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1. IntEgrating Smoking Cessation treatment As part of usual Psychological care for dEpression and anxiety (ESCAPE): protocol for a randomised and controlled, multicentre, acceptability, feasibility and implementation trial

Author

Taylor, G, Aveyard, P, Bartlem, K, Shaw, A, Player, J, Metcalfe, C, Kessler, D, and Munafò, M

Subjects
Study Protocol, lcsh:R5-920, lcsh:Medicine (General)
Abstract

Background People with depression/anxiety are twice as likely to smoke and are less responsive to standard tobacco treatments, leading to a reduced life expectancy of up to 13.6 years compared to people without depression/anxiety. However, this group of smokers is motivated to quit, and as a result of quitting smoking, their depression/anxiety is likely to improve. In England, people with depression/anxiety are referred to a primary care-based psychological therapies service known as ‘Improving Access to Psychological Therapies’ (IAPT), which could offer smoking cessation treatment as part of usual care but currently does not. In this study, we aim (1) to establish the feasibility and acceptability of delivering a smoking cessation treatment alongside IAPT usual care and (2) to establish the feasibility of a multi-centre randomised trial to compare the combined smoking cessation and IAPT treatment to usual IAPT treatment alone. Methods A randomised and controlled, multi-centre trial to test the acceptability, feasibility and implementation of smoking cessation treatment as offered alongside usual IAPT care, compared to usual care alone, with nested qualitative methods. We will include adult daily smokers with depression/anxiety, who would like help to quit smoking and are about to start IAPT treatment. Follow-up will be conducted at 3-months after baseline. The main outcome will be retention in the smoking cessation treatment. Secondary outcomes are smoking-related (biochemically-verified 7-day point prevalence smoking cessation, number of cigarettes smoked per day, Heaviness of Smoking Index), mental health-related (PHQ-9), service-related (number of ‘Did Not Attends’, number of planned and completed IAPT sessions), acceptability and feasibility (participant and clinician acceptability and satisfaction of intervention as assessed by questionnaires and qualitative interviews, interviews will also explore acceptability and feasibility of data collection procedures and impact of smoking cessation treatment on usual care and mental health recovery) and implementation-related (intervention delivery checklist, qualitative analysis of intervention delivery). Discussion If the intervention is shown to be acceptable, feasible and suitably implemented, we can conduct a randomised controlled trial. In a future trial, we would examine whether adding smoking cessation treatment increases smoking abstinence and improves depression and anxiety more than usual care, which would lead to long-term health improvement. Trial registration ISRCTN99531779 Electronic supplementary material The online version of this article (10.1186/s40814-018-0385-2) contains supplementary material, which is available to authorized users.

Published
2019
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2. MC1R variants in childhood and adolescent melanoma: a retrospective pooled analysis of a multicentre cohort

Author

Pellegrini, C. Botta, F. Massi, D. Martorelli, C. Facchetti, F. Gandini, S. Maisonneuve, P. Avril, M.-F. Demenais, F. Bressac-de Paillerets, B. Hoiom, V. Cust, A.E. Anton-Culver, H. Gruber, S.B. Gallagher, R.P. Marrett, L. Zanetti, R. Dwyer, T. Thomas, N.E. Begg, C.B. Berwick, M. Puig, S. Potrony, M. Nagore, E. Ghiorzo, P. Menin, C. Manganoni, A.M. Rodolfo, M. Brugnara, S. Passoni, E. Sekulovic, L.K. Baldini, F. Guida, G. Stratigos, A. Ozdemir, F. Ayala, F. Fernandez-de-Misa, R. Quaglino, P. Ribas, G. Romanini, A. Migliano, E. Stanganelli, I. Kanetsky, P.A. Pizzichetta, M.A. García-Borrón, J.C. Nan, H. Landi, M.T. Little, J. Newton-Bishop, J. Sera, F. Fargnoli, M.C. Raimondi, S. Alaibac, M. Ferrari, A. Valeri, B. Sicher, M. Mangiola, D. Nazzaro, G. Tosti, G. Mazzarol, G. Giudice, G. Ribero, S. Astrua, C. Mazzoni, L. Orlow, I. Mujumdar, U. Hummer, A. Busam, K. Roy, P. Canchola, R. Clas, B. Cotignola, J. Monroe, Y. Armstrong, B. Kricker, A. Litchfield, M. Tucker, P. Stephens, N. Switzer, T. Theis, B. From, L. Chowdhury, N. Vanasse, L. Purdue, M. Northrup, D. Rosso, S. Sacerdote, C. Leighton, N. Gildea, M. Bonner, J. Jeter, J. Klotz, J. Wilcox, H. Weiss, H. Millikan, R. Mattingly, D. Player, J. Tse, C.-K. Rebbeck, T. Walker, A. Panossian, S. Setlow, R. Mohrenweiser, H. Autier, P. Han, J. Caini, S. Hofman, A. Kayser, M. Liu, F. Nijsten, T. Uitterlinden, A.G. Kumar, R. Bishop, T. Elliott, F. Lazovich, D. Polsky, D. Hansson, J. Pastorino, L. Gruis, N.A. Bouwes Bavinck, J.N. Aguilera, P. Badenas, C. Carrera, C. Gimenez-Xavier, P. Malvehy, J. Puig-Butille, J.A. Tell-Marti, G. Blizzard, L. Cochrane, J. Branicki, W. Debniak, T. Morling, N. Johansen, P. Mayne, S. Bale, A. Cartmel, B. Ferrucci, L. Pfeiffer, R. Palmieri, G. Kypreou, K. Bowcock, A. Cornelius, L. Council, M.L. Motokawa, T. Anno, S. Helsing, P. Andresen, P.A. Guida, S. Wong, T.H. IMI Study Group GEM Study Group M-SKIP Study Group

Abstract

Background: Germline variants in the melanocortin 1 receptor gene (MC1R) might increase the risk of childhood and adolescent melanoma, but a clear conclusion is challenging because of the low number of studies and cases. We assessed the association of MC1R variants with childhood and adolescent melanoma in a large study comparing the prevalence of MC1R variants in child or adolescent patients with melanoma to that in adult patients with melanoma and in healthy adult controls. Methods: In this retrospective pooled analysis, we used the M-SKIP Project, the Italian Melanoma Intergroup, and other European groups (with participants from Australia, Canada, France, Greece, Italy, the Netherlands, Serbia, Spain, Sweden, Turkey, and the USA) to assemble an international multicentre cohort. We gathered phenotypic and genetic data from children or adolescents diagnosed with sporadic single-primary cutaneous melanoma at age 20 years or younger, adult patients with sporadic single-primary cutaneous melanoma diagnosed at age 35 years or older, and healthy adult individuals as controls. We calculated odds ratios (ORs) for childhood and adolescent melanoma associated with MC1R variants by multivariable logistic regression. Subgroup analysis was done for children aged 18 or younger and 14 years or younger. Findings: We analysed data from 233 young patients, 932 adult patients, and 932 healthy adult controls. Children and adolescents had higher odds of carrying MC1R r variants than did adult patients (OR 1·54, 95% CI 1·02–2·33), including when analysis was restricted to patients aged 18 years or younger (1·80, 1·06–3·07). All investigated variants, except Arg160Trp, tended, to varying degrees, to have higher frequencies in young patients than in adult patients, with significantly higher frequencies found for Val60Leu (OR 1·60, 95% CI 1·05–2·44; p=0·04) and Asp294His (2·15, 1·05–4·40; p=0·04). Compared with those of healthy controls, young patients with melanoma had significantly higher frequencies of any MC1R variants. Interpretation: Our pooled analysis of MC1R genetic data of young patients with melanoma showed that MC1R r variants were more prevalent in childhood and adolescent melanoma than in adult melanoma, especially in patients aged 18 years or younger. Our findings support the role of MC1R in childhood and adolescent melanoma susceptibility, with a potential clinical relevance for developing early melanoma detection and preventive strategies. Funding: SPD-Pilot/Project-Award-2015; AIRC-MFAG-11831. © 2019 Elsevier Ltd

Published
2019

3. Variants in autophagy-related genes and clinical characteristics in melanoma: a population-based study

Author

White, KAM, Luo, L, Thompson, TA, Torres, S, Hu, CAA, Thomas, NE, Lilyquist, J, Anton-Culver, H, Gruber, SB, From, L, Busam, KJ, Orlow, I, Kanetsky, PA, Marrett, LD, Gallagher, RP, Sacchetto, L, Rosso, S, Dwyer, T, Cust, AE, Begg, CB, Berwick, M, Mujumdar, U, Roy, P, Armstrong, B, Kricker, A, Litchfield, M, Tucker, P, Venn, A, Stephens, N, Switzer, T, Marrett, L, Theis, E, Chowdhury, N, Vanasse, L, Zanetti, R, Sacerdote, C, Leighton, N, Jeter, J, Klotz, J, Wilcox, H, Weiss, H, Mattingly, D, Player, J, Rebbeck, T, Walker, A, Panossian, S, Taylor, JL, and Madronich, S

Abstract

© 2016 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy-related (ATG) genes have been investigated in relation to melanoma progression. We examined five single-nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population-based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression.

Published
2016
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5. Notes.

Author

Bremner, J. M., Shaw, K., Kilroe-Smith, T. A., de Gier, Jeanne F., Kent, P. W., Whitehouse, M. W., Johnson, E. A., Newman, E. J., Zeller, Howard D., and Player, J. H.

Published
1955
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13. Evaluation of the Wright 1902 Glider Using Full-Scale Wind-Tunnel Data.

Author

Kochersberger, K. B., Landman, D., Player, J. L., and Hyde, K. W.

Subjects
*GLIDERS (Aeronautics), *WIND tunnels, *AERODYNAMICS, *GLIDING & soaring, *FLIGHT training
Abstract

A reproduction of the Wright 1902 glider was wind-tunnel tested at the NASA Langley Research Center Full-Scale Tunnel through a range of conditions similar to those experienced 102 years ago. Data were collected over a range of angle of attack from -4 to 20 deg, and a range of sideslip angles from -20 to 20 deg. Both the canard and wing warp controls were actuated to determine control power, and a canard-only test was performed to augment estimates of pitch control power. An optimal lift/drag of 7.4:1 in ground effect was determined, comparing favorably with the Wrights' observations. This aircraft displayed levels of longitudinal and lateral control power that allowed, for the first time, control of an aircraft without reliance on weight shift. Because of its low pitch inertia and damping, the aircraft is sensitive in pitch and requires constant pilot attention to maintain an attitude. Laterally, the aircraft shows adequate roll rate and turn coordination, although a moderate sideslip will develop in turning maneuvers due to the lack of vertical surface area. Validation of the handling characteristics was aided through the use of a six-degree-of-freedom, commercially available flight simulator. [ABSTRACT FROM AUTHOR]

Published
2005
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14. MC1R variants in childhood and adolescent melanoma: a retrospective pooled analysis of a multicentre cohort

Author

Pellegrini, Cristina, Botta, Francesca, Massi, Daniela, Martorelli, Claudia, Facchetti, Fabio, Gandini, Sara, Maisonneuve, Patrick, Avril, Marie-Françoise, Demenais, Florence, Bressac-de Paillerets, Brigitte, Hoiom, Veronica, Cust, Anne E, Anton-Culver, Hoda, Gruber, Stephen B, Gallagher, Richard P, Marrett, Loraine, Zanetti, Roberto, Dwyer, Terence, Thomas, Nancy E, Begg, Colin B, Berwick, Marianne, Puig, Susana, Potrony, Miriam, Nagore, Eduardo, Ghiorzo, Paola, Menin, Chiara, Manganoni, Ausilia Maria, Rodolfo, Monica, Brugnara, Sonia, Passoni, Emanuela, Sekulovic, Lidija Kandolf, Baldini, Federica, Guida, Gabriella, Stratigos, Alexandros, Ozdemir, Fezal, Ayala, Fabrizio, Fernandez-de-Misa, Ricardo, Quaglino, Pietro, Ribas, Gloria, Romanini, Antonella, Migliano, Emilia, Stanganelli, Ignazio, Kanetsky, Peter A, Pizzichetta, Maria Antonietta, García-Borrón, Jose Carlos, Nan, Hongmei, Landi, Maria Teresa, Little, Julian, Newton-Bishop, Julia, Sera, Francesco, Fargnoli, Maria Concetta, Raimondi, Sara, Alaibac, Mauro, Ferrari, Andrea, Valeri, Barbara, Sicher, Mariacristina, Mangiola, Daniela, Nazzaro, Gianluca, Tosti, Giulio, Mazzarol, Giovanni, Giudice, Giuseppe, Ribero, Simone, Astrua, Chiara, Mazzoni, Laura, Orlow, Irene, Mujumdar, Urvi, Hummer, Amanda, Busam, Klaus, Roy, Pampa, Canchola, Rebecca, Clas, Brian, Cotignola, Javiar, Monroe, Yvette, Armstrong, Bruce, Kricker, Anne, Litchfield, Melisa, Tucker, Paul, Stephens, Nicola, Switzer, Teresa, Theis, Beth, From, Lynn, Chowdhury, Noori, Vanasse, Louise, Purdue, Mark, Northrup, David, Rosso, Stefano, Sacerdote, Carlotta, Leighton, Nancy, Gildea, Maureen, Bonner, Joe, Jeter, Joanne, Klotz, Judith, Wilcox, Homer, Weiss, Helen, Millikan, Robert, Mattingly, Dianne, Player, Jon, Tse, Chiu-Kit, Rebbeck, Timothy, Walker, Amy, Panossian, Saarene, Setlow, Richard, Mohrenweiser, Harvey, Autier, Philippe, Han, Jiali, Caini, Saverio, Hofman, Albert, Kayser, Manfred, Liu, Fan, Nijsten, Tamar, Uitterlinden, Andre G., Kumar, Rajiv, Bishop, Tim, Elliott, Faye, Lazovich, Deann, Polsky, David, Hansson, Johan, Pastorino, Lorenza, Gruis, Nelleke A., Bouwes Bavinck, Jan Nico, Aguilera, Paula, Badenas, Celia, Carrera, Cristina, Gimenez-Xavier, Pol, Malvehy, Josep, Puig-Butille, Joan Anton, Tell-Marti, Gemma, Blizzard, Leigh, Cochrane, Jennifer, Branicki, Wojciech, Debniak, Tadeusz, Morling, Niels, Johansen, Peter, Mayne, Susan, Bale, Allen, Cartmel, Brenda, Ferrucci, Leah, Pfeiffer, Ruth, Palmieri, Giuseppe, Kypreou, Katerina, Bowcock, Anne, Cornelius, Lynn, Council, M. Laurin, Motokawa, Tomonori, Anno, Sumiko, Helsing, Per, Andresen, Per Arne, Guida, Stefania, Wong, Collaborators (98): Alaibac M, Terence H., Ferrari, A, Valeri, B, Et, Al., Pellegrini, C., Botta, F., Massi, D., Martorelli, C., Facchetti, F., Gandini, S., Maisonneuve, P., Avril, M. -F., Demenais, F., Bressac-de Paillerets, B., Hoiom, V., Cust, A. E., Anton-Culver, H., Gruber, S. B., Gallagher, R. P., Marrett, L., Zanetti, R., Dwyer, T., Thomas, N. E., Begg, C. B., Berwick, M., Puig, S., Potrony, M., Nagore, E., Ghiorzo, P., Menin, C., Manganoni, A. M., Rodolfo, M., Brugnara, S., Passoni, E., Sekulovic, L. K., Baldini, F., Guida, G., Stratigos, A., Ozdemir, F., Ayala, F., Fernandez-de-Misa, R., Quaglino, P., Ribas, G., Romanini, A., Migliano, E., Stanganelli, I., Kanetsky, P. A., Pizzichetta, M. A., Garcia-Borron, J. C., Nan, H., Landi, M. T., Little, J., Newton-Bishop, J., Sera, F., Fargnoli, M. C., Raimondi, S., Alaibac, M., Ferrari, A., Valeri, B., Sicher, M., Mangiola, D., Nazzaro, G., Tosti, G., Mazzarol, G., Giudice, G., Ribero, S., Astrua, C., Mazzoni, L., Orlow, I., Mujumdar, U., Hummer, A., Busam, K., Roy, P., Canchola, R., Clas, B., Cotignola, J., Monroe, Y., Armstrong, B., Kricker, A., Litchfield, M., Tucker, P., Stephens, N., Switzer, T., Theis, B., From, L., Chowdhury, N., Vanasse, L., Purdue, M., Northrup, D., Rosso, S., Sacerdote, C., Leighton, N., Gildea, M., Bonner, J., Jeter, J., Klotz, J., Wilcox, H., Weiss, H., Millikan, R., Mattingly, D., Player, J., Tse, C. -K., Rebbeck, T., Walker, A., Panossian, S., Setlow, R., Mohrenweiser, H., Autier, P., Han, J., Caini, S., Hofman, A., Kayser, M., Liu, F., Nijsten, T., Uitterlinden, A. G., Kumar, R., Bishop, T., Elliott, F., Lazovich, D., Polsky, D., Hansson, J., Pastorino, L., Gruis, N. A., Bouwes Bavinck, J. N., Aguilera, P., Badenas, C., Carrera, C., Gimenez-Xavier, P., Malvehy, J., Puig-Butille, J. A., Tell-Marti, G., Blizzard, L., Cochrane, J., Branicki, W., Debniak, T., Morling, N., Johansen, P., Mayne, S., Bale, A., Cartmel, B., Ferrucci, L., Pfeiffer, R., Palmieri, G., Kypreou, K., Bowcock, A., Cornelius, L., Council, M. L., Motokawa, T., Anno, S., Helsing, P., Andresen, P. A., Guida, S., Wong, T. H., Ege Üniversitesi, Epidemiology, Genetic Identification, and Dermatology

Subjects
Male, Skin Neoplasms, Pediatrics, Cohort Studies, 0302 clinical medicine, Odds Ratio, Developmental and Educational Psychology, Pediatrics, Perinatology and Child Health, 030212 general & internal medicine, Child, Cancer, Pediatric, Tumor, childhood disease, Middle Aged, Perinatology and Child Health, cohort analysis, Meta-analysis, Melanocortin, Cohort, Female, MC1R gene, Receptor, Melanocortin, Type 1, Receptor, Type 1, Cohort study, Adult, medicine.medical_specialty, adolescent, melanoma, cohort analysi, Subgroup analysis, Article, 03 medical and health sciences, Genetic, Clinical Research, 030225 pediatrics, Internal medicine, Genetics, Biomarkers, Tumor, medicine, Humans, Genetic Predisposition to Disease, Polymorphism, Germ-Line Mutation, Aged, Retrospective Studies, Polymorphism, Genetic, business.industry, Prevention, Case-control study, Retrospective cohort study, GEM Study Group, Odds ratio, Logistic Models, M-SKIP Study Group, Case-Control Studies, Cutaneous melanoma, IMI Study Group, business, Biomarkers
Abstract

Ferrari, Andrea/0000-0002-4724-0517; Pellegrini, Cristina/0000-0003-2168-8097; Migliano, Emilia/0000-0002-5316-8937; Maisonneuve, Patrick/0000-0002-5309-4704; Guida, Stefania/0000-0002-8221-6694; Pastorino, Lorenza/0000-0002-2575-8331; CARRERA, CRISTINA/0000-0003-1608-8820; Paillerets, Brigitte Bressac-de/0000-0003-0245-8608; Sekulovic, Lidija Kandolf/0000-0002-5221-5068; Caini, Saverio/0000-0002-2262-1102; Potrony, Miriam/0000-0003-2766-0765; Pizzichetta, Maria Antonietta/0000-0002-4201-8490; Little, Julian/0000-0001-5026-5531; Nagore, Eduardo/0000-0003-3433-8707; Polsky, David/0000-0001-9554-5289; Demenais, Florence/0000-0001-8361-0936; Nazzaro, Gianluca/0000-0001-8534-6497; gandini, sara/0000-0002-1348-4548; Cornelius, Lynn A/0000-0002-6329-2819; Palmieri, Giuseppe/0000-0002-4350-2276; Cotignola, Javier/0000-0003-4473-9854; Ghiorzo, Paola/0000-0002-3651-8173; Autier, Philippe/0000-0003-1538-5321; Bishop, Tim/0000-0002-8752-8785; Sera, Francesco/0000-0002-8890-6848; Newton-Bishop, Julia/0000-0001-9147-6802; Litchfield, Melisa/0000-0003-0002-7724, WOS: 000464254100018, PubMed: 30872112, Background Germline variants in the melanocortin 1 receptor gene (MC1R) might increase the risk of childhood and adolescent melanoma, but a clear conclusion is challenging because of the low number of studies and cases. We assessed the association of MC1R variants with childhood and adolescent melanoma in a large study comparing the prevalence of MC1R variants in child or adolescent patients with melanoma to that in adult patients with melanoma and in healthy adult controls. Methods in this retrospective pooled analysis, we used the M-SKIP Project, the Italian Melanoma Intergroup, and other European groups (with participants from Australia, Canada, France, Greece, Italy, the Netherlands, Serbia, Spain, Sweden, Turkey, and the USA) to assemble an international multicentre cohort. We gathered phenotypic and genetic data from children or adolescents diagnosed with sporadic single-primary cutaneous melanoma at age 20 years or younger, adult patients with sporadic single-primary cutaneous melanoma diagnosed at age 35 years or older, and healthy adult individuals as controls. We calculated odds ratios (ORs) for childhood and adolescent melanoma associated with MC1R variants by multivariable logistic regression. Subgroup analysis was done for children aged 18 or younger and 14 years or younger. Findings We analysed data from 233 young patients, 932 adult patients, and 932 healthy adult controls. Children and adolescents had higher odds of carrying MC1R r variants than did adult patients (OR 1.54, 95% CI 1.02-2.33), including when analysis was restricted to patients aged 18 years or younger (1.80, 1.06-3.07). All investigated variants, except Arg160Trp, tended, to varying degrees, to have higher frequencies in young patients than in adult patients, with significantly higher frequencies found for Val60Leu (OR 1.60, 95% CI 1.05-2.44; p=0.04) and Asp294His (2.15, 1.05-4.40; p=0.04). Compared with those of healthy controls, young patients with melanoma had significantly higher frequencies of any MC1R variants. Interpretation Our pooled analysis of MC1R genetic data of young patients with melanoma showed that MC1R r variants were more prevalent in childhood and adolescent melanoma than in adult melanoma, especially in patients aged 18 years or younger. Our findings support the role of MC1R in childhood and adolescent melanoma susceptibility, with a potential clinical relevance for developing early melanoma detection and preventive strategies. Copyright (c) 2019 Elsevier Ltd. All rights reserved., [AIRC-MFAG-11831]; NATIONAL CANCER INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P30CA016086, P01CA206980, P30CA016086, P30CA016086] Funding Source: NIH RePORTER, SPD-Pilot/Project-Award-2015; AIRC-MFAG-11831.

Published
2019

15. Polymorphisms in nucleotide excision repair genes, smoking and breast cancer in African Americans and whites: a population-based case-control study.

Author

Mechanic LE, Millikan RC, Player J, de Cotret AR, Winkel S, Worley K, Heard K, Heard K, Tse CK, and Keku T

Subjects
Adult, Aged, Breast Neoplasms ethnology, Breast Neoplasms genetics, Case-Control Studies, Female, Genetic Predisposition to Disease, Genotype, Humans, Middle Aged, Odds Ratio, Polymerase Chain Reaction, Polymorphism, Genetic, Black or African American genetics, Breast Neoplasms etiology, DNA Repair genetics, Smoking adverse effects, White People genetics
Abstract

Polymorphisms exist in several genes involved in nucleotide excision repair (NER), the principal pathway for removal of smoking-induced DNA damage. An epidemiologic study was conducted to determine whether these polymorphisms modify the association between smoking and breast cancer. DNA samples and exposure histories were analyzed as part of a large population-based case-control study of breast cancer in North Carolina. The study population included 2311 cases (894 African Americans, 1417 whites) and 2022 controls (788 African Americans, 1234 whites). Odds ratios (ORs) were calculated for breast cancer and smoking, and for breast cancer and nine non-synonymous coding polymorphisms in six NER genes (XPD codons 312 and 751, RAD23B codon 249, XPG codon 1104, XPC codon 939, XPF codons 415 and 662, and ERCC6 codons 1213 and 1230). Modification of ORs for smoking by single and combined NER genotypes was investigated. In this study population, smoking was more strongly associated with breast cancer in African American women compared with white women. Among African American women, the association of breast cancer and smoking was strongest among women with specific combinations of NER genotypes. Evidence for multiplicative interaction was found between combined NER genotypes and smoking dose (likelihood ratio test P = 0.06), duration (P = 0.09), time since cessation (P = 0.02), age at initiation (P = 0.04) and former smoking (P = 0.03). No interactions were observed in white women. Therefore, polymorphisms in NER genes may modify the relationship between breast cancer and smoking. These results are consistent with previous evidence of exposure-specific p53 mutations in breast tumors from current and former smokers, suggesting that smoking may play a role in breast cancer etiology.

Published
2006
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16. COX-2 polymorphism, use of nonsteroidal anti-inflammatory drugs, and risk of colon cancer in African Americans (United States).

Author

Sansbury LB, Millikan RC, Schroeder JC, North KE, Moorman PG, Keku TO, de Cotret AR, Player J, and Sandler RS

Subjects
Aged, Anti-Inflammatory Agents, Non-Steroidal administration & dosage, Colonic Neoplasms prevention & control, Female, Humans, Male, Middle Aged, North Carolina epidemiology, Odds Ratio, Risk Factors, United States epidemiology, Black or African American, Anti-Inflammatory Agents, Non-Steroidal therapeutic use, Aspirin therapeutic use, Colonic Neoplasms ethnology, Colonic Neoplasms genetics, Cyclooxygenase 2, Polymorphism, Genetic genetics
Abstract

Introduction: The inducible Cyclooxygenase (COX)-2 enzyme plays an important role in inflammation and carcinogenesis. Recent reports suggest that single nucleotide polymorphisms (SNPs) in the COX-2 gene may alter enzyme function and in turn modify an individual's risk of colon cancer. We explored the association between the COX-2 Val511Ala SNP and risk of colon cancer among 240 African American cases and 326 African American controls in a population-based, case-control study in North Carolina., Methods: We used unconditional logistic regression models to determine the odds ratios (ORs) for genotype and risk of colon cancer., Results: We observed a non-statistically significant inverse association between any Ala COX-2 genotype and risk of colon cancer (OR = 0.62, 95% CI: 0.33, 1.16) among African Americans. The inverse association was present among non-regular NSAID users, use < or = 3 times/week, (OR = 0.66; 95% CI: 0.32, 1.37) and regular NSAID users, use > or =3 times/week for > or =3 months, (OR = 0.41; 95% CI: 0.11, 1.54)., Conclusions: Our results suggest that the COX-2 Val511Ala SNP does not antagonize the effect of NSAIDs on colon cancer risk and provides support that NSAID use and the COX-2 Val511Ala SNP may contribute to a reduced risk of colon cancer among African Americans.

Published
2006
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17. Polymorphisms in nucleotide excision repair genes and risk of multiple primary melanoma: the Genes Environment and Melanoma Study.

Author

Millikan RC, Hummer A, Begg C, Player J, de Cotret AR, Winkel S, Mohrenweiser H, Thomas N, Armstrong B, Kricker A, Marrett LD, Gruber SB, Culver HA, Zanetti R, Gallagher RP, Dwyer T, Rebbeck TR, Busam K, From L, Mujumdar U, and Berwick M

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Case-Control Studies, Child, Female, Genotype, Humans, Male, Melanoma etiology, Middle Aged, Odds Ratio, Risk Factors, Skin Neoplasms etiology, DNA Repair, Melanoma genetics, Polymorphism, Genetic, Skin Neoplasms genetics, Xeroderma Pigmentosum Group D Protein genetics
Abstract

Polymorphisms in six genes involved in nucleotide excision repair of DNA were examined in a large population-based case-control study of melanoma. Genotyping was conducted for 2485 patients with a single primary melanoma (controls) and 1238 patients with second or higher order primary melanomas (cases). Patients were ascertained from nine geographic regions in Australia, Canada, Italy and the United States. Positive associations were observed for XPD 312 Asn/Asn versus Asp/Asp [odds ratio (OR) = 1.5, 95% confidence interval (CI) 1.2-1.9] and XPD 751 Gln/Gln versus Lys/Lys (OR = 1.4, 95% CI 1.1-1.7) genotypes and melanoma. The combined XPD Asn (A) 312 + Gln (C) 751 haplotype was significantly more frequent in cases (32%) compared with controls (29%) (P = 0.003) and risk of melanoma increased significantly with one and two copies of the haplotype (ORs 1.2, 95% CI 1.0-1.4, and 1.6, 95% CI 1.2-2.0, trend P = 0.002). No significant associations were observed for HR23B codon 249, XPG codon 1104, XPC codon 939, XPF codon 415, XPF nt 2063, ERCC6 codon 1213 or ERCC6 codon 1230. ORs for XPD and XPC genotypes were stronger for melanoma diagnosed at an early age, but tests for interaction were not statistically significant. The results provide further evidence for a role of XPD in the etiology of melanoma.

Published
2006
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18. Manganese superoxide dismutase Ala-9Val polymorphism and risk of breast cancer in a population-based case-control study of African Americans and whites.

Author

Millikan RC, Player J, de Cotret AR, Moorman P, Pittman G, Vannappagari V, Tse CK, and Keku T

Subjects
Adult, Alleles, Amino Acid Substitution genetics, Breast Neoplasms epidemiology, Case-Control Studies, Female, Genetic Predisposition to Disease epidemiology, Genetic Predisposition to Disease genetics, Humans, Middle Aged, Molecular Epidemiology methods, Molecular Epidemiology statistics & numerical data, North Carolina, Black or African American genetics, Alanine genetics, Breast Neoplasms genetics, Polymorphism, Genetic genetics, Population Surveillance methods, Superoxide Dismutase genetics, Valine genetics, White People genetics
Abstract

Introduction: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies. Results suggest that the Ala allele increases the risk of breast cancer and modifies the effects of environmental exposures that produce oxidative damage to DNA., Methods: We examined the role of the MnSOD Ala-9Val polymorphism in a population-based case-control study of invasive and in situ breast cancer in North Carolina. Genotypes were evaluated for 2025 cases (760 African Americans and 1265 whites) and for 1812 controls (677 African Americans and 1135 whites)., Results: The odds ratio for MnSOD Ala/Ala versus any MnSOD Val genotypes was not elevated in African Americans (odds ratio = 0.9, 95% confidence interval = 0.7-1.2) or in whites (odds ratio = 1.0, 95% confidence interval = 0.8-1.2). Greater than additive joint effects were observed for the Ala/Ala genotype and smoking, radiation to the chest, and occupational exposure to ionizing radiation. Antagonism was observed between the Ala/Ala genotype and the use of nonsteroidal anti-inflammatory drugs., Conclusions: The MnSOD genotype may contribute to an increased risk of breast cancer in the presence of specific environmental exposures. These results provide further evidence for the importance of reactive oxygen species and of oxidative DNA damage in the etiology of breast cancer.

Published
2004
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19. Pain after laparoscopy: an observational study and a randomized trial of local anesthetic.

Author

Johnson N, Onwude JL, Player J, Hicks N, Yates A, Bryce F, Tuffnell D, Jarvis G, MacDonald H, and Griffiths-Jones M

Subjects
Anesthesia, General, Body Height, Body Weight, Dilatation and Curettage, Double-Blind Method, Female, Humans, Pain Measurement, Pain, Postoperative epidemiology, Pneumoperitoneum, Artificial, Prospective Studies, Sterilization, Reproductive, Time Factors, Anesthesia, Local, Bupivacaine, Laparoscopy, Pain, Postoperative prevention & control
Abstract

Our objective was to determine if local anesthesia reduces pain after a laparoscopy. Eighty women were assigned randomly 10 ml of 0.5% bupivacaine or 0.9% saline flushed over the peritoneal folds and into the abdominal wall after laparoscopy under general anesthesia. Pain scores from the deep abdomen, skin, shoulder, and back were collected 30 min, 2 h, 4 h, and the day following laparoscopy. Pain scores also were correlated with patients' height, weight, operative findings, surgical technique and procedure, and volume of gas insufflated into the abdomen. Bupivacaine has a small effect on abdominal and skin pain 2 h after surgery (p = 0.01) but has no effect on shoulder or back discomfort. Women who have been sterilized, have not had previous abdominal surgery, or have evidence of old pelvic inflammation report more postoperative backache and deep abdominal pain but no greater skin or shoulder discomfort. Weight, height, whether the abdominal wall was picked up, and the volume of gas used to insufflate the abdomen are independent of all postoperative pain scores. Local anaesthetic instilled down the laparoscopy trocar reduces skin discomfort 2 h after surgery, but this beneficial effect is small compared with other factors influencing pain after laparoscopy.

Published
1994
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20. The economic importance of nurses.

Author

Player JM

Subjects
Female, Humans, Male, Nurse Administrators, Nursing Service, Hospital economics, Nursing Staff, Hospital psychology, Salaries and Fringe Benefits
Published
1982

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