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Sökning: WFRF:(Chen S) > Jönköping University

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1.
  • Antoniou, A. C., et al. (författare)
  • Common breast cancer susceptibility alleles and the risk of breast cancer for BRCA1 and BRCA2 mutation carriers : Implications for risk prediction
  • 2010
  • Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:23, s. 9742-9754
  • Tidskriftsartikel (refereegranskat)abstract
    • The known breast cancer susceptibility polymorphisms in FGFR2, TNRC9/TOX3, MAP3K1, LSP1, and 2q35 confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. We evaluated the associations of 3 additional single nucleotide polymorphisms (SNPs), rs4973768 in SLC4A7/NEK10, rs6504950 in STXBP4/COX11, and rs10941679 at 5p12, and reanalyzed the previous associations using additional carriers in a sample of 12,525 BRCA1 and 7,409 BRCA2 carriers. Additionally, we investigated potential interactions between SNPs and assessed the implications for risk prediction. The minor alleles of rs4973768 and rs10941679 were associated with increased breast cancer risk for BRCA2 carriers (per-allele HR = 1.10, 95% CI: 1.03-1.18, P = 0.006 and HR = 1.09, 95% CI: 1.01-1.19, P = 0.03, respectively). Neither SNP was associated with breast cancer risk for BRCA1 carriers, and rs6504950 was not associated with breast cancer for either BRCA1 or BRCA2 carriers. Of the 9 polymorphisms investigated, 7 were associated with breast cancer for BRCA2 carriers (FGFR2, TOX3, MAP3K1, LSP1, 2q35, SLC4A7, 5p12, P = 7 × 10-11 - 0.03), but only TOX3 and 2q35 were associated with the risk for BRCA1 carriers (P = 0.0049, 0.03, respectively). All risk-associated polymorphisms appear to interact multiplicatively on breast cancer risk for mutation carriers. Based on the joint genotype distribution of the 7 risk-associated SNPs in BRCA2 mutation carriers, the 5% of BRCA2 carriers at highest risk (i.e., between 95th and 100th percentiles) were predicted to have a probability between 80% and 96% of developing breast cancer by age 80, compared with 42% to 50% for the 5% of carriers at lowest risk. Our findings indicated that these risk differences might be sufficient to influence the clinical management of mutation carriers.
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2.
  • Osorio, A., et al. (författare)
  • Evaluation of a candidate breast cancer associated SNP in ERCC4 as a risk modifier in BRCA1 and BRCA2 mutation carriers. Results from the consortium of investigators of modifiers of BRCA1/BRCA2 (CIMBA)
  • 2009
  • Ingår i: British Journal of Cancer. - : Nature Publishing Group. - 0007-0920 .- 1532-1827. ; 101:12, s. 2048-2054
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: In this study we aimed to evaluate the role of a SNP in intron 1 of the ERCC4 gene (rs744154), previously reported to be associated with a reduced risk of breast cancer in the general population, as a breast cancer risk modifier in BRCA1 and BRCA2 mutation carriers. Methods: We have genotyped rs744154 in 9408 BRCA1 and 5632 BRCA2 mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) and assessed its association with breast cancer risk using a retrospective weighted cohort approach. Results: We found no evidence of association with breast cancer risk for BRCA1 (per-allele HR: 0.98, 95% CI: 0.93-1.04, P0.5) or BRCA2 (per-allele HR: 0.97, 95% CI: 0.89-1.06, P0.5) mutation carriers. Conclusion: This SNP is not a significant modifier of breast cancer risk for mutation carriers, though weak associations cannot be ruled out.
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3.
  • Antoniou, A. C., et al. (författare)
  • Common variants in LSP1, 2q35 and 8q24 and breast cancer risk for BRCA1 and BRCA2 mutation carriers
  • 2009
  • Ingår i: Human Molecular Genetics. - [Antoniou, Antonis C.; McGuffog, Lesley; Peock, Susan; Cook, Margaret; Frost, Debra; Oliver, Clare; Platte, Radka; Pooley, Karen A.; Easton, Douglas F.] Univ Cambridge, Dept Publ Hlth & Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England. [Sinilnikova, Olga M.; Leone, Melanie] Univ Lyon, CNRS, Hosp Civils Lyon,Ctr Leon Berard,UMR5201, Unite Mixte Genet Constitut Canc Frequents, Lyon, France. [Healey, Sue; Spurdle, Amanda B.; Beesley, Jonathan; Chen, Xiaoqing; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4029, Australia. [Nevanlinna, Heli; Heikkinen, Tuomas] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland. [Simard, Jacques] Univ Laval, Quebec City, PQ, Canada. [Simard, Jacques] Univ Quebec, Ctr Hosp, Canada Res Chair Oncogenet, Canc Genom Lab, Quebec City, PQ, Canada. Peter MacCallum Canc Inst, Melbourne, Vic 3002, Australia. [Neuhausen, Susan L.; Ding, Yuan C.] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA. [Couch, Fergus J.; Wang, Xianshu; Fredericksen, Zachary] Mayo Clin, Rochester, MN USA. [Peterlongo, Paolo; Peissel, Bernard; Radice, Paolo] Fdn IRCCS Ist Nazl Tumori, Milan, Italy. [Peterlongo, Paolo; Radice, Paolo] Fdn Ist FIRC Oncol Molecolare, Milan, Italy. [Bonanni, Bernardo; Bernard, Loris] Ist Europeo Oncol, Milan, Italy. [Viel, Alessandra] IRCCS, Ctr Riferimento Oncol, Aviano, Italy. [Bernard, Loris] Cogentech, Consortium Genom Technol, Milan, Italy. [Szabo, Csilla I.] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN USA. [Foretova, Lenka] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic. [Zikan, Michal] Charles Univ Prague, Dept Biochem & Expt Oncol, Fac Med 1, Prague, Czech Republic. [Claes, Kathleen] Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium. [Greene, Mark H.; Mai, Phuong L.] US Natl Canc Inst, Clin Genet Branch, Rockville, MD USA. [Rennert, Gad; Lejbkowicz, Flavio] CHS Natl Canc Control Ctr, Haifa, Israel. [Rennert, Gad; Lejbkowicz, Flavio] Carmel Hosp, Dept Community Med & Epidemiol, Haifa, Israel. [Rennert, Gad; Lejbkowicz, Flavio] B Rappaport Fac Med, Haifa, Israel. [Andrulis, Irene L.; Glendon, Gord] Canc Care Ontario, Ontario Canc Genet Network, Toronto, ON M5G 2L7, Canada. [Andrulis, Irene L.] Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Samuel Lunenfeld Res Inst, Toronto, ON, Canada. [Andrulis, Irene L.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada. [Gerdes, Anne-Marie; Thomassen, Mads] Odense Univ Hosp, Dept Biochem Pharmacol & Genet, DK-5000 Odense, Denmark. [Sunde, Lone] Aarhus Univ Hosp, Dept Clin Genet, DK-8000 Aarhus, Denmark. [Caligo, Maria A.] Univ Pisa, Div Surg Mol & Ultrastructural Pathol, Dept Oncol, Pisa, Italy. [Caligo, Maria A.] Pisa Univ Hosp, Pisa, Italy. [Laitman, Yael; Kontorovich, Tair; Cohen, Shimrit; Friedman, Eitan] Chaim Sheba Med Ctr, Susanne Levy Gertner Oncogenet Unit, IL-52621 Tel Hashomer, Israel. [Kaufman, Bella] Chaim Sheba Med Ctr, Inst Oncol, IL-52621 Tel Hashomer, Israel. [Kaufman, Bella; Friedman, Eitan] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel. [Dagan, Efrat; Baruch, Ruth Gershoni] Rambam Med Ctr, Genet Inst, Haifa, Israel. [Harbst, Katja] Lund Univ, Dept Oncol, S-22100 Lund, Sweden. [Barbany-Bustinza, Gisela; Rantala, Johanna] Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden. [Ehrencrona, Hans] Uppsala Univ, Dept Genet & Pathol, Uppsala, Sweden. [Karlsson, Per] Sahlgrenska Univ, Dept Oncol, Gothenburg, Sweden. [Domchek, Susan M.; Nathanson, Katherine L.] Univ Penn, Philadelphia, PA 19104 USA. [Osorio, Ana; Benitez, Javier] Ctr Invest Biomed Red Enfermedades Raras CIBERERE, Inst Salud Carlos III, Madrid, Spain. [Osorio, Ana; Benitez, Javier] Spanish Natl Canc Ctr CNIO, Human Canc Genet Programme, Human Genet Grp, Madrid, Spain. [Blanco, Ignacio] Catalan Inst Oncol ICO, Canc Genet Counseling Program, Barcelona, Spain. [Lasa, Adriana] Hosp Santa Creu & Sant Pau, Genet Serv, Barcelona, Spain. [Hamann, Ute] Deutsch Krebsforschungszentrum, Neuenheimer Feld 580 69120, D-6900 Heidelberg, Germany. [Hogervorst, Frans B. L.] Netherlands Canc Inst, Dept Pathol, Family Canc Clin, NL-1066 CX Amsterdam, Netherlands. [Rookus, Matti A.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands. [Collee, J. Margriet] Erasmus Univ, Dept Clin Genet, Rotterdam Family Canc Clin, Med Ctr, NL-3000 DR Rotterdam, Netherlands. [Devilee, Peter] Dept Genet Epidemiol, Leiden, Netherlands. [Wijnen, Juul] Leiden Univ, Med Ctr, Ctr Human & Clin Genet, Leiden, Netherlands. [Ligtenberg, Marjolijn J.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 ED Nijmegen, Netherlands. [van der Luijt, Rob B.] Univ Utrecht, Med Ctr, Dept Clin Mol Genet, NL-3508 TC Utrecht, Netherlands. [Aalfs, Cora M.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands. [Waisfisz, Quinten] Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Amsterdam, Netherlands. [van Roozendaal, Cornelis E. P.] Univ Med Ctr, Dept Clin Genet, Maastricht, Netherlands. [Evans, D. Gareth; Lalloo, Fiona] Cent Manchester Univ Hosp, NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England. [Eeles, Rosalind] Inst Canc Res, Translat Canc Genet Team, London SW3 6JB, England. [Eeles, Rosalind] Royal Marsden NHS Fdn Trust, London, England. [Izatt, Louise] Guys Hosp, Clin Genet, London SE1 9RT, England. [Davidson, Rosemarie] Ferguson Smith Ctr Clin Genet, Glasgow, Lanark, Scotland. [Chu, Carol] Yorkshire Reg Genet Serv, Leeds, W Yorkshire, England. [Eccles, Diana] Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England. [Cole, Trevor] Birmingham Womens Hosp Healthcare, NHS Trust, W Midlands Reg Genet Serv, Birmingham, W Midlands, England. [Hodgson, Shirley] Univ London, Dept Canc Genet, St Georges Hosp, London, England. [Godwin, Andrew K.; Daly, Mary B.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. [Stoppa-Lyonnet, Dominique] Univ Paris 05, Paris, France. [Stoppa-Lyonnet, Dominique] Inst Curie, INSERM U509, Serv Genet Oncol, Paris, France. [Buecher, Bruno] Inst Curie, Dept Genet, Paris, France. [Bressac-de Paillerets, Brigitte; Remenieras, Audrey; Lenoir, Gilbert M.] Inst Cancrol Gustave Roussy, Dept Genet, Villejuif, France. [Bressac-de Paillerets, Brigitte] Inst Cancerol Gustave Roussy, INSERM U946, Villejuif, France. [Caron, Olivier] Inst Cancerol Gustave Roussy, Dept Med, Villejuif, France. [Lenoir, Gilbert M.] Inst Cancerol Gustave Roussy, CNRS FRE2939, Villejuif, France. [Sevenet, Nicolas; Longy, Michel] Inst Bergonie, Lab Genet Constitutionnelle, Bordeaux, France. [Longy, Michel] Inst Bergonie, INSERM U916, Bordeaux, France. [Ferrer, Sandra Fert] Hop Hotel Dieu, Ctr Hosp, Lab Genet Chromosom, Chambery, France. [Prieur, Fabienne] CHU St Etienne, Serv Genet Clin Chromosom, St Etienne, France. [Goldgar, David] Univ Utah, Dept Dermatol, Salt Lake City, UT 84112 USA. [Miron, Alexander; Yassin, Yosuf] Dana Farber Canc Inst, Boston, MA 02115 USA. [John, Esther M.] No Calif Canc Ctr, Fremont, CA USA. [John, Esther M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA. [Buys, Saundra S.] Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Salt Lake City, UT USA. [Hopper, John L.] Univ Melbourne, Melbourne, Australia. [Terry, Mary Beth] Columbia Univ, New York, NY USA. [Singer, Christian; Gschwantler-Kaulich, Daphne; Staudigl, Christine] Med Univ Vienna, Div Special Gynecol, Dept OB GYN, Vienna, Austria. [Hansen, Thomas V. O.] Univ Copenhagen, Rigshosp, Dept Clin Biochem, DK-2100 Copenhagen, Denmark. [Barkardottir, Rosa Bjork] Landspitali Univ Hosp, Dept Pathol, Reykjavik, Iceland. [Kirchhoff, Tomas; Pal, Prodipto; Kosarin, Kristi; Offit, Kenneth] Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA. [Piedmonte, Marion] Roswell Pk Canc Inst, GOG Stat & Data Ctr, Buffalo, NY 14263 USA. [Rodriguez, Gustavo C.] Evanston NW Healthcare, NorthShore Univ Hlth Syst, Evanston, IL 60201 USA. [Wakeley, Katie] Tufts Univ, New England Med Ctr, Boston, MA 02111 USA. [Boggess, John F.] Univ N Carolina, Chapel Hill, NC 27599 USA. [Basil, Jack] St Elizabeth Hosp, Edgewood, KY 41017 USA. [Schwartz, Peter E.] Yale Univ, Sch Med, New Haven, CT 06510 USA. [Blank, Stephanie V.] New York Univ, Sch Med, New York, NY 10016 USA. [Toland, Amanda E.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA. [Toland, Amanda E.] Ohio State Univ, Div Human Canc Genet, Ctr Comprehens Canc, Columbus, OH 43210 USA. [Montagna, Marco; Casella, Cinzia] IRCCS, Ist Oncologico Veneto, Immunol & Mol Oncol Unit, Padua, Italy. [Imyanitov, Evgeny N.] NN Petrov Inst Res Inst, St Petersburg, Russia. [Allavena, Anna] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy. [Schmutzler, Rita K.; Versmold, Beatrix; Arnold, Norbert] Univ Cologne, Dept Obstet & Gynaecol, Div Mol Gynaeco Oncol, Cologne, Germany. [Engel, Christoph] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany. [Meindl, Alfons] Tech Univ Munich, Dept Obstet & Gynaecol, Munich, Germany. [Ditsch, Nina] Univ Munich, Dept Obstet & Gynecol, Munich, Germany. Univ Schleswig Holstein, Dept Obstet & Gynaecol, Campus Kiel, Germany. [Niederacher, Dieter] Univ Duesseldorf, Dept Obstet & Gynaecol, Mol Genet Lab, Dusseldorf, Germany. [Deissler, Helmut] Univ Ulm, Dept Obstet & Gynaecol, Ulm, Germany. [Fiebig, Britta] Univ Regensburg, Inst Human Genet, Regensburg, Germany. [Suttner, Christian] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany. [Schoenbuchner, Ines] Univ Wurzburg, Inst Human Genet, D-8700 Wurzburg, Germany. [Gadzicki, Dorothea] Med Univ, Inst Cellular & Mol Pathol, Hannover, Germany. [Caldes, Trinidad; de la Hoya, Miguel] Hosp Clinico San Carlos 28040, Madrid, Spain. : Oxford University Press. - 0964-6906 .- 1460-2083. ; 18:22, s. 4442-4456
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome-wide association studies of breast cancer have identified multiple single nucleotide polymorphisms (SNPs) that are associated with increased breast cancer risks in the general population. In a previous study, we demonstrated that the minor alleles at three of these SNPs, in FGFR2, TNRC9 and MAP3K1, also confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. Three additional SNPs rs3817198 at LSP1, rs13387042 at 2q35 and rs13281615 at 8q24 have since been reported to be associated with breast cancer in the general population, and in this study we evaluated their association with breast cancer risk in 9442 BRCA1 and 5665 BRCA2 mutation carriers from 33 study centres. The minor allele of rs3817198 was associated with increased breast cancer risk only for BRCA2 mutation carriers [hazard ratio (HR) = 1.16, 95% CI: 1.07-1.25, P-trend = 2.8 × 10-4]. The best fit for the association of SNP rs13387042 at 2q35 with breast cancer risk was a dominant model for both BRCA1 and BRCA2 mutation carriers (BRCA1: HR = 1.14, 95% CI: 1.04-1.25, P = 0.0047; BRCA2: HR = 1.18 95% CI: 1.04-1.33, P = 0.0079). SNP rs13281615 at 8q24 was not associated with breast cancer for either BRCA1 or BRCA2 mutation carriers, but the estimated association for BRCA2 mutation carriers (per-allele HR = 1.06, 95% CI: 0.98-1.14) was consistent with odds ratio estimates derived from population-based case-control studies. The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers. There was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not. 
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4.
  • Johnatty, S. E., et al. (författare)
  • No evidence that GATA3 rs570613 SNP modifies breast cancer risk
  • 2009
  • Ingår i: Breast Cancer Research and Treatment. - : Springer. - 0167-6806 .- 1573-7217. ; 117:2, s. 371-379
  • Tidskriftsartikel (refereegranskat)abstract
    • GATA-binding protein 3 (GATA3) is a transcription factor that is crucial to mammary gland morphogenesis and differentiation of progenitor cells, and has been suggested to have a tumor suppressor function. The rs570613 single nucleotide polymorphism (SNP) in intron 4 of GATA3 was previously found to be associated with a reduction in breast cancer risk in the Cancer Genetic Markers of Susceptibility project and in pooled analysis of two case-control studies from Norway and Poland (P trend = 0.004), with some evidence for a stronger association with estrogen receptor (ER) negative tumours [Garcia-Closas M et al. (2007) Cancer Epidemiol Biomarkers Prev 16:2269-2275]. We genotyped GATA3 rs570613 in 6,388 cases and 4,995 controls from the Breast Cancer Association Consortium (BCAC) and 5,617 BRCA1 and BRCA2 carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). We found no association between this SNP and breast cancer risk in BCAC cases overall (ORper-allele = 1.00, 95% CI 0.94-1.05), in ER negative BCAC cases (ORper-allele = 1.02, 95% CI 0.91-1.13), in BRCA1 mutation carriers RRper-allele = 0.99, 95% CI 0.90-1.09) or BRCA2 mutation carriers (RRper-allele = 0.93, 95% CI 0.80-1.07). We conclude that there is no evidence that either GATA3 rs570613, or any variant in strong linkage disequilibrium with it, is associated with breast cancer risk in women. 
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5.
  • Huang, Y. -T, et al. (författare)
  • Specific Internet Disorders in University Students in Taiwan and Hong Kong : Psychometric Properties with Invariance Testing for the Traditional Chinese Version of the Assessment of Criteria for Specific Internet-Use Disorders (ACSID-11)
  • 2024
  • Ingår i: International Journal of Mental Health and Addiction. - : Springer. - 1557-1874 .- 1557-1882.
  • Tidskriftsartikel (refereegranskat)abstract
    • The Assessment of Criteria for Specific Internet-use Disorder (ACSID-11) is a psychometric instrument assessing different types of problematic internet use. The aim of the present study was to assess the psychometric properties of the traditional Chinese version and evaluate whether the traditional Chinese version showed similar and robust psychometric evidence to that of original ACSID-11 using a German sample. The present study was longitudinal and comprised 1257 university students in the first study and 409 university students in the follow-up study. Cronbach’s α and McDonald’s ω were used for testing internal consistency of the ACSID-11. A confirmatory factor analysis (CFA) was conducted to examine construct validity. Multi-group CFA was performed to assess the invariance of the factor structure across region and sex. Moreover, Pearson correlations were conducted to examine the test–retest reliability and concurrent validity of ACSID-11. The results suggested satisfactory levels of test–retest reliability, internal consistency, and validity of the ACSID-11. The four-factor structure of the ACSID-11 was replicated and confirmed in both Taiwan and Hong Kong samples. The study findings demonstrated that the traditional Chinese version of the ACSID-11 is reliable and valid for assessing and distinguishing specific internet-use disorders and is applicable across regions and sexes among emerging adults in Taiwan and Hong Kong.
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6.
  • Chang, K. -C, et al. (författare)
  • Comparisons of psychological distress and self-stigma among three types of substance use disorders receiving treatment-as-usual approaches : real-world data from a 9-month longitudinal study
  • 2022
  • Ingår i: Therapeutic Advances in Chronic Disease. - : Sage Publications. - 2040-6223 .- 2040-6231. ; 13
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Substance use is an important issue worldwide and people with substance use disorders (SUDs) have been reported to have high levels of psychological distress and self-stigma. Therefore, psychological distress and self-stigma in people with SUDs are considerable. Objective: The present study used a longitudinal design to examine whether treatment-as-usual approaches in Taiwan improve psychological distress and self-stigma among people with three types of SUDs (heroin, amphetamine, and alcohol use disorders). Design: A 9-month longitudinal design involving four assessments spaced 3 months apart. Methods: Convenience sampling was used to recruit people with heroin (n = 112), amphetamine (n = 151), and alcohol (n = 56) use disorders from outpatient psychiatric center in Southern Taiwan. Psychological distress was assessed using the Depression, Anxiety, Stress Scale (DASS-21), and self-stigma was assessed using the Self-Stigma Scale–Short (SSS-S). Generalized estimating equation (GEE) models were constructed to understand between-group differences in psychological distress and self-stigma over time. Results: Patients with heroin and amphetamine use disorders had lower levels of psychological distress as compared with those with alcohol use disorder. Levels of psychological distress were lower at Time 2 to Time 4 as compared with Time 1. Patients with heroin and amphetamine use disorders had higher levels of self-stigma as compared with those with alcohol use disorder. Self-stigma levels remained stable over time. The dropout rate of receiving treatment-as-usual approach in the 9-month study was 60%. Conclusion: Treatment as usual for SUDs among outpatients in Taiwan may decrease psychological distress but not self-stigma. However, such effects need to be further examined given the high drop-out rates and absence of a control condition. The findings suggest that self-stigma may warrant additional treatment for patients with SUDs.
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7.
  • Engel, C., et al. (författare)
  • Association of the variants CASP8 D302H and CASP10 V410I with breast and ovarian cancer risk in BRCA1 and BRCA2 mutation carriers
  • 2010
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 19:11, s. 2859-2868
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The genes caspase-8 (CASP8) and caspase-10 (CASP10) functionally cooperate and play a key role in the initiation of apoptosis. Suppression of apoptosis is one of the major mechanisms underlying the origin and progression of cancer. Previous case-control studies have indicated that the polymorphisms CASP8 D302H and CASP10 V410I are associated with a reduced risk of breast cancer in the general population.Methods: To evaluate whether the CASP8 D302H (CASP10 V410I) polymorphisms modify breast or ovarian cancer risk in BRCA1 and BRCA2 mutation carriers, we analyzed 7,353 (7,227) subjects of white European origin provided by 19 (18) study groups that participate in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). A weighted cohort approach was used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI).Results: The minor allele of CASP8 D302H was significantly associated with a reduced risk of breast cancer (per-allele HR, 0.85; 95% CI, 0.76-0.97; Ptrend = 0.011) and ovarian cancer (per-allele HR, 0.69; 95% CI, 0.53-0.89; Ptrend = 0.004) for BRCA1 but not for BRCA2 mutation carriers. The CASP10 V410I polymorphism was not associated with breast or ovarian cancer risk for BRCA1 or BRCA2 mutation carriers.Conclusions: CASP8 D302H decreases breast and ovarian cancer risk for BRCA1 mutation carriers but not for BRCA2 mutation carriers.Impact: The combined application of these and other recently identified genetic riskmodifiers could in the future allow better individual risk calculation and could aid in the individualized counseling and decision making with respect to preventive options in BRCA1 mutation carriers.
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8.
  • Huang, P. -C, et al. (författare)
  • Temporal associations between physical activity and three types of problematic use of the internet : A six-month longitudinal study
  • 2022
  • Ingår i: Journal of Behavioral Addictions. - : Akademiai Kiado. - 2062-5871 .- 2063-5303. ; 11:4, s. 1055-1067
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and aims: Internet use has become an important part of daily living. However, for a minority it may become problematic. Moreover, problematic use of the Internet/smartphone (PUIS) has been associated with low physical activity. The present study investigated the temporal associations between three types of PUIS (i.e., problematic smartphone use [PSPU], problematic social media use [PSMU] and problematic gaming [PG]) and physical activity among Taiwanese university students. Methods: A six-month longitudinal survey study comprising three time points for assessments was conducted. From the original 974 participants, a total of 452 completed all three waves of an online survey comprising the International Physical Activity Questionnaire Short Form (IPAQ-SF) assessing physical activity level, Smartphone Application-Based Addiction Scale (SABAS) assessing PSPU, Bergen Social Media Addiction Scale (BSMAS) assessing PSMU, and Internet Gaming Disorder Short Form (IGDS9-SF) assessing PG. Results: The linear mixed effects model found positive temporal associations of PSMU and PG with physical activity level (PSMU: B = 85.88, SE = 26.24; P = 0.001; PG: B = 36.81, SE = 15.17; P = 0.02). PSPU was not associated with physical activity level (B = 40.54, SE = 22.99; P = 0.08). Additionally, the prevalence rates were 44.4% for at-risk/PSPU, 24.6% for at-risk/PSMU, and 12.3% for at-risk/PG. Discussion and Conclusions: PSMU and PG unexpectedly demonstrated correlations with higher physical activity level. The nature of these relationships warrants additional investigation into the underlying mechanisms in order to promote healthy lifestyles among university students.
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9.
  • Chang, K. -C, et al. (författare)
  • A longitudinal study of the effects of problematic smartphone use on social functioning among people with schizophrenia : Mediating roles for sleep quality and self-stigma
  • 2022
  • Ingår i: Journal of Behavioral Addictions. - : Akademiai Kiado. - 2062-5871 .- 2063-5303. ; 11:2, s. 567-576
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and aims: Individuals with schizophrenia may often experience poor sleep, self-stigma, impaired social functions, and problematic smartphone use. However, the temporal relationships between these factors have not been investigated. The present study used a longitudinal design to examine potential mediating roles of poor sleep and self-stigma in associations between problematic smartphone use and impaired social functions among individuals with schizophrenia. Methods: From April 2019 to August 2021, 193 individuals with schizophrenia (mean [SD] age = 41.34 [9.01] years; 88 [45.6%] males) were recruited and asked to complete three psychometric scales: the Smartphone Application-Based Addiction Scale to assess problematic smartphone use; the Pittsburgh Sleep Quality Index to assess sleep quality; and the Self-Stigma Scale-Short Scale to assess self-stigma. Social functioning was evaluated by a psychiatrist using the Personal and Social Performance Scale. All measures were assessed five times (one baseline and four follow-ups) at three-month intervals between assessments. Results: General estimating equations found that problematic smartphone use (coefficient =-0.096, SE = 0.021; P < 0.001), sleep quality (coefficient =-0.134, SE = 0.038; P < 0.001), and self-stigma (coefficient =-0.612, SE = 0.192; P = 0.001) were significant statistical predictors for social functioning. Moreover, sleep quality and self-stigma mediated associations between problematic smartphone use and social functioning. Conclusion: Problematic smartphone use appears to impact social functioning longitudinally among individuals with schizophrenia via poor sleep and self-stigma concerns. Interventions aimed at reducing problematic smartphone use, improving sleep, and addressing self-stigma may help improve social functioning among individuals with schizophrenia.
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10.
  • Kukreti, S., et al. (författare)
  • Post-traumatic stress disorder in Chinese teachers during covid-19 pandemic : Roles of fear of COVID-19, nomophobia, and psychological distress
  • 2021
  • Ingår i: Healthcare. - : MDPI. - 2227-9032. ; 9:10
  • Tidskriftsartikel (refereegranskat)abstract
    • There are limited data concerning the prevalence of post-traumatic stress disorder (PTSD) among teachers. Therefore, the present study estimated the prevalence of PTSD among mainland Chinese teachers during the COVID-19 pandemic and to construct a model with mediation and moderation effects to explain the PTSD. Data collection was conducted in schools in the Jiangxi province between October and November 2020 among k-12 schoolteachers. An online survey, including five different psychometric scales, was used to collect data. All participants were assessed for PTSD using the Chinese version of the PTSD Checklist for DSM-5 (PCL-5). Hayes’ PROCESS Model 8 was used to examine the potential factors explaining a higher PTSD scores. A total of 2603 teachers from k-12 schools participated. With the cutoff score at 31, the prevalence of PTSD was 12.3% but decreased to 1.0% when the cutoff score was at 49. Nomophobia moderated the effects of Fear of COVID-19 Scale on PTSD. The findings suggest that fear of COVID-19 among teachers leads to PTSD via psychological distress, highlighting the moderating effect of nomophobia in this association. Based on the study’s findings, psychological interventions and educational training are needed to reduce fear among teachers at higher risk of developing PTSD.
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