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Publications (10 of 159) Show all publications
Du, M., Xin, J., Zheng, R., Yuan, Q., Wang, Z., Liu, H., . . . Christiani, D. C. (2024). Cyp2a6 activity and cigarette consumption interact in smoking-related lung cancer susceptibility. Cancer Research, 84(4), 616-625
Open this publication in new window or tab >>Cyp2a6 activity and cigarette consumption interact in smoking-related lung cancer susceptibility
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2024 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 84, no 4, p. 616-625Article in journal (Refereed) Published
Abstract [en]

Cigarette smoke, containing both nicotine and carcinogens, causes lung cancer. However, not all smokers develop lung cancer, highlighting the importance of the interaction between host susceptibility and environmental exposure in tumorigenesis. Here, we aimed to delineate the interaction between metabolizing ability of tobacco carcinogens and smoking intensity in mediating genetic susceptibility to smoking-related lung tumorigenesis. Single-variant and gene-based associations of 43 tobacco carcinogen–metabolizing genes with lung cancer were analyzed using summary statistics and individual-level genetic data, followed by causal inference of Mendelian randomization, mediation analysis, and structural equation modeling. Cigarette smoke–exposed cell models were used to detect gene expression patterns in relation to specific alleles. Data from the International Lung Cancer Consortium (29,266 cases and 56,450 controls) and UK Biobank (2,155 cases and 376,329 controls) indicated that the genetic variant rs56113850 C>T located in intron 4 of CYP2A6 was significantly associated with decreased lung cancer risk among smokers (OR = 0.88, 95% confidence interval = 0.85–0.91, P = 2.18 X 10-16), which might interact (Pinteraction = 0.028) with and partially be mediated (ORindirect = 0.987) by smoking status. Smoking intensity accounted for 82.3% of the effect of CYP2A6 activity on lung cancer risk but entirely mediated the genetic effect of rs56113850. Mechanistically, the rs56113850 T allele rescued the downregulation of CYP2A6 caused by cigarette smoke exposure, potentially through preferential recruitment of transcription factor helicase-like transcription factor. Together, this study provides additional insights into the interplay between host susceptibility and carcinogen exposure in smoking-related lung tumorigenesis.

Place, publisher, year, edition, pages
American Association For Cancer Research (AACR), 2024
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:umu:diva-222228 (URN)10.1158/0008-5472.CAN-23-0900 (DOI)1163685000010 ()38117513 (PubMedID)2-s2.0-85185218849 (Scopus ID)
Available from: 2024-03-14 Created: 2024-03-14 Last updated: 2024-03-14Bibliographically approved
Zhao, X., Yang, M., Fan, J., Wang, M., Wang, Y., Qin, N., . . . Dai, J. (2024). Identification of genetically predicted DNA methylation markers associated with non–small cell lung cancer risk among 34,964 cases and 448,579 controls. Cancer, 130(6), 913-926
Open this publication in new window or tab >>Identification of genetically predicted DNA methylation markers associated with non–small cell lung cancer risk among 34,964 cases and 448,579 controls
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2024 (English)In: Cancer, ISSN 0008-543X, E-ISSN 1097-0142, Vol. 130, no 6, p. 913-926Article in journal (Refereed) Published
Abstract [en]

Background: Although the associations between genetic variations and lung cancer risk have been explored, the epigenetic consequences of DNA methylation in lung cancer development are largely unknown. Here, the genetically predicted DNA methylation markers associated with non–small cell lung cancer (NSCLC) risk by a two-stage case-control design were investigated.

Methods: The genetic prediction models for methylation levels based on genetic and methylation data of 1595 subjects from the Framingham Heart Study were established. The prediction models were applied to a fixed-effect meta-analysis of screening data sets with 27,120 NSCLC cases and 27,355 controls to identify the methylation markers, which were then replicated in independent data sets with 7844 lung cancer cases and 421,224 controls. Also performed was a multi-omics functional annotation for the identified CpGs by integrating genomics, epigenomics, and transcriptomics and investigation of the potential regulation pathways.

Results: Of the 29,894 CpG sites passing the quality control, 39 CpGs associated with NSCLC risk (Bonferroni-corrected p ≤ 1.67 × 10−6) were originally identified. Of these, 16 CpGs remained significant in the validation stage (Bonferroni-corrected p ≤ 1.28 × 10−3), including four novel CpGs. Multi-omics functional annotation showed nine of 16 CpGs were potentially functional biomarkers for NSCLC risk. Thirty-five genes within a 1-Mb window of 12 CpGs that might be involved in regulatory pathways of NSCLC risk were identified.

Conclusions: Sixteen promising DNA methylation markers associated with NSCLC were identified. Changes of the methylation level at these CpGs might influence the development of NSCLC by regulating the expression of genes nearby.

Plain Language Summary: The epigenetic consequences of DNA methylation in lung cancer development are still largely unknown. This study used summary data of large-scale genome-wide association studies to investigate the associations between genetically predicted levels of methylation biomarkers and non–small cell lung cancer risk at the first time. This study looked at how well larotrectinib worked in adult patients with sarcomas caused by TRK fusion proteins. These findings will provide a unique insight into the epigenetic susceptibility mechanisms of lung cancer.

Place, publisher, year, edition, pages
John Wiley & Sons, 2024
Keywords
association study, DNA methylation, gene expression, genetic prediction, non–small cell lung cancer risk
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:umu:diva-217717 (URN)10.1002/cncr.35130 (DOI)001114272200001 ()38055287 (PubMedID)2-s2.0-85178394580 (Scopus ID)
Available from: 2023-12-11 Created: 2023-12-11 Last updated: 2024-04-30Bibliographically approved
Li, Y., Xiao, X., Li, J., Han, Y., Cheng, C., Fernandes, G. F., . . . Amos, C. I. (2024). Lung cancer in ever- and never-smokers: findings from multi-population GWAS studies. Cancer Epidemiology, Biomarkers and Prevention, 33(3), 389-399
Open this publication in new window or tab >>Lung cancer in ever- and never-smokers: findings from multi-population GWAS studies
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2024 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 33, no 3, p. 389-399Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Clinical, molecular, and genetic epidemiology studies displayed remarkable differences between ever- and never-smoking lung cancer.

METHODS: We conducted a stratified multi-population (European, East Asian, and African descent) association study on 44,823 ever-smokers and 20,074 never-smokers to identify novel variants that were missed in the non-stratified analysis. Functional analysis including expression quantitative trait loci (eQTL) colocalization and DNA damage assays, and annotation studies were conducted to evaluate the functional roles of the variants. We further evaluated the impact of smoking quantity on lung cancer risk for the variants associated with ever-smoking lung cancer.

RESULTS: Five novel independent loci, GABRA4, intergenic region 12q24.33, LRRC4C, LINC01088, and LCNL1 were identified with the association at two or three populations (P < 5 × 10-8). Further functional analysis provided multiple lines of evidence suggesting the variants affect lung cancer risk through excessive DNA damage (GABRA4) or cis-regulation of gene expression (LCNL1). The risk of variants from 12 independent regions, including the well-known CHRNA5, associated with ever-smoking lung cancer was evaluated for never-smokers, light-smokers (packyear ≤ 20), and moderate-to-heavy-smokers (packyear > 20). Different risk patterns were observed for the variants among the different groups by smoking behavior.

CONCLUSIONS: We identified novel variants associated with lung cancer in only ever- or never-smoking groups that were missed by prior main-effect association studies. IMPACT: Our study highlights the genetic heterogeneity between ever- and never-smoking lung cancer and provides etiologic insights into the complicated genetic architecture of this deadly cancer.

Place, publisher, year, edition, pages
American Association For Cancer Research (AACR), 2024
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:umu:diva-222350 (URN)10.1158/1055-9965.EPI-23-0613 (DOI)38180474 (PubMedID)2-s2.0-85186745004 (Scopus ID)
Funder
NIH (National Institutes of Health)
Available from: 2024-03-18 Created: 2024-03-18 Last updated: 2024-03-18Bibliographically approved
Luyapan, J., Bossé, Y., Li, Z., Xiao, X., Rosenberger, A., Hung, R. J., . . . Amos, C. I. (2023). Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk. Human Molecular Genetics, 32(18), 2842-2855
Open this publication in new window or tab >>Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk
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2023 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 32, no 18, p. 2842-2855Article in journal (Refereed) Published
Abstract [en]

Pulmonary surfactant is a lipoprotein synthesized and secreted by alveolar type II cells in lung. We evaluated the associations between 200,139 single nucleotide polymorphisms (SNPs) of 40 surfactant-related genes and lung cancer risk using genotyped data from two independent lung cancer genome-wide association studies. Discovery data included 18,082 cases and 13,780 controls of European ancestry. Replication data included 1,914 cases and 3,065 controls of European descent. Using multivariate logistic regression, we found novel SNPs in surfactant-related genes CTSH [rs34577742 C > T, odds ratio (OR) = 0.90, 95% confidence interval (CI) = 0.89-0.93, P = 7.64 × 10-9] and SFTA2 (rs3095153 G > A, OR = 1.16, 95% CI = 1.10-1.21, P = 1.27 × 10-9) associated with overall lung cancer in the discovery data and validated in an independent replication data-CTSH (rs34577742 C > T, OR = 0.88, 95% CI = 0.80-0.96, P = 5.76 × 10-3) and SFTA2 (rs3095153 G > A, OR = 1.14, 95% CI = 1.01-1.28, P = 3.25 × 10-2). Among ever smokers, we found SNPs in CTSH (rs34577742 C > T, OR = 0.89, 95% CI = 0.85-0.92, P = 1.94 × 10-7) and SFTA2 (rs3095152 G > A, OR = 1.20, 95% CI = 1.14-1.27, P = 4.25 × 10-11) associated with overall lung cancer in the discovery data and validated in the replication data-CTSH (rs34577742 C > T, OR = 0.88, 95% CI = 0.79-0.97, P = 1.64 × 10-2) and SFTA2 (rs3095152 G > A, OR = 1.15, 95% CI = 1.01-1.30, P = 3.81 × 10-2). Subsequent transcriptome-wide association study using expression weights from a lung expression quantitative trait loci study revealed genes most strongly associated with lung cancer are CTSH (PTWAS = 2.44 × 10-4) and SFTA2 (PTWAS = 2.32 × 10-6).

Place, publisher, year, edition, pages
Oxford University Press, 2023
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-214250 (URN)10.1093/hmg/ddad095 (DOI)37471639 (PubMedID)2-s2.0-85169846740 (Scopus ID)
Funder
NIH (National Institutes of Health), 5U01CA209414; T32LM012204; 5U01CA209414
Available from: 2023-09-18 Created: 2023-09-18 Last updated: 2023-09-18Bibliographically approved
Shi, J., Grankvist, K. & Lan, Q. (2023). Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population. Nature Communications, 14(1), Article ID 3043.
Open this publication in new window or tab >>Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population
2023 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 14, no 1, article id 3043Article in journal (Refereed) Published
Abstract [en]

Lung adenocarcinoma is the most common type of lung cancer. Known risk variants explain only a small fraction of lung adenocarcinoma heritability. Here, we conducted a two-stage genome-wide association study of lung adenocarcinoma of East Asian ancestry (21,658 cases and 150,676 controls; 54.5% never-smokers) and identified 12 novel susceptibility variants, bringing the total number to 28 at 25 independent loci. Transcriptome-wide association analyses together with colocalization studies using a Taiwanese lung expression quantitative trait loci dataset (n = 115) identified novel candidate genes, including FADS1 at 11q12 and ELF5 at 11p13. In a multi-ancestry meta-analysis of East Asian and European studies, four loci were identified at 2p11, 4q32, 16q23, and 18q12. At the same time, most of our findings in East Asian populations showed no evidence of association in European populations. In our studies drawn from East Asian populations, a polygenic risk score based on the 25 loci had a stronger association in never-smokers vs. individuals with a history of smoking (Pinteraction = 0.0058). These findings provide new insights into the etiology of lung adenocarcinoma in individuals from East Asian populations, which could be important in developing translational applications.

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Medical Genetics Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-210530 (URN)10.1038/s41467-023-38196-z (DOI)37236969 (PubMedID)2-s2.0-85160220141 (Scopus ID)
Available from: 2023-06-22 Created: 2023-06-22 Last updated: 2024-03-26Bibliographically approved
Cheng, C., Hong, W., Li, Y., Xiao, X., McKay, J., Han, Y., . . . Amos, C. I. (2023). Mosaic chromosomal alterations are associated with increased lung cancer risk: insight from the INTEGRAL-ILCCO cohort analysis. Journal of Thoracic Oncology
Open this publication in new window or tab >>Mosaic chromosomal alterations are associated with increased lung cancer risk: insight from the INTEGRAL-ILCCO cohort analysis
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2023 (English)In: Journal of Thoracic Oncology, ISSN 1556-0864, E-ISSN 1556-1380Article in journal (Refereed) In press
Abstract [en]

Introduction: Mosaic chromosomal alterations (mCAs) detected in white blood cells represent a type of clonal hematopoiesis (CH) that is understudied compared with CH-related somatic mutations. A few recent studies indicated their potential link with nonhematological cancers, especially lung cancer. Methods: In this study, we investigated the association between mCAs and lung cancer using the high-density genotyping data from the OncoArray study of INTEGRAL-ILCCO, the largest single genetic study of lung cancer with 18,221 lung cancer cases and 14,825 cancer-free controls. Results: We identified a comprehensive list of autosomal mCAs, ChrX mCAs, and mosaic ChrY (mChrY) losses from these samples. Autosomal mCAs were detected in 4.3% of subjects, in addition to ChrX mCAs in 3.6% of females and mChrY losses in 9.6% of males. Multivariable logistic regression analysis indicated that the presence of autosomal mCAs in white blood cells was associated with an increased lung cancer risk after adjusting for key confounding factors, including age, sex, smoking status, and race. This association was mainly driven by a specific type of mCAs: copy-neutral loss of heterozygosity on autosomal chromosomes. The association between autosome copy-neutral loss of heterozygosity and increased risk of lung cancer was further confirmed in two major histologic subtypes, lung adenocarcinoma and squamous cell carcinoma. In addition, we observed a significant increase of ChrX mCAs and mChrY losses in smokers compared with nonsmokers and racial differences in certain types of mCA events. Conclusions: Our study established a link between mCAs in white blood cells and increased risk of lung cancer.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Clonal hematopoiesis, Loss of heterozygosity, Lung cancer risk, Mosaic chromosomal alterations
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:umu:diva-212103 (URN)10.1016/j.jtho.2023.05.001 (DOI)37150255 (PubMedID)2-s2.0-85163295925 (Scopus ID)
Funder
NIH (National Institutes of Health), 1R01CA269764
Available from: 2023-07-17 Created: 2023-07-17 Last updated: 2024-03-26
Smith-Byrne, K., Cerani, A., Guida, F., Zhou, S., Agudo, A., Aleksandrova, K., . . . Richards, J. B. (2022). Circulating Isovalerylcarnitine and Lung Cancer Risk: evidence from Mendelian Randomization and Prediagnostic Blood Measurements. Cancer Epidemiology, Biomarkers and Prevention, 31(10), 1966-1974
Open this publication in new window or tab >>Circulating Isovalerylcarnitine and Lung Cancer Risk: evidence from Mendelian Randomization and Prediagnostic Blood Measurements
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2022 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 31, no 10, p. 1966-1974Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Tobacco exposure causes 8 of 10 lung cancers, and identifying additional risk factors is challenging due to confounding introduced by smoking in traditional observational studies.

MATERIALS AND METHODS: We used Mendelian randomization (MR) to screen 207 metabolites for their role in lung cancer predisposition using independent genome-wide association studies (GWAS) of blood metabolite levels (n = 7,824) and lung cancer risk (n = 29,266 cases/56,450 controls). A nested case-control study (656 cases and 1,296 matched controls) was subsequently performed using prediagnostic blood samples to validate MR association with lung cancer incidence data from population-based cohorts (EPIC and NSHDS).

RESULTS: An MR-based scan of 207 circulating metabolites for lung cancer risk identified that blood isovalerylcarnitine (IVC) was associated with a decreased odds of lung cancer after accounting for multiple testing (log10-OR = 0.43; 95% CI, 0.29-0.63). Molar measurement of IVC in prediagnostic blood found similar results (log10-OR = 0.39; 95% CI, 0.21-0.72). Results were consistent across lung cancer subtypes.

CONCLUSIONS: Independent lines of evidence support an inverse association of elevated circulating IVC with lung cancer risk through a novel methodologic approach that integrates genetic and traditional epidemiology to efficiently identify novel cancer biomarkers.

IMPACT: Our results find compelling evidence in favor of a protective role for a circulating metabolite, IVC, in lung cancer etiology. From the treatment of a Mendelian disease, isovaleric acidemia, we know that circulating IVC is modifiable through a restricted protein diet or glycine and L-carnatine supplementation. IVC may represent a modifiable and inversely associated biomarker for lung cancer.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-200447 (URN)10.1158/1055-9965.EPI-21-1033 (DOI)000868221500001 ()35839461 (PubMedID)2-s2.0-85139570941 (Scopus ID)
Available from: 2022-10-25 Created: 2022-10-25 Last updated: 2023-09-05Bibliographically approved
Byun, J., Han, Y., Li, Y., Xia, J., Long, E., Choi, J., . . . Amos, C. I. (2022). Cross-ancestry genome-wide meta-analysis of 61,047 cases and 947,237 controls identifies new susceptibility loci contributing to lung cancer. Nature Genetics, 54(8), 1167-1177
Open this publication in new window or tab >>Cross-ancestry genome-wide meta-analysis of 61,047 cases and 947,237 controls identifies new susceptibility loci contributing to lung cancer
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2022 (English)In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 54, no 8, p. 1167-1177Article in journal (Refereed) Published
Abstract [en]

To identify new susceptibility loci to lung cancer among diverse populations, we performed cross-ancestry genome-wide association studies in European, East Asian and African populations and discovered five loci that have not been previously reported. We replicated 26 signals and identified 10 new lead associations from previously reported loci. Rare-variant associations tended to be specific to populations, but even common-variant associations influencing smoking behavior, such as those with CHRNA5 and CYP2A6, showed population specificity. Fine-mapping and expression quantitative trait locus colocalization nominated several candidate variants and susceptibility genes such as IRF4 and FUBP1. DNA damage assays of prioritized genes in lung fibroblasts indicated that a subset of these genes, including the pleiotropic gene IRF4, potentially exert effects by promoting endogenous DNA damage.

Place, publisher, year, edition, pages
Nature Research, 2022
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-198568 (URN)10.1038/s41588-022-01115-x (DOI)000834739900001 ()35915169 (PubMedID)2-s2.0-85135272569 (Scopus ID)
Funder
NIH (National Institutes of Health)
Available from: 2022-08-12 Created: 2022-08-12 Last updated: 2023-03-24Bibliographically approved
Li, Y., Xiao, X., Li, J., Byun, J., Cheng, C., Bossé, Y., . . . Amos, C. I. (2022). Genome-wide interaction analysis identified low-frequency variants with sex disparity in lung cancer risk. Human Molecular Genetics, 31(16), 2831-2843
Open this publication in new window or tab >>Genome-wide interaction analysis identified low-frequency variants with sex disparity in lung cancer risk
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2022 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 31, no 16, p. 2831-2843Article in journal (Refereed) Published
Abstract [en]

Differences by sex in lung cancer incidence and mortality have been reported which cannot be fully explained by sex differences in smoking behavior, implying existence of genetic and molecular basis for sex disparity in lung cancer development. However, the information about sex dimorphism in lung cancer risk is quite limited despite the great success in lung cancer association studies. By adopting a stringent two-stage analysis strategy, we performed a genome-wide gene-sex interaction analysis using genotypes from a lung cancer cohort including ~ 47 000 individuals with European ancestry. Three low-frequency variants (minor allele frequency < 0.05), rs17662871 [odds ratio (OR) = 0.71, P = 4.29×10-8); rs79942605 (OR = 2.17, P = 2.81×10-8) and rs208908 (OR = 0.70, P = 4.54×10-8) were identified with different risk effect of lung cancer between men and women. Further expression quantitative trait loci and functional annotation analysis suggested rs208908 affects lung cancer risk through differential regulation of Coxsackie virus and adenovirus receptor gene expression in lung tissues between men and women. Our study is one of the first studies to provide novel insights about the genetic and molecular basis for sex disparity in lung cancer development.

Place, publisher, year, edition, pages
Oxford University Press, 2022
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-199395 (URN)10.1093/hmg/ddac030 (DOI)000769849700001 ()35138370 (PubMedID)2-s2.0-85137124752 (Scopus ID)
Available from: 2022-09-28 Created: 2022-09-28 Last updated: 2023-05-04Bibliographically approved
Nilsson, K., Brulin, C., Grankvist, K. & Juthberg, C. (2022). Senior nursing students' reflections on deviations from guideline adherence regarding venous blood specimen collection practice: A qualitative study. Nurse Education Today, 115, Article ID 105375.
Open this publication in new window or tab >>Senior nursing students' reflections on deviations from guideline adherence regarding venous blood specimen collection practice: A qualitative study
2022 (English)In: Nurse Education Today, ISSN 0260-6917, E-ISSN 1532-2793, Vol. 115, article id 105375Article in journal (Refereed) Published
Abstract [en]

Background: Venous blood specimen collection is a common procedure within healthcare and both diagnoses as well as treatment evaluation, are often based on results from these analyses. However, studies among both students and staff have demonstrated suboptimal adherence to venous blood specimen collection practice guidelines which in turn might jeopardize patient safety.

Objectives: This study aimed to describe final semester nursing students' experiences of deviations from venous blood specimen collection practice guidelines during clinical training.

Methods: This study adopted a qualitative design. Twentysix final (6th) semester nursing students were recruited through purposive sampling at a Swedish university. Data were collected through semi-structured, face-to-face, focus group interviews in September 2015. The transcribed interviews were analyzed using qualitative content analysis.

Results: The students' experiences generated two categories; 1) Striving to blend in (subcategories Feeling uncomfortable and Adapting to the prevailing practice culture) and 2) Diminished confidence (subcategories Being confused due to inconsistency and Being uncertain about guideline usefulness) forming the overall theme Being a copycat.

Conclusion: The research concludes that nursing students adapt to the prevailing practice culture encountered during clinical training, often at the expense of guidelines adherence. Since the students are being assessed during clinical training, the eagerness to belong to the team and be well-liked might be stronger than the ambition to follow guidelines. As a consequence, nursing students in clinical training might become copycats by aligning themselves with the prevailing practice culture which in turn might jeopardize adherence with VBSC guideline practice and thereby patient safety. With the ambition to support nursing students' learning in clinical training, facilitators of learning to comprise both students and supervisors need to be further addressed. Tweetable abstract: Nursing students adapt to the prevailing venous blood sample collection practice culture and become copycats.

Place, publisher, year, edition, pages
Elsevier, 2022
Keywords
Clinical training, Content analysis, Nursing students, Professional socialization, Venous blood specimen collection
National Category
Nursing
Identifiers
urn:nbn:se:umu:diva-203217 (URN)10.1016/j.nedt.2022.105375 (DOI)35653918 (PubMedID)2-s2.0-85131554870 (Scopus ID)
Available from: 2023-01-17 Created: 2023-01-17 Last updated: 2023-01-17Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-4289-2097

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