10 research outputs found
An Empirical Study of Commercial Banks in Kenya
No full textFull TextThis study investigates the influence of strategic planning and planning outcomes;
planning outcomes and firm performance. Measures of strategic planning were seven
dimensions namely internal orientation, external orientation, functional integration, key
personnel involvement in planning, use of planning techniques, creativity in planning,
focus on control. Measures of planning outcomes comprised direction and focus,
sustainable competitive advantage, firm-environment fit, efficiency in allocation of
resources, improved innovation, greater organizational commitment, improved coordination
and control of organization activities, improved organizational analysis.
Measures of firm performance were both financial and non financial. Financial items
composed of Gross Profit Margin, Return on Investment and Return on Asset. Non
financial items comprised of ability to evaluate alternatives, ability to avoid mistakes,
improved budget process. Commercial banks in Kenya were studied using both primary
and secondary data. In this study, a census of 44 commercial banks in Nairobi Kenya
was done. The majority (80 per cent) of the respondents were managers in charge of
planning and 20 per cent were either heads of human resource departments or business
and marketing department. Various data analysis procedures were applied including
descriptive analysis, Pearson Moment Correlation Coefficient; F-statistics were used in
order to accomplish the objectives of the study. Hypotheses H1, H2, H3 were tested for
correlation. The study found that there are a positive and significant relationship
between strategic planning (seven dimensions of planning) and firm performance;
strategic planning and planning outcomes and finally planning outcomes and firm
performance. Thus, the study suggests that effective and focused strategic planning lead
to positive change in firm performance. This study therefore is significant since it has
contributed immensely to the body of knowledge more specifically in strategic planning
where key variables of the study have been linked individually to organizational
performance. The study also impacts positively to the readers and scholars where they
are able to relate strategic planning, planning outcomes and performance in a real
working environment and interrogate the existing theories and concepts in the area of
strategic management in the African context.University of Nairob
The effect of the multi-cultural environment on the central managment of the human resources in the Czech MNC
Full text linkkatedra: KOB; přílohy: 1 CD ROM; rozsah: 92 s. (120 764 znaků)The goal of this thesis is to analyze the influence of the various cultures on the human resources management in the multinational corporation LINET. LINET is on of the largest companies operating in the medical bed branch. The company uses subsidiaries in many countries all around the world, in order to secure its?market position. Therefore a perfect communication between the Czech headquarters and subsidiaries is essential. This is directly connected with all of the HR processes within the international environment of the company. These processes are influenced, at certain level, by the variety of the cultures of the different countries, where the subsidiaries based in. This thesis defines the factors, which can be influenced by the cultural diversity, in the area mentioned above. The author creates and prepares a research, which will be in the form of questionnaires for the employees in the subsidiaries of the LINET Company. This research will result in an internal manual of the LINET Company, which will include hints and recommendations to the communication and behaviour within the intercultural communication in the area of the human resources management.Předmětem této diplomové práce je zpracování vlivu rozdílných kultur na řízení lidských zdrojů v nadnárodní společnosti LINET. Firma LINET je jednou z největších firem v oblasti nemocničních lůžek. Na této pozici se udržuje mimo jiné také díky svým zahraničním pobočkám a dceřiným společnostem. Z toho plyne nutnost dokonalé komunikace mezi pobočkami a českou centrálou. S tím jsou spojeny veškeré HR procesy v rámci mezinárodního prostředí firmy. Tyto procesy jsou do jisté míry ovlivňovány odlišností kultur jednotlivých zemí, kde mají pobočky sídlo. Tato práce vymezuje faktory, které v této oblasti mohou být ovlivněny rozdílností kultur. Následně autor práce vytváří a natavuje parametry průzkumu, který formou dotazníkového šetření proběhne ve společnosti LINET. K tomuto průzkumu jsou v rámci této diplomové práce sestaveny vlastní dotazníky v on-line platformě. Výstupem průzkumu, který bude probíhat i v období po odevzdání této práce, bude interní manuál společnosti LINET, který bude obsahovat doporučení a rady k postupům a chování v rámci mezikulturní komunikace v oblasti řízení lidských zdrojů
THE GROWING ROLE OF LABOR MARKET INTERMEDIARIES ON EMPLOYMENT RELATIONS AND IT’S IMPLICATIONS OF HUMAN RESOURCES MANAGEMENT
Full text linkThe role of labor market intermediaries has evolved drastically over the past few years andstill evolving due to global competition, selection and placement, legal constrictions,changes in employee-employer relations and leadership styles combined precipitate asignificant rise in their roles. The continued rise of labour market intermediaries hasraised more questions than answers questions about their functionality and rationale in thelabour market, and their value to people’s employment notions. Few studies have beencarried out on the emerging trends in work relations, the growing role of labour marketintermediaries and their implications on human resources management. A gap which thiscritical review seeks to fill by determining the different relations that exist in the workplaceand their effects on individuals and the management while trying understand traitscharacteristics that make them to be who they are for instance; mentors, trailblazers,communicators, foes, acquaintances and advocates in addition to establishing how labourmarket intermediaries carry out their activities in regard to work relations. Labourmarket intermediaries have been in existence for many years under different pretext suchas labor unions, expertise association, and professional licensing boards among others.Previous studies into work place relations mostly dwelt on their effects on job satisfaction,employee motivation, employee turnover and retention
Estimation and projection of the national profile of cancer mortality in China: 1991-2005.
Full text linkThere are no national-level data on cancer mortality in China since two surveys in 1973-1975 and 1990-1992 (a 10% sample), but ongoing surveillance systems, based on nonrandom selected populations, give an indication as to the trends for major cancers. Based on a log-linear regression model with Poisson errors, the annual rates of change for 10 cancers and all other cancers combined, by age, sex and urban/rural residence were estimated from the data of the surveillance system of the Center for Health Information and Statistics, covering about 10% of the national population. These rates of change were applied to the survey data of 1990-1992 to estimate national mortality in the year 2000, and to make projections for 2005. Mortality rates for all cancers combined, adjusted for age, are predicted to change little between 1991 and 2005 (-0.8% in men and +2.5% in women), but population growth and ageing will result in an increasing number of deaths, from 1.2 to 1.8 million. The largest predicted increases are for the numbers of female breast (+155.4%) and lung cancers (+112.1% in men, +153.5% in women). For these two sites, mortality rates will almost double. Cancer will make an increasing contribution to the burden of diseases in China in the 21st century. The marked increases in risk of cancers of the lung, female breast and large bowel indicate priorities for prevention and control. The increasing trends in young age groups for cancers of the cervix, lung and female breast suggest that their predicted increases may be underestimated, and that more attention should be paid to strategies for their prevention and control
The use of mobile phones and the risk of brain tumors among children and adolescents
Full text linkMobile phones experienced a steep rise in popularity among children and adolescents during the last decade. The increase in popularity has been reflected in both increased ownership and increased usage of mobile phones. Most children start to use mobile phones when they are around 9–10 years old, but usage before school age is not uncommon. The increase in mobile phone use has raised concerns about possible adverse health effects. Brain tumors have been a main concern because the brain absorbs most of the radio frequency energy emitted by mobile phones during calls. In addition, it has been hypothesized that children may be more vulnerable to radio frequency electromagnetic fields (RF-EMFs) because their nervous system is developing, their brain tissue is more conductive than that of adults, and RF-EMFs penetrate in to regions that are deeper in their brains. Radio frequency radiation emitted by mobile phones has insufficient energy to directly damage the DNA and the only known effect of RF-EMFs is heating of the tissue. Studies about mobile phone use and brain tumor risk among adults have shown no increased risk for regular users but have been inconclusive regarding long-term (≥10 years) and heavy mobile phone use. The largest case-control study so far, INTERPHONE, found an increased risk for glioma among heavy users (≥1640 lifetime calls). Another study from a Swedish research group reported a five-fold increased risk for astrocytoma for adults who first used mobile phones before the age of 20. No study has addressed the association between mobile phone use and brain tumor risk among children and adolescents so far. The goal of this thesis was to assess whether there is a relationship between mobile phone use and brain tumor risk among children and adolescents or not. In 2006, we set up CEFALO, an international case-control study about the relationship between mobile phone use and brain tumor risk in children and adolescents aged 7–19 years. CEFALO was performed in Denmark, Sweden, Norway, and Switzerland. The study period ranged from 2004 through 2008. Children and adolescents of age 7–19 years who were diagnosed during the study period with a primary brain tumor were eligible. For each case patient, we selected two healthy controls matched by age, sex and geographical region of residence using population registries. Exposure data was collected by face to face interviews with the study participants accompanied by at least one parent. Risk estimates for brain tumors were calculated for various exposure surrogates. We also examined the gender and age-adjusted brain tumor incidence rates among Swedish children and adolescents aged 5–19 years from 1990 to 2008 including hypothetical incidence rate trends based on the risk estimates found in our analyses. Lastly, we compared the self-reported amount of mobile phone use with objectively recorded data by network operators. Regular users of mobile phones were not statistically significantly more likely to have been diagnosed with brain tumors compared with non-regular users (OR=1.36, 95%-CI: 0.92 to 2.02). No clear exposure-response relationship was observed for any exposure surrogate. Moreover, no exposure-response relationship was seen in terms of localization of the tumor. For the study participants for whom operator-recorded data were available, we found a statistically significantly increased risk among users with more than 2.8 years since the start of the first subscription (OR=2.15). The odds ratio for brain tumor risk among ipsilateral regular users of mobile phones was not higher than the odds ratio of contralateral regular users. The risk estimate of 2.15 after 3 years of regular mobile phone use is incompatible with the stable (or even downward) incidence trends observed among Swedish children and adolescents aged 5–19 years from 1990 to 2008. This indicates that short-term use of mobile phones does not cause brain tumors in children and adolescents. In the validation study, cases overestimated their cumulative number of calls by 9% on average and controls by 34%. Cases also overestimated their cumulative duration of calls by 52% on average and controls by 163%. We found little evidence for differential recall errors. CEFALO is the first study to investigate the relationship between mobile phone use and brain tumor risk in children and adolescents. We found no consistent evidence for a causal association between short-term mobile phone use and brain tumor risk among children and adolescents. The lack of an exposure-response relationship either in terms of the amount of mobile phone use or by localization of the brain tumor argues against a causal relationship. These findings are corroborated by the fact that brain tumor incidence rates among children and adolescents have not increased in many countries in recent times. We cannot, however, exclude the possibility of a small increase in brain tumor risk due to mobile phone use. As we found that self-reported mobile phone use is affected with large random and some systematic recall errors, we emphasize the importance of future studies with objective exposure assessment or the use of prospectively collected exposure data. We also recommend the monitoring of time trends in brain tumor incidence rates as increased risks should be reflected in future brain tumor incidence rate trends
Assessing interactions between the associations of common genetic susceptibility variants, reproductive history and body mass index with breast cancer risk in the breast cancer association consortium: a combined case-control study.
Full text linkINTRODUCTION: Several common breast cancer genetic susceptibility variants have recently been identified. We aimed to determine how these variants combine with a subset of other known risk factors to influence breast cancer risk in white women of European ancestry using case-control studies participating in the Breast Cancer Association Consortium. METHODS: We evaluated two-way interactions between each of age at menarche, ever having had a live birth, number of live births, age at first birth and body mass index (BMI) and each of 12 single nucleotide polymorphisms (SNPs) (10q26-rs2981582 (FGFR2), 8q24-rs13281615, 11p15-rs3817198 (LSP1), 5q11-rs889312 (MAP3K1), 16q12-rs3803662 (TOX3), 2q35-rs13387042, 5p12-rs10941679 (MRPS30), 17q23-rs6504950 (COX11), 3p24-rs4973768 (SLC4A7), CASP8-rs17468277, TGFB1-rs1982073 and ESR1-rs3020314). Interactions were tested for by fitting logistic regression models including per-allele and linear trend main effects for SNPs and risk factors, respectively, and single-parameter interaction terms for linear departure from independent multiplicative effects. RESULTS: These analyses were applied to data for up to 26,349 invasive breast cancer cases and up to 32,208 controls from 21 case-control studies. No statistical evidence of interaction was observed beyond that expected by chance. Analyses were repeated using data from 11 population-based studies, and results were very similar. CONCLUSIONS: The relative risks for breast cancer associated with the common susceptibility variants identified to date do not appear to vary across women with different reproductive histories or body mass index (BMI). The assumption of multiplicative combined effects for these established genetic and other risk factors in risk prediction models appears justified
Ionizing and non-ionizing radiation and the risk of childhood cancer-illustrated with domestic radon and radio frequency electromagnetic field exposure
Full text linkBackground
Children are exposed to many different environmental factors, including exposure to low-dose ionizing radiation and to non-ionizing radiation.
Low-dose ionizing radiation comprises anthropogenic modified radiation and natural ionizing radiation from cosmic rays from the atmosphere, terrestrial gamma radiation from radionuclides in rocks and soils and radiation from radon.
Non-ionizing radiation comprises optical radiation and radiation from electromagnetic fields. The latter comprises radiation from extremely low-frequency electromagnetic fields (ELF-EMF; high voltage power lines, electrical installations) and radiofrequency electromagnetic fields (RF-EMF; broadcast transmitters, mobile phone base stations, mobile and cordless phones).
Both ionizing and non-ionizing radiation are assumed to be associated with childhood cancer.
Aims
Within this dissertation, we primarily aimed to assess whether there is an association between domestic radon exposure and childhood cancers. We further investigated whether there is an association between low-dose ionizing gamma radiation and childhood cancers. We finally assessed whether there is an association between RF-EMF exposure from broadcast transmitters and childhood cancers.
Methods
We performed prospective census-based cohort designs, considering all children, aged less than 16 years and living in Switzerland at the date of census 2000 (December 5th 2000). Time at risk was set to begin at census and lasted until the date of diagnosis, death, emigration, a child’s 16th birthday or until the end of the year 2008. In terms of non-ionizing radiation from far-field RF-EMF sources from broadcast transmitters, we carried out a further prospective cohort analysis, considering all children, aged less than 16 years and living in Switzerland between 1985 and 2008.
We assessed exposure at baseline (date of census 2000) for each child’s home address. For the analyses on RF-EMF exposure to broadcast transmitters and childhood cancers where a longer follow-up was considered, we considered exposure at the time of diagnosis.
For the analyses on domestic radon exposure and childhood cancers, exposure assessment was based on a nationwide radon prediction model. For the analyses on low-dose ionizing gamma radiation and childhood cancers, exposure assessment was based on modelled and measured dose rates from outdoor gamma radiation. For the analyses on RF-EMF exposure to broadcast transmitters and childhood cancers, exposure assessment was based on modeled field strengths.
Results
We estimated arithmetic mean radon concentrations to be 85.7 Bq/m³ (range: 6.9-337.2 Bq/m³) for childhood cancer cases and 85.9 Bq/m³ (range: 0.7-490.1 Bq/m³) for the rest of the study population. Despite relative high radon levels in Switzerland, we found no evidence for an association between domestic radon exposure and childhood cancers.
We found increased leukaemia risk (including acute lymphoblastic leukaemia) with respect to gamma radiation for children who lived at the same address between 1995 and 2000.
Finally, we found no increased leukaemia risk but increased central nervous system (CNS) tumour risks with respect to RF-EMF exposure from broadcast transmitters.
Conclusions and Outlook
The findings of our analyses, indicating no association between domestic radon exposure and childhood cancers were consistent with past studies that estimated doses of domestic radon concentrations for different body organs (lung, red bone marrow, brain).
The results of the analyses on gamma radiation and childhood cancers indicate that low dose ionizing gamma radiation might be relevant in terms of childhood leukaemia. These results were also found to be consistent with dose estimations for different body organs (red bone marrow, brain). They indicated that the same gamma radiation dose to the red bone marrow over a longer time period is probably necessary for gamma radiation to lead to childhood leukaemia.
The findings from the analyses on RF-EMF exposure from broadcasting and childhood leukaemia were found to be consistent with results from animal, in-vitro and laboratory studies. On the contrary, the findings indicating increased CNS tumours from RF-EMF exposure to broadcast transmitters contradict results from former studies. Our results are further in contradiction to a previous case-control study on wireless phones. This study could not find an increased risk for CNS tumours from the use of wireless phones that lead to substantially higher exposure to the head.
Although no evidence for an association with childhood cancers was found, domestic radon exposure is of public health relevance with regard to lung cancer in adults.
The findings from the analyses on gamma radiation and childhood cancers indicate that gamma radiation is of public health relevance as well, especially when children are exposed to the same gamma radiation dose over a longer time period.
Statements on possible public health relevance concerning non-ionizing radiation of RF-EMF from broadcasting on the other hand are not yet possible, as the results for CNS tumours need further clarification
Strengthening the Reporting of Observational Studies in Epidemiology (STROBE): Explanation and elaboration
Full text linkMuch medical research is observational. The reporting of observational studies is often of insufficient quality. Poor reporting hampers the assessment of the strengths and weaknesses of a study and the generalisability of its results. Taking into account empirical evidence and theoretical considerations, a group of methodologists, researchers, and editors developed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) recommendations to improve the quality of reporting of observational studies. The STROBE Statement consists of a checklist of 22 items, which relate to the title, abstract, introduction, methods, results and discussion sections of articles. Eighteen items are common to cohort studies, casecontrol studies and cross-sectional studies and four are specific to each of the three study designs. The STROBE Statement provides guidance to authors about how to improve the reporting of observational studies and facilitates critical appraisal and interpretation of studies by reviewers, journal editors and readers. This explanatory and elaboration document is intended to enhance the use, understanding, and dissemination of the STROBE Statement. The meaning and rationale for each checklist item are presented. For each item, one or several published examples and, where possible, references to relevant empirical studies and methodological literature are provided. Examples of useful flow diagrams are also included. The STROBE Statement, this document, and the associated Web site (http://www. strobe-statement.org/) should be helpful resources to improve reporting of observational research. © 2007 Vandenbroucke et al
Aggregation tests identify new gene associations with breast cancer in populations with diverse ancestry
Full text linkLow-frequency variants play an important role in breast cancer (BC) susceptibility. Gene-based methods can increase power by combining multiple variants in the same gene and help identify target genes. We evaluated the potential of gene-based aggregation in the Breast Cancer Association Consortium cohorts including 83,471 cases and 59,199 controls. Low-frequency variants were aggregated for individual genes' coding and regulatory regions. Association results in European ancestry samples were compared to single-marker association results in the same cohort. Gene-based associations were also combined in meta-analysis across individuals with European, Asian, African, and Latin American and Hispanic ancestry. In European ancestry samples, 14 genes were significantly associated (q < 0.05) with BC. Of those, two genes, FMNL3 (P = 6.11 × 10 ) and AC058822.1 (P = 1.47 × 10 ), represent new associations. High FMNL3 expression has previously been linked to poor prognosis in several other cancers. Meta-analysis of samples with diverse ancestry discovered further associations including established candidate genes ESR1 and CBLB. Furthermore, literature review and database query found further support for a biologically plausible link with cancer for genes CBLB, FMNL3, FGFR2, LSP1, MAP3K1, and SRGAP2C. Using extended gene-based aggregation tests including coding and regulatory variation, we report identification of plausible target genes for previously identified single-marker associations with BC as well as the discovery of novel genes implicated in BC development. Including multi ancestral cohorts in this study enabled the identification of otherwise missed disease associations as ESR1 (P = 1.31 × 10 ), demonstrating the importance of diversifying study cohorts. [Abstract copyright: © 2023. The Author(s).
A genome-wide gene-environment interaction study of breast cancer risk for women of European ancestry
Full text linkFunding Open Access funding enabled and organized by Projekt DEAL. BCAC is funded by the European Union's Horizon 2020 Research and Innovation Programme (grant numbers 634935 and 633784 for BRIDGES and B-CAST respectively), and the PERSPECTIVE I&I project, funded by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research, the Ministère de l’Économie et de l'Innovation du Québec through Genome Québec, the Quebec Breast Cancer Foundation. The EU Horizon 2020 Research and Innovation Programme funding source had no role in study design, data collection, data analysis, data interpretation or writing of the report. Additional funding for BCAC is provided via the Confluence project which is funded with intramural funds from the National Cancer Institute Intramural Research Program, National Institutes of Health. Genotyping of the OncoArray was funded by the NIH Grant U19 CA148065, and Cancer Research UK Grant C1287/A16563 and the PERSPECTIVE project supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (grant GPH-129344) and, the Ministère de l’Économie, Science et Innovation du Québec through Genome Québec and the PSRSIIRI-701 grant, and the Quebec Breast Cancer Foundation. Funding for iCOGS came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009–223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112—the GAME-ON initiative), the Department of Defence (W81XWH-10–1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, and Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. The BRIDGES panel sequencing was supported by the European Union Horizon 2020 research and innovation program BRIDGES (grant number, 634935) and the Wellcome Trust (v203477/Z/16/Z). The Australian Breast Cancer Family Study (ABCFS) was supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Australia) and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow. M.C.S. is a NHMRC Senior Research Fellow. The ABCS study was supported by the Dutch Cancer Society [grants NKI 2007–3839; 2009 4363]. The Australian Breast Cancer Tissue Bank (ABCTB) was supported by the National Health and Medical Research Council of Australia, The Cancer Institute NSW and the National Breast Cancer Foundation. The AHS study is supported by the intramural research program of the National Institutes of Health, the National Cancer Institute (grant number Z01-CP010119), and the National Institute of Environmental Health Sciences (grant number Z01-ES049030). The work of the BBCC was partly funded by ELAN-Fond of the University Hospital of Erlangen. The BCEES was funded by the National Health and Medical Research Council, Australia and the Cancer Council Western Australia and acknowledges funding from the National Breast Cancer Foundation (JS). For the BCFR-NY, BCFR-PA, BCFR-UT this work was supported by grant UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. The BCINIS study is supported in part by the Breast Cancer Research Foundation (BCRF). The BREast Oncology GAlician Network (BREOGAN) is funded by Acción Estratégica de Salud del Instituto de Salud Carlos III FIS PI12/02125/Cofinanciado and FEDER PI17/00918/Cofinanciado FEDER; Acción Estratégica de Salud del Instituto de Salud Carlos III FIS Intrasalud (PI13/01136); Programa Grupos Emergentes, Cancer Genetics Unit, Instituto de Investigacion Biomedica Galicia Sur. Xerencia de Xestion Integrada de Vigo-SERGAS, Instituto de Salud Carlos III, Spain; Grant 10CSA012E, Consellería de Industria Programa Sectorial de Investigación Aplicada, PEME I + D e I + D Suma del Plan Gallego de Investigación, Desarrollo e Innovación Tecnológica de la Consellería de Industria de la Xunta de Galicia, Spain; Grant EC11-192. Fomento de la Investigación Clínica Independiente, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain; and Grant FEDER-Innterconecta. Ministerio de Economia y Competitividad, Xunta de Galicia, Spain. CBCS is funded by the Canadian Cancer Society (grant # 313404) and the Canadian Institutes of Health Research. CCGP is supported by funding from the University of Crete. The CECILE study was supported by Fondation de France, Institut National du Cancer (INCa), Ligue Nationale contre le Cancer, Agence Nationale de Sécurité Sanitaire, de l'Alimentation, de l'Environnement et du Travail (ANSES), Agence Nationale de la Recherche (ANR). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council, and Herlev and Gentofte Hospital. The CNIO-BCS was supported by the Instituto de Salud Carlos III, the Red Temática de Investigación Cooperativa en Cáncer and grants from the Asociación Española Contra el Cáncer and the Fondo de Investigación Sanitario (PI11/00923 and PI12/00070). The American Cancer Society funds the creation, maintenance, and updating of the CPS-II cohort. The California Teachers Study (CTS) and the research reported in this publication were supported by the National Cancer Institute of the National Institutes of Health under award number U01-CA199277; P30-CA033572; P30-CA023100; UM1-CA164917; and R01-CA077398. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Cancer Institute or the National Institutes of Health. The collection of cancer incidence data used in the California Teachers Study was supported by the California Department of Public Health pursuant to California Health and Safety Code Sect. 103885; Centers for Disease Control and Prevention’s National Program of Cancer Registries, under cooperative agreement 5NU58DP006344; the National Cancer Institute’s Surveillance, Epidemiology and End Results Program under contract HHSN261201800032I awarded to the University of California, San Francisco, contract HHSN261201800015I awarded to the University of Southern California, and contract HHSN261201800009I awarded to the Public Health Institute. The opinions, findings, and conclusions expressed herein are those of the author(s) and do not necessarily reflect the official views of the State of California, Department of Public Health, the National Cancer Institute, the National Institutes of Health, the Centers for Disease Control and Prevention or their Contractors and Subcontractors, or the Regents of the University of California, or any of its programs. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom). The ESTHER study was supported by a grant from the Baden Württemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Krebshilfe). PROCAS thank NIHR for funding. The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0 and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, the Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, as well as the Department of Internal Medicine, Johanniter GmbH Bonn, Johanniter Krankenhaus, Bonn, Germany. The GESBC was supported by the Deutsche Krebshilfe e. V. [70492] and the German Cancer Research Center (DKFZ). The KARMA study was supported by Märit and Hans Rausings Initiative Against Breast Cancer. The KBCP was financially supported by the special Government Funding (VTR) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, and by the strategic funding of the University of Eastern Finland. kConFab is supported by a grant from the National Breast Cancer Foundation, and previously by the National Health and Medical Research Council (NHMRC), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. Financial support for the AOCS was provided by the United States Army Medical Research and Materiel Command [DAMD17-01–1-0729], Cancer Council Victoria, Queensland Cancer Fund, Cancer Council New South Wales, Cancer Council South Australia, The Cancer Foundation of Western Australia, Cancer Council Tasmania and the National Health and Medical Research Council of Australia (NHMRC; 400413, 400281, 199600). G.C.T. and P.W. are supported by the NHMRC. RB was a Cancer Institute NSW Clinical Research Fellow. LMBC is supported by the 'Stichting tegen Kanker'. DL is supported by the FWO. The MARIE study was supported by the Deutsche Krebshilfe e.V. [70–2892-BR I, 106332, 108253, 108419, 110826, 110828], the Hamburg Cancer Society, the German Cancer Research Center (DKFZ) and the Federal Ministry of Education and Research (BMBF) Germany [01KH0402]. The MCBCS was supported by the NIH grants R35CA253187, R01CA192393, R01CA116167, R01CA176785 a NIH Specialized Program of Research Excellence (SPORE) in Breast Cancer [P50CA116201], and the Breast Cancer Research Foundation. The Melbourne Collaborative Cohort Study (MCCS) cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further augmented by Australian National Health and Medical Research Council grants 209057, 396414 and 1074383 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry and the Australian Institute of Health and Welfare, including the National Death Index and the Australian Cancer Database. The MEC was supported by NIH Grants CA63464, CA54281, CA098758, CA132839 and CA164973. The MISS study was supported by funding from ERC-2011-294576 Advanced grant, Swedish Cancer Society CAN 2018/675, Swedish Research Council, Local hospital funds, Berta Kamprad Foundation FBKS 2021–19, Gunnar Nilsson. The MMHS study was supported by NIH grants CA97396, CA128931, CA116201, CA140286 and CA177150. MSKCC is supported by grants from the Breast Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer Genetics Initiative. The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The Northern California Breast Cancer Family Registry (NC-BCFR) and Ontario Familial Breast Cancer Registry (OFBCR) were supported by grant U01CA164920 from the USA National Cancer Institute of the National Institutes of Health. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The Carolina Breast Cancer Study (NCBCS) was funded by Komen Foundation, the National Cancer Institute (P50 CA058223, U54 CA156733, U01 CA179715), and the North Carolina University Cancer Research Fund. The NHS was supported by NIH grants P01 CA87969, UM1 CA186107, and U19 CA148065. The NHS2 was supported by NIH grants UM1 CA176726 and U19 CA148065. The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. Genotyping for PLCO was supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The PLCO is supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health. The SASBAC study was supported by funding from the Agency for Science, Technology and Research of Singapore (A*STAR), the US National Institute of Health (NIH) and the Susan G. Komen Breast Cancer Foundation. The SBCS was supported by Sheffield Experimental Cancer Medicine Centre and Breast Cancer Now Tissue Bank. SEARCH is funded by Cancer Research UK [C490/A10124, C490/A16561] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academic Reserve. The Sister Study (SISTER) is supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES049033). The SMC is funded by the Swedish Cancer Foundation and the Swedish Research Council (VR 2017–00644) grant for the Swedish Infrastructure for Medical Population-based Life-course Environmental Research (SIMPLER). The USRT Study was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The WHI program is funded by the National Heart, Lung, and Blood Institute, the US National Institutes of Health and the US Department of Health and Human Services (HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C and HHSN271201100004C). This work was also funded by NCI U19 CA148065-01.Peer reviewe
