-small Cell Lung Cancer

Author

Coate, Linda E., primary, Cuffe, Sinead, additional, McDowell, Dermot, additional, Gately, Kathy, additional, Barr, Martin, additional, Meaney, James, additional, O’Connell, Finbar, additional, Nicholson, Siobhan, additional, Young, Vincent, additional, and O’Byrne, Kenneth, additional

Published
2007
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149. The emerging role of microRNAs in resistance to lung cancer treatments.

Author

MacDonagh, Lauren, Gray, Steven G, Finn, Stephen P, Cuffe, Sinead, O'Byrne, Kenneth J, and Barr, Martin P

Abstract

One of the major challenges in the treatment of lung cancer is the development of drug resistance. This represents a major obstacle in the treatment of patients, limiting the efficacy of both conventional chemotherapy and biological therapies. Deciphering the mechanisms of resistance is critical to further understanding the multifactorial pathways involved, and in developing more specific targeted treatments. To date, numerous studies have reported the potential role of microRNAs (miRNAs) in resistance to various cancer treatments. MicroRNAs are a family of small non-coding RNAs that regulate gene expression by sequence-specific targeting of mRNAs causing translational repression or mRNA degradation. More than 1200 validated human miRNAs have been identified to date. While as little as one miRNA can regulate hundreds of targets, a single target can also be affected by multiple miRNAs. Evidence suggests that dysregulation of specific miRNAs may be involved in the acquisition of resistance to a number of cancer treatments, thereby modulating the sensitivity of cancer cells to such therapies. Therefore, targeting miRNAs may be an attractive strategy for developing novel and more effective individualized therapies, improving drug efficiency, and for predicting patient response to different treatments. In this review, we provide an overview on the role of miRNAs in resistance to current lung cancer therapies and novel biological agents. [ABSTRACT FROM AUTHOR]

Published
2015
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150. The role of DNA repair pathways in cisplatin resistant lung cancer.

Author

O’Grady, Shane, Finn, Stephen P., Cuffe, Sinead, Richard, Derek J., O’Byrne, Kenneth J., and Barr, Martin P.

Abstract

Platinum chemotherapeutic agents such as cisplatin are currently used in the treatment of various malignancies such as lung cancer. However, their efficacy is significantly hindered by the development of resistance during treatment. While a number of factors have been reported that contribute to the onset of this resistance phenotype, alterations in the DNA repair capacity of damaged cells is now recognised as an important factor in mediating this phenomenon. The mode of action of cisplatin has been linked to its ability to crosslink purine bases on the DNA, thereby interfering with DNA repair mechanisms and inducing DNA damage. Following DNA damage, cells respond by activating a DNA-damage response that either leads to repair of the lesion by the cell thereby promoting resistance to the drug, or cell death via activation of the apoptotic response. Therefore, DNA repair is a vital target to improving cancer therapy and reduce the resistance of tumour cells to DNA damaging agents currently used in the treatment of cancer patients. To date, despite the numerous findings that differential expression of components of the various DNA repair pathways correlate with response to cisplatin, translation of such findings in the clinical setting are still warranted. The identification of alterations in specific proteins and pathways that contribute to these unique DNA repair pathways in cisplatin resistant cancer cells may potentially lead to a renewed interest in the development of rational novel therapies for cisplatin resistant cancers, in particular, lung cancer. [ABSTRACT FROM AUTHOR]

Published
2014
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