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2. Contributors

Author

Abbas, Ghulam, primary, Adelstein, David J., additional, Aigner, Clemens, additional, Alifano, Marco, additional, Allen, Mark S., additional, Altorki, Nasser K., additional, Andrade, Rafael S., additional, Andritsos, Michael J., additional, Arruda, M. Janine, additional, Ashiku, Simon K., additional, Ashrafi, Ahmad S., additional, Backer, Carl Lewis, additional, Bains, Majit S., additional, Baker, Mark E., additional, Banki, Farzaneh, additional, Bartlett, Nancy L., additional, Battafarano, Richard J., additional, Beauchamp, Gilles, additional, Bello, Ricardo A., additional, Bennett, W. Fred, additional, Bergeron, Michel G., additional, Bergeron, Yves, additional, Bhalla, Sanjeev, additional, Bizekis, Costas, additional, Boland, Brendan J., additional, Bousamra, Michael, additional, Bradley, Jeffrey D., additional, Brandolino, Mario, additional, Bredenberg, Carl E., additional, Bremner, Ross M., additional, Bronner, Mary P., additional, Bryant, Ayesha, additional, Burack, Joshua H., additional, Burgos, Raul, additional, Bussières, Jean S., additional, Campos, Javier H., additional, Cannie, Mieke, additional, Cassivi, Stephen D., additional, Casson, Alan G., additional, Castedo, Evaristo, additional, Cerfolio, Robert James, additional, Cetindag, Ibrahim Bulent, additional, Chelly, Jacques E., additional, Chiu, Priscilla, additional, Christie, Neil A., additional, Chung, Andy T.A., additional, Claytor, R. Brannon, additional, Cooper, Joel D., additional, Costantini, Mario, additional, Courcoulas, Anita P., additional, D'Amico, Thomas A., additional, Darling, Gail, additional, Dartevelle, Philippe, additional, de Hoyos, Alberto, additional, de Perrot, Marc, additional, De Wet, Charl J., additional, Debeer, Anne, additional, DeCamp, Malcolm M., additional, Dehdashti, Farrokh, additional, DeMeester, Steven R., additional, DeMeester, Tom R., additional, Deprest, Jan, additional, Deschamps, Claude, additional, Deslauriers, Jean, additional, Detterbeck, Frank C., additional, Díaz, Ismael A. Conti, additional, Doné, Elise, additional, Doody, Daniel P., additional, Downey, Gregory P., additional, Downey, Robert J., additional, Ducko, Christopher T., additional, Dumot, John A., additional, Duncan, Brian W., additional, Duranceau, André, additional, Edmundowicz, Steven A., additional, Einstein, David M., additional, Ellis, F. Henry, additional, Fadel, Elie, additional, Fell, Stanley C., additional, Fenske, Timothy S., additional, Ferguson, Mark K., additional, Fernandez, Felix G., additional, Fernando, Hiran C., additional, Ferraro, Pasquale, additional, Ferri, Lorenzo E., additional, Ferson, Peter F., additional, Finks, Jonathan F., additional, Finley, Richard J., additional, Flores, Raja M., additional, Fokin, Alexander A., additional, Fortin, Dalilah, additional, Fréchette, Éric, additional, Gaissert, Henning A., additional, Gamliel, Ziv, additional, Gandhi, Sanjiv K., additional, Ghefter, Mario C., additional, Gierada, David S., additional, Gilbert, Sebastien, additional, Goldstein, Allan M., additional, Govindan, Ramaswamy, additional, Graeber, Geoffrey M., additional, Grégoire, Jocelyn, additional, Griffin, Noreen, additional, Grillo, Hermes C., additional, Grunenwald, Dominique, additional, Gucciardo, Leonardo, additional, Gullane, Patrick J., additional, Hagen, Jeffrey A., additional, Lee Hall, Bruce, additional, Hantler, Charles, additional, Harpole, David H., additional, Harrison-Phipps, Karen, additional, Haughey, Bruce H., additional, Haustermans, Karin, additional, Hazelrigg, Stephen R., additional, Henschke, Claudia I., additional, Herridge, Margaret S., additional, Hiebert, Clement A., additional, Holinger, Lauren, additional, Hölscher, Arnulf H., additional, Hoover, Susan J., additional, Huang, Jasmine, additional, Huddleston, Charles B., additional, Hunter, John G., additional, Iannettoni, Mark D., additional, Ilson, David H., additional, Inculet, Richard I., additional, Irshad, Kashif, additional, Jacobsohn, Eric, additional, Jani, Jacques, additional, Javidan-Nejad, Cylen, additional, Jones, David R., additional, Jones, William G., additional, Jurkovich, Gregory, additional, Kaiser, Larry R., additional, Karmy-Jones, Riyad, additional, Keller, Steven M., additional, Kent, Michael S., additional, Keshavjee, Shaf, additional, Kesler, Kenneth A., additional, Klepetko, Walter, additional, Konstantakos, Anastasios, additional, Korst, Robert J., additional, Kozower, Benjamin D., additional, Krakovitz, Paul, additional, Krasna, Mark J., additional, Kreisel, Daniel, additional, Krishna, Priya D., additional, Krupnick, Alexander S., additional, Kucharczuk, John C., additional, Kwong, King F., additional, Landreneau, Rodney J., additional, Lang, Florian, additional, Langer, Jacob C., additional, Lara-Guerra, Humberto, additional, Lardinois, Didier, additional, Law, Simon, additional, Lefrak, Stephen S., additional, Leighl, Natasha B., additional, Leo, Francesco, additional, Lerut, Antoon (Toni) E.M.R., additional, Liebermann-Meffert, Dorothea, additional, Linden, Philip A., additional, Litle, Virginia R., additional, Little, Sherard, additional, Locadia, Mirjam, additional, Losso, Luis C., additional, Louie, Brian E., additional, Low, Donald E., additional, Luketich, James D., additional, Lundell, Lars, additional, Lutey, Barbara A., additional, Macchiarini, Paolo, additional, Mackinnon, Susan E., additional, Maddaus, Michael A., additional, Malthaner, Richard A., additional, Mason, David P., additional, Mathisen, Douglas J., additional, Mattioli, Sandro, additional, Mavroudis, Constantine, additional, Maziak, Donna E., additional, Mazur, Paul, additional, McLoud, Theresa, additional, McRae, Karen M., additional, Mehran, Reza John, additional, Mekhail, Tarek, additional, Merritt, Robert E., additional, Meyers, Bryan F., additional, Meyerson, Shari L., additional, Miller, Daniel L., additional, Miller, Joseph I., additional, Mineo, Tommaso C., additional, Minsky, Bruce D., additional, Moley, Jeffrey, additional, Monnier, Philippe, additional, Montano, Rachel, additional, Moreira, Andre L., additional, Morse, Christopher R., additional, Mouroux, Jérôme, additional, Müller, Nestor L., additional, Mulligan, Michael, additional, Murthy, Sudish C., additional, Naunheim, Keith, additional, Nelems, Bill, additional, Ng, Calvin S.H., additional, Nguyen, Ninh T., additional, Nichols, Francis C., additional, Novak, Christine B., additional, Odell, Michael J., additional, Ollyo, Jean-Baptiste, additional, Onaitis, Mark W., additional, Onders, Raymond P., additional, Ong, Sharon, additional, Orringer, Mark B., additional, Ouellette, Denise, additional, Pairolero, Peter C., additional, Papsin, Blake C., additional, Park, Bernard J., additional, Parsons, Alden M., additional, Partrick, David A., additional, Pasche, Philippe, additional, Pastorino, Ugo, additional, Patel, Amit N., additional, Patterson, G. Alexander, additional, Pearson, F. Griffith, additional, Peitzman, Andrew B., additional, Pennathur, Arjun, additional, Pera, Manuel, additional, Peracchia, Alberto, additional, Pereira, Sérgio Tadeu L.F., additional, Peters, Jeffrey H., additional, Pettiford, Brian, additional, Phillips, Kacy, additional, Pierre, Andrew F., additional, Pompeo, Eugenio, additional, Pop, Daniel, additional, Poylin, Vitaliy, additional, Propst, Evan J., additional, Putnam, Joe B., additional, Qadeer, Mohammed A., additional, Raghu, Ganesh, additional, Rayyan, Maissa, additional, Razzuk, Linda M., additional, Razzuk, Maruf A., additional, Rendina, Erino A., additional, Rice, Thomas W., additional, Richter, Joel E., additional, Ritter, Jon H., additional, Rizk, Nabil P., additional, Robicsek, Francis, additional, Rocco, Gaetano, additional, Rosati, Riccardo, additional, Rosen, Clark A., additional, Rusch, Valerie W., additional, Salzman, Steve H., additional, Sampliner, Richard E., additional, Savary, Marcel, additional, Sbragia, Lourenço, additional, Schipper, Paul H., additional, Schrump, David S., additional, Sciurba, Frank C., additional, Shepherd, Frances A., additional, Shrager, Joseph B., additional, Siegel, Barry A., additional, Sihoe, Alan D.L., additional, Singhal, Sunil, additional, Slinger, Peter D., additional, Smith, Philip W., additional, Soper, Nathaniel J., additional, Souza, Carolina A., additional, Sprangers, Mirjam A.G., additional, Stewart, Robert D., additional, Stroobants, Sigrid G., additional, Sugarbaker, David J., additional, Sullivan, Erin A., additional, Sundaresan, Sudhir R., additional, Swanström, Lee L., additional, Temes, R. Thomas, additional, Tronc, François, additional, Ugalde, Paula A., additional, Urschel, Harold C., additional, Vaezi, Michael F., additional, Vallières, Eric, additional, van Berge Henegouwen, Mark I., additional, Van de Velde, Marc, additional, van Lanschot, Jan J.B., additional, Van Mieghem, Tim, additional, Van Natta, Timothy L., additional, Van Schoubroeck, Dominique, additional, Varela, Andrés, additional, Veeramachaneni, Nirmal K., additional, Venissac, Nicolas, additional, Venuta, Federico, additional, Videtic, Gregory M.M., additional, Vivó, Jorge Nin, additional, Waddell, Thomas K., additional, Walsh, Garrett L., additional, Warren, William H., additional, Waters, Paul F., additional, Watson, Thomas J., additional, Watts, Larry T., additional, Weder, Walter, additional, Wick, Mark R., additional, Wigle, Dennis A., additional, Wildes, Troy S., additional, Wilkins, Earl Wayne, additional, Withers, H. Rodney, additional, Witterick, Ian, additional, Wizorek, Joseph J., additional, Wong, John, additional, Wood, Douglas E., additional, Wright, Cameron D., additional, Wrightson, William, additional, Ximenes-Netto, Manoel, additional, Yang, Steve, additional, Yankelevitz, David F., additional, Yazbeck, Salam, additional, Yim, Anthony P.C., additional, Zakowski, Maureen, additional, and Zuccaro, Gregory, additional

Published
2008
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3. Polymorphisms Near TBX5 and GDF7 Are Associated With Increased Risk for Barrett’s Esophagus

Author

Palles, Claire, Chegwidden, Laura, Li, Xinzhong, Findlay, John M., Farnham, Garry, Castro Giner, Francesc, Peppelenbosch, Maikel P., Kovac, Michal, Adams, Claire L., Prenen, Hans, Briggs, Sarah, Harrison, Rebecca, Sanders, Scott, MacDonald, David, Haigh, Chris, Tucker, Art, Love, Sharon, Nanji, Manoj, deCaestecker, John, Ferry, David, Rathbone, Barrie, Hapeshi, Julie, Barr, Hugh, Moayyedi, Paul, Watson, Peter, Zietek, Barbara, Maroo, Neera, Gay, Laura, Underwood, Tim, Boulter, Lisa, McMurtry, Hugh, Monk, David, Patel, Praful, Ragunath, Krish, Al Dulaimi, David, Murray, Iain, Koss, Konrad, Veitch, Andrew, Trudgill, Nigel, Nwokolo, Chuka, Rembacken, Bjorn, Atherfold, Paul, Green, Elaine, Ang, Yeng, Kuipers, Ernst J., Chow, Wu, Paterson, Stuart, Kadri, Sudarshan, Beales, Ian, Grimley, Charles, Mullins, Paul, Beckett, Conrad, Farrant, Mark, Dixon, Andrew, Kelly, Sean, Johnson, Matthew, Wajed, Shahjehan, Dhar, Anjan, Sawyer, Elinor, Roylance, Rebecca, Onstad, Lynn, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Bird, Nigel C., Hardie, Laura J., Reid, Brian J., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Casson, Alan G., Fitzgerald, Rebecca, Whiteman, David C., Risch, Harvey A., Levine, David M., Vaughan, Tom L., Verhaar, Auke P., van den Brande, Jan, Toxopeus, Eelke L., Spaander, Manon C., Wijnhoven, Bas P.L., van der Laan, Luc J.W., Krishnadath, Kausilia, Wijmenga, Cisca, Trynka, Gosia, McManus, Ross, Reynolds, John V., O’Sullivan, Jacintha, MacMathuna, Padraic, McGarrigle, Sarah A., Kelleher, Dermot, Vermeire, Severine, Cleynen, Isabelle, Bisschops, Raf, Tomlinson, Ian, Jankowski, Janusz, Palles, Claire, Chegwidden, Laura, Li, Xinzhong, Findlay, John M., Farnham, Garry, Castro Giner, Francesc, Peppelenbosch, Maikel P., Kovac, Michal, Adams, Claire L., Prenen, Hans, Briggs, Sarah, Harrison, Rebecca, Sanders, Scott, MacDonald, David, Haigh, Chris, Tucker, Art, Love, Sharon, Nanji, Manoj, deCaestecker, John, Ferry, David, Rathbone, Barrie, Hapeshi, Julie, Barr, Hugh, Moayyedi, Paul, Watson, Peter, Zietek, Barbara, Maroo, Neera, Gay, Laura, Underwood, Tim, Boulter, Lisa, McMurtry, Hugh, Monk, David, Patel, Praful, Ragunath, Krish, Al Dulaimi, David, Murray, Iain, Koss, Konrad, Veitch, Andrew, Trudgill, Nigel, Nwokolo, Chuka, Rembacken, Bjorn, Atherfold, Paul, Green, Elaine, Ang, Yeng, Kuipers, Ernst J., Chow, Wu, Paterson, Stuart, Kadri, Sudarshan, Beales, Ian, Grimley, Charles, Mullins, Paul, Beckett, Conrad, Farrant, Mark, Dixon, Andrew, Kelly, Sean, Johnson, Matthew, Wajed, Shahjehan, Dhar, Anjan, Sawyer, Elinor, Roylance, Rebecca, Onstad, Lynn, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Bird, Nigel C., Hardie, Laura J., Reid, Brian J., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Casson, Alan G., Fitzgerald, Rebecca, Whiteman, David C., Risch, Harvey A., Levine, David M., Vaughan, Tom L., Verhaar, Auke P., van den Brande, Jan, Toxopeus, Eelke L., Spaander, Manon C., Wijnhoven, Bas P.L., van der Laan, Luc J.W., Krishnadath, Kausilia, Wijmenga, Cisca, Trynka, Gosia, McManus, Ross, Reynolds, John V., O’Sullivan, Jacintha, MacMathuna, Padraic, McGarrigle, Sarah A., Kelleher, Dermot, Vermeire, Severine, Cleynen, Isabelle, Bisschops, Raf, Tomlinson, Ian, and Jankowski, Janusz

Abstract

Background & Aims Barrett's esophagus (BE) increases the risk of esophageal adenocarcinoma (EAC). We found the risk to be BE has been associated with single nucleotide polymorphisms (SNPs) on chromosome 6p21 (within the HLA region) and on 16q23, where the closest protein-coding gene is FOXF1. Subsequently, the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON) identified risk loci for BE and esophageal adenocarcinoma near CRTC1 and BARX1, and within 100 kb of FOXP1. We aimed to identify further SNPs that increased BE risk and to validate previously reported associations. Methods We performed a genome-wide association study (GWAS) to identify variants associated with BE and further analyzed promising variants identified by BEACON by genotyping 10,158 patients with BE and 21,062 controls. Results We identified 2 SNPs not previously associated with BE: rs3072 (2p24.1; odds ratio [OR] = 1.14; 95% CI: 1.09–1.18; P = 1.8 × 10−11) and rs2701108 (12q24.21; OR = 0.90; 95% CI: 0.86–0.93; P = 7.5 × 10−9). The closest protein-coding genes were respectively GDF7 (rs3072), which encodes a ligand in the bone morphogenetic protein pathway, and TBX5 (rs2701108), which encodes a transcription factor that regulates esophageal and cardiac development. Our data also supported in BE cases 3 risk SNPs identified by BEACON (rs2687201, rs11789015, and rs10423674). Meta-analysis of all data identified another SNP associated with BE and esophageal adenocarcinoma: rs3784262, within ALDH1A2 (OR = 0.90; 95% CI: 0.87–0.93; P = 3.72 × 10−9). Conclusions We identified 2 loci associated with risk of BE and provided data to support a further locus. The genes we found to be associated with risk for BE encode transcription factors involved in thoracic, diaphragmatic, and esophageal development or proteins involved in the inflammatory response.

Published
2015

5. The importance of exposure rate on odds ratios by cigarette smoking and alcohol consumption for esophageal adenocarcinoma and squamous cell carcinoma in the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium.

Author

Lubin JH, Cook MB, Pandeya N, Vaughan TL, Abnet CC, Giffen C, Webb PM, Murray LJ, Casson AG, Risch HA, Ye W, Kamangar F, Bernstein L, Sharp L, Nyrén O, Gammon MD, Corley DA, Wu AH, Brown LM, Chow WH, Ward MH, Freedman ND, and Whiteman DC

Subjects
Adenocarcinoma etiology, Age Factors, Aged, Alcohol Drinking epidemiology, Body Mass Index, Carcinoma, Squamous Cell etiology, Case-Control Studies, Esophageal Neoplasms etiology, Esophagogastric Junction pathology, Female, Gastroesophageal Reflux epidemiology, Humans, Male, Middle Aged, Models, Statistical, Odds Ratio, Risk Factors, Sex Factors, Smoking epidemiology, Time Factors, Adenocarcinoma epidemiology, Alcohol Drinking adverse effects, Carcinoma, Squamous Cell epidemiology, Esophageal Neoplasms epidemiology, Smoking adverse effects
Abstract

Background: Cigarette smoking is associated with esophageal adenocarcinoma (EAC), esophagogastric junctional adenocarcinoma (EGJA) and esophageal squamous cell carcinoma (ESCC), and alcohol consumption with ESCC. However, no analyses have examined how delivery rate modifies the strength of odds ratio (OR) trends with total exposure, i.e., the impact on the OR for a fixed total exposure of high exposure rate for short duration compared with low exposure rate for long duration., Methods: The authors pooled data from 12 case-control studies from the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium (BEACON), including 1242 (EAC), 1263 (EGJA) and 954 (ESCC) cases and 7053 controls, modeled joint ORs for cumulative exposure and exposure rate for cigarette smoking and alcohol consumption, and evaluated effect modification by sex, body mass index (BMI), age and self-reported acid reflux., Results: For smoking, all sites exhibited inverse delivery rate effects, whereby ORs with pack-years increased, but trends weakened with increasing cigarettes/day. None of the examined factors modified associations, except for ESCC where younger ages at diagnosis enhanced smoking effects (P<0.01). For EAC and EGJA, ORs with drink-years exhibited inverse associations in <5 drinks/day consumers and no association in heavier consumers. For ESCC, ORs with drink-years increased, with trends strengthening with greater drinks/day. There was no significant effect modification, except for EAC and EGJA where acid reflux mitigated the inverse associations (P=0.02). For ESCC, younger ages at diagnosis enhanced drinking-related ORs (P<0.01)., Conclusions: Patterns of ORs by pack-years and drink-years, delivery rate effects and effect modifiers revealed common as well as distinct etiologic elements for these diseases., (Published by Elsevier Ltd.)

Published
2012
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7. A polymorphic variant of the insulin-like growth factor type I receptor gene modifies risk of obesity for esophageal adenocarcinoma.

Author

MacDonald K, Porter GA, Guernsey DL, Zhao R, and Casson AG

Subjects
Adenocarcinoma epidemiology, Adenocarcinoma pathology, Barrett Esophagus epidemiology, Barrett Esophagus genetics, Barrett Esophagus pathology, Case-Control Studies, Esophageal Neoplasms epidemiology, Esophageal Neoplasms pathology, Gastroesophageal Reflux epidemiology, Gastroesophageal Reflux genetics, Gastroesophageal Reflux pathology, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Humans, Insulin-Like Growth Factor I metabolism, Multivariate Analysis, Risk Factors, Adenocarcinoma genetics, Esophageal Neoplasms genetics, Obesity complications, Obesity genetics, Polymorphism, Genetic, Receptor, IGF Type 1 genetics
Abstract

Background: To investigate potential biologic mechanisms underlying the association between obesity and risk for esophageal adenocarcinoma (EADC), we studied the frequency of a common polymorphism of the insulin-like growth factor I receptor (IGF-IR) gene in patients with either gastroesophageal reflux disease (GERD), premalignant Barrett esophagus (BE) and or invasive EADC., Methods: Using a well characterized series of 431 individuals enrolled in a case-control study, we studied the frequency of the IGF-IR gene polymorphism, G1013A., Results: On multivariate analysis controlling for age and gender, in comparison to asymptomatic controls, obese individuals with the polymorphic A-variant (G/A, A/A) were found to have significantly increased risk for EADC (OR 4.81; 95%CI 1.09-21.15), whereas obese individuals with the G/G variant were not at statistically significant increased risk (OR 2.69; 95%CI 0.41-17.62). Similarly, compared to asymptomatic controls, only obese individuals with the A-variant (G/A, A/A) were at increased risk for BE (OR 3.11; 95%CI 1.12-8.63), while obese individuals with the G/G variant were not at increased risk for BE (OR 2.91; 95%CI 0.69-12.15)., Conclusion: We conclude that the common IGF-IR gene polymorphism G1013A modulates the risk of obesity for EADC, an effect most likely mediated by altered the receptor function by influencing gene transcription or mRNA stability. These findings further implicate the insulin-like growth factor axis in the molecular pathogenesis of EADC, and represent a plausible mechanistic link underlying the association between obesity and malignancy.

Published
2009
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9. Genetic polymorphisms of microsomal epoxide hydroxylase and glutathione S-transferases M1, T1 and P1, interactions with smoking, and risk for esophageal (Barrett) adenocarcinoma.

Author

Casson AG, Zheng Z, Porter GA, and Guernsey DL

Subjects
Adenocarcinoma genetics, Alleles, Barrett Esophagus genetics, Case-Control Studies, Esophageal Neoplasms pathology, Female, Gastroesophageal Reflux genetics, Genetic Predisposition to Disease, Genotype, Humans, Male, Middle Aged, Risk Factors, Epoxide Hydrolases genetics, Esophageal Neoplasms genetics, Glutathione S-Transferase pi genetics, Glutathione Transferase genetics, Polymorphism, Genetic genetics, Smoking adverse effects
Abstract

Background: The aim of this case-control study was to test the hypothesis that polymorphisms of the microsomal epoxide hydroxylase (mEH) and glutathione S-transferase (GST) genes modulate the susceptibility to esophageal adenocarcinoma (EADC) associated with smoking., Methods: Cases included patients with gastroesophageal reflux disease (GERD) (n=126), Barrett esophagus (BE) (n=125), and EADC (n=56); controls comprised 95 strictly asymptomatic individuals. Genomic DNA was extracted from blood samples, and PCR-based assays were used to genotype mEH (slow allele, fast allele, predicted activity) and GSTM1, GSTT1 and GSTP1. Logistic regression was used to study associations between smoking and genotype, adjusting for age, gender and alcohol consumption., Results: Relative to asymptomatic controls, no significant differences were found for the distribution of mEH and GST polymorphic variants in cases with GERD, BE or EADC. Smoking was a risk factor for EADC, especially when cigarette exposure was greater than 30 pack-years (adjusted odds ratio [OR] 6.11, 95% confidence interval [CI] 2.2-17.32; P=0.001). The strong association between smoking and EADC was seen preferentially in patients with the active allele of either GSTM1 (OR 7.9, 95% CI 1.14-54.76; P=0.003) or GSTT1 (OR 3.2, 95% CI 1.23-8.35; P=0.004)., Conclusions: Cigarette smoking is an independent risk factor for EADC, and in particular for heavy smokers. The strong statistical association between smoking and risk for EADC in individuals with the active allele of either GSTM1 or GSTT1 may have potential clinical application in endoscopic surveillance programs to identify individuals with BE at increased risk for progression to EADC.

Published
2006
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