@Article{hjelmborg_bmi_2008,
  Title                    = {{{G}enetic influences on growth traits of {B}{M}{I}: a longitudinal study of adult twins}},
  Author                   = {Hjelmborg, J. v. and Fagnani, C. and Silventoinen, K. and McGue, M. and Korkeila, M. and Christensen, K. and Rissanen, A. and Kaprio, J. },
  Journal                  = {Obesity (Silver Spring)},
  Year                     = {2008},
  Month                    = {Apr},
  Number                   = {4},
  Pages                    = {847--852},
  Volume                   = {16}
}

@Article{korkeila_bmi_1991,
  Title                    = {{{E}ffects of gender and age on the heritability of body mass index}},
  Author                   = {Korkeila, M. and Kaprio, J. and Rissanen, A. and Koskenvuo, M. },
  Journal                  = {Int J Obes},
  Year                     = {1991},
  Month                    = {Oct},
  Number                   = {10},
  Pages                    = {647--654},
  Volume                   = {15}
}

@article{twinstutter,
author = {Corrado Fagnani and Steen Fibiger and Axel Skytthe and Jacob V. B. Hjelmborg},
title = {Heritability and environmental effects for self-reported
                  periods with stuttering: A twin study from Denmark},
journal = {Logopedics Phoniatrics Vocology},
volume = {36},
number = {3},
pages = {114-120},
year = {2011},
doi = {10.3109/14015439.2010.534503},
abstract = { AbstractGenetic influence for stuttering was studied based on adult self-reporting. Using nation-wide questionnaire answers from 33,317 Danish twins, a univariate biometric analysis based on the liability threshold model was performed in order to estimate the heritability of stuttering. The self-reported incidences for stuttering were from less than 4\% for females to near 9\% for males. Both probandwise concordance rate and tetrachoric correlation were substantially higher for monozygotic compared to dizygotic pairs, indicating substantial genetic influence on individual liability. Univariate biometric analyses showed that additive genetic and unique environmental factors best explained the observed concordance patterns. Heritability estimates for males/females were 0.84/0.81. Moderate unique environmental effects were also found. }
}

@Article{TRACE,
  Title                    = {Does in-hospital ventricular fibrillation affect prognosis after myocardial infarction?},
  Author                   = {Jensen, G.V. and Torp-Pedersen, C. and Hildebrandt, P. and Kober, L. and Nielsen, F. E. and Melchior, T. and Joen, T. and P. K. Andersen},
  Journal                  = {European Heart Journal},
  Year                     = {1997},
  Pages                    = {919-924},
  Volume                   = {18}
}



@Article{Cederkvist2018,
  author        = {Cederkvist, Luise and Holst, Klaus K and Andersen, Klaus K and Scheike, Thomas H},
  title         = {Modeling the cumulative incidence function of multivariate competing risks data allowing for within-cluster dependence of risk and timing},
  journal       = {Biostatistics},
  year          = {2018},
  __markedentry = {[bhd252:6]},
}

@Article{Cederkvist2017,
  author    = {Luise Cederkvist and Holst, {Klaus K.} and Andersen, {Klaus K.} and Glidden, {David V.} and Kirsten Frederiksen and Kjaer, {Susanne K.} and Scheike, {Thomas H.}},
  title     = {Incorporation of the time aspect into the liability-threshold model for case-control-family data},
  journal   = {Statistics in Medicine},
  year      = {2017},
  month     = {1},
  note      = {Copyright © 2017 John Wiley \& Sons, Ltd.},
  issn      = {0277-6715},
  doi       = {10.1002/sim.7229},
  abstract  = {Familial aggregation and the role of genetic and environmental factors can be investigated through family studies analysed using the liability-threshold model. The liability-threshold model ignores the timing of events including the age of disease onset and right censoring, which can lead to estimates that are difficult to interpret and are potentially biased. We incorporate the time aspect into the liability-threshold model for case-control-family data following the same approach that has been applied in the twin setting. Thus, the data are considered as arising from a competing risks setting and inverse probability of censoring weights are used to adjust for right censoring. In the case-control-family setting, recognising the existence of competing events is highly relevant to the sampling of control probands. Because of the presence of multiple family members who may be censored at different ages, the estimation of inverse probability of censoring weights is not as straightforward as in the twin setting but requires consideration. We propose to employ a composite likelihood conditioning on proband status that markedly simplifies adjustment for right censoring. We assess the proposed approach using simulation studies and apply it in the analysis of two Danish register-based case-control-family studies: one on cancer diagnosed in childhood and adolescence, and one on early-onset breast cancer. Copyright © 2017 John Wiley & Sons, Ltd.},
  publisher = {JohnWiley \& Sons Ltd.},
}

@Article{Hjelmborg2016,
  author    = {Jacob Hjelmborg and Tellervo Korhonen and Klaus Holst and Axel Skytthe and Eero Pukkala and Julia Kutschke and Harris, {Jennifer R.} and Mucci, {Lorelei A.} and Kaare Christensen and Kamila Czene and Adami, {Hans Olov} and Thomas Scheike and Jaakko Kaprio},
  title     = {Lung cancer, genetic predisposition and smoking: The Nordic Twin Study of Cancer},
  journal   = {Thorax},
  year      = {2016},
  month     = {11},
  pages     = {1--7},
  issn      = {0040-6376},
  doi       = {10.1136/thoraxjnl-2015-207921},
  abstract  = {Background: We aimed to disentangle genetic and environmental causes in lung cancer while considering smoking status. Methods: Four Nordic twin cohorts (43 512 monozygotic (MZ) and 71 895 same sex dizygotic (DZ) twin individuals) had smoking data before cancer diagnosis. We used time-to-event analyses accounting for censoring and competing risk of death to estimate incidence, concordance risk and heritability of liability to develop lung cancer by smoking status. Results: During a median of 28.5 years of follow-up, we recorded 1508 incident lung cancers. Of the 30 MZ and 28 DZ pairs concordant for lung cancer, nearly all were current smokers at baseline and only one concordant pair was seen among never smokers. Among ever smokers, the case-wise concordance of lung cancer, that is the risk before a certain age conditional on lung cancer in the co-twin before that age, was significantly increased compared with the cumulative incidence for both MZ and DZ pairs. This ratio, the relative recurrence risk, significantly decreased by age for MZ but was constant for DZ pairs. Heritability of lung cancer was 0.41 (95% CI 0.26 to 0.56) for currently smoking and 0.37 (95% CI 0.25 to 0.49) for ever smoking pairs. Among smoking discordant pairs, the pairwise HR for lung cancer of the ever smoker twin compared to the never smoker co-twin was 5.4 (95% CI 2.1 to 14.0) in MZ pairs and 5.0 (95% CI 3.2 to 7.9) in DZ pairs. Conclusions: The contribution of familial effects appears to decrease by age. The discordant pair analysis confirms that smoking causes lung cancer.},
  publisher = {B M J Group},
}

@Article{Holst2016,
  author    = {Holst, {Klaus K.} and Thomas Scheike and Hjelmborg, {Jacob B.}},
  title     = {The liability threshold model for censored twin data},
  journal   = {Computational Statistics \& Data Analysis},
  year      = {2016},
  volume    = {93},
  month     = {1},
  pages     = {324–335},
  issn      = {0167-9473},
  doi       = {10.1016/j.csda.2015.01.014},
  abstract  = {Family studies provide an important tool for understanding etiology of diseases, with the key aim of discovering evidence of family aggregation and to determine if such aggregation can be attributed to genetic components. Heritability and concordance estimates are routinely calculated in twin studies of diseases, as a way of quantifying such genetic contribution. The endpoint in these studies are typically defined as occurrence of a disease versus death without the disease. However, a large fraction of the subjects may still be alive at the time of follow-up without having experienced the disease thus still being at risk. Ignoring this right-censoring can lead to severely biased estimates. The classical liability threshold model can be extended with inverse probability of censoring weighting of complete observations. This leads to a flexible way of modelling twin concordance and obtaining consistent estimates of heritability. The method is demonstrated in simulations and applied to data from the population based Danish twin cohort to describe the dependence in prostate cancer occurrence in twins.},
  keywords  = {Competing risks, Cumulative incidence, Heritability, Liability-threshold, Polygenic model, Probit model, Random effects, Right censoring, Twins},
  publisher = {Elsevier BV},
}

@Article{Martinussen2016,
  author    = {Torben Martinussen and Holst, {Klaus K.} and Scheike, {Thomas H.}},
  title     = {Cox regression with missing covariate data using a modified partial likelihood method},
  journal   = {Lifetime Data Analysis},
  year      = {2016},
  volume    = {22},
  number    = {4},
  month     = {10},
  pages     = {570–588},
  issn      = {1380-7870},
  doi       = {10.1007/s10985-015-9351-y},
  abstract  = {Missing covariate values is a common problem in survival analysis. In this paper we propose a novel method for the Cox regression model that is close to maximum likelihood but avoids the use of the EM-algorithm. It exploits that the observed hazard function is multiplicative in the baseline hazard function with the idea being to profile out this function before carrying out the estimation of the parameter of interest. In this step one uses a Breslow type estimator to estimate the cumulative baseline hazard function. We focus on the situation where the observed covariates are categorical which allows us to calculate estimators without having to assume anything about the distribution of the covariates. We show that the proposed estimator is consistent and asymptotically normal, and derive a consistent estimator of the variance-covariance matrix that does not involve any choice of a perturbation parameter. Moderate sample size performance of the estimators is investigated via simulation and by application to a real data example.},
  publisher = {Springer New York LLC},
}

@Article{Mucci2016,
  author    = {Mucci, {Lorelei A.} and Hjelmborg, {Jacob B.} and Harris, {Jennifer R.} and Kamila Czene and Havelick, {David J.} and Thomas Scheike and Graff, {Rebecca E.} and Klaus Holst and Søren Møller and Unger, {Robert H.} and Christina McIntosh and Elizabeth Nuttall and Ingunn Brandt and Penney, {Kathryn L.} and Mikael Hartman and Peter Kraft and Giovanni Parmigiani and Kaare Christensen and Markku Koskenvuo and Holm, {Niels V.} and Kauko Heikkila and Eero Pukkala and Axel Skytthe and Hans-Olov Adami and Jaakko Kaprio},
  title     = {Familial Risk and Heritability of Cancer Among Twins in Nordic Countries},
  journal   = {J A M A: The Journal of the American Medical Association},
  year      = {2016},
  volume    = {315},
  number    = {1},
  month     = {1},
  pages     = {68--76},
  issn      = {0098-7484},
  doi       = {10.1001/jama.2015.17703},
  abstract  = {Importance: Estimates of familial cancer risk from population-based studies are essential components of cancer risk prediction.Objective: To estimate familial risk and heritability of cancer types in a large twin cohort.Design, Setting, and Participants: Prospective study of 80 309 monozygotic and 123 382 same-sex dizygotic twin individuals (N = 203 691) within the population-based registers of Denmark, Finland, Norway, and Sweden. Twins were followed up a median of 32 years between 1943 and 2010. There were 50 990 individuals who died of any cause, and 3804 who emigrated and were lost to follow-up.Exposures: Shared environmental and heritable risk factors among pairs of twins.Main Outcomes and Measures: The main outcome was incident cancer. Time-to-event analyses were used to estimate familial risk (risk of cancer in an individual given a twin’s development of cancer) and heritability (proportion of variance in cancer risk due to interindividual genetic differences) with follow-up via cancer registries. Statistical models adjusted for age and follow-up time, and accounted for censoring and competing risk of death.Results: A total of 27 156 incident cancers were diagnosed in 23 980 individuals, translating to a cumulative incidence of 32%. Cancer was diagnosed in both twins among 1383 monozygotic (2766 individuals) and 1933 dizygotic (2866 individuals) pairs. Of these, 38% of monozygotic and 26% of dizygotic pairs were diagnosed with the same cancer type. There was an excess cancer risk in twins whose co-twin was diagnosed with cancer, with estimated cumulative risks that were an absolute 5% (95% CI, 4%-6%) higher in dizygotic (37%; 95% CI, 36%-38%) and an absolute 14% (95% CI, 12%-16%) higher in monozygotic twins (46%; 95% CI, 44%-48%) whose twin also developed cancer compared with the cumulative risk in the overall cohort (32%). For most cancer types, there were significant familial risks and the cumulative risks were higher in monozygotic than dizygotic twins. Heritability of cancer overall was 33% (95% CI, 30%-37%). Significant heritability was observed for the cancer types of skin melanoma (58%; 95% CI, 43%-73%), prostate (57%; 95% CI, 51%-63%), nonmelanoma skin (43%; 95% CI, 26%-59%), ovary (39%; 95% CI, 23%-55%), kidney (38%; 95% CI, 21%-55%), breast (31%; 95% CI, 11%-51%), and corpus uteri (27%; 95% CI, 11%-43%).Conclusions and Relevance: In this long-term follow-up study among Nordic twins, there was significant excess familial risk for cancer overall and for specific types of cancer, including prostate, melanoma, breast, ovary, and uterus. This information about hereditary risks of cancers may be helpful in patient education and cancer risk counseling.},
  publisher = {American Medical Association},
}

@Article{Moeller2016,
  author    = {Sören Möller and Mucci, {Lorelei A} and Harris, {Jennifer R} and Thomas Scheike and Klaus Holst and Ulrich Halekoh and Hans-Olov Adami and Kamila Czene and Kaare Christensen and Holm, {Niels V} and Eero Pukkala and Axel Skytthe and Jaakko Kaprio and Hjelmborg, {Jacob B}},
  title     = {The Heritability of Breast Cancer among women in the Nordic Twin Study of Cancer.},
  journal   = {Cancer Epidemiology, Biomarkers \& Prevention},
  year      = {2016},
  volume    = {25},
  month     = {1},
  pages     = {145--150},
  issn      = {1055-9965},
  doi       = {10.1158/1055-9965.EPI-15-0913},
  abstract  = {Background Family history is an established risk factor for breast cancer. Although some important genetic factors have been identified, the extent to which familial risk can be attributed to genetic factors versus common environment remains unclear. Methods We estimated the familial concordance and heritability of breast cancer among 21,054 monozygotic and 30,939 dizygotic female twin pairs from the Nordic Twin Study of Cancer, the largest twin study of cancer in the world. We accounted for left-censoring, right-censoring, as well as the competing risk of death. Results From 1943 through 2010, 3,933 twins were diagnosed with breast cancer. The cumulative lifetime incidence of breast cancer taking competing risk of death into account was 8.1% for both zygosities, while the cumulative risk for twins whose co-twins had breast cancer was 28% among monozygotic and 20% among dizygotic twins. The heritability of liability to breast cancer was 31% (95% CI 10% - 51%) and the common environmental component was 16% (95% CI 10% - 32%). For pre-menopausal breast cancer these estimates were 27% and 12%, respectively and for postmenopausal breast cancer 22% and 16%, respectively. The relative contributions of genetic and environmental factors were constant between ages 50 and 96. Our results are compatible with the Peto-Mack hypothesis. Conclusion Our findings indicate that familial factors explain almost half of the variation in liability to develop breast cancer, and results were similar for pre- and post-menopausal breast cancer. Impact We estimate heritability of breast cancer, taking until now ignored sources of bias into account.},
  publisher = {American Association for Cancer Research (A A C R)},
}

@Article{holst-hjelmborg-scheike-2014,
  author  = {Holst, Klaus K. and Scheike, Thomas H. and Hjelmborg, Jacob B.},
  title   = {The Liability Threshold Model for Censored Twin Data},
  journal = {Computational Statistics and Data Analysis},
  year    = {2015},
  volume  = {to appear},
  doi     = {10.1016/j.csda.2015.01.014},
  url     = {http://dx.doi.org/10.1016/j.csda.2015.01.014},
}

@Article{behav-scheike-hjelmborg-holst-2015,
  author    = {Scheike, {Thomas H} and Hjelmborg, {Jacob B} and Holst, {Klaus K}},
  title     = {Estimating Twin Pair Concordance for Age of Onset},
  journal   = {Behavior Genetics},
  year      = {2015},
  issn      = {0001-8244},
  doi       = {10.1007/s10519-015-9729-3},
  keywords  = {FIRST},
  owner     = {first},
  publisher = {Springer New York LLC},
}

@Article{Scheike2015,
  author    = {Thomas Scheike and Holst, {Klaus K} and Hjelmborg, {Jacob B}},
  title     = {Measuring early or late dependence for bivariate lifetimes of twins},
  journal   = {Lifetime Data Analysis},
  year      = {2015},
  volume    = {21},
  number    = {2},
  month     = {4},
  pages     = {280--299},
  issn      = {1380-7870},
  doi       = {10.1007/s10985-014-9309-5},
  abstract  = {We consider data from the Danish twin registry and aim to study in detail how lifetimes for twin-pairs are correlated. We consider models where we specify the marginals using a regression structure, here Cox's regression model or the additive hazards model. The best known such model is the Clayton-Oakes model. This model can be extended in several directions. One extension is to allow the dependence parameter to depend on covariates. Another extension is to model dependence via piecewise constant cross-hazard ratio models. We show how both these models can be implemented for large sample data, and suggest a computational solution for obtaining standard errors for such models for large registry data. In addition we consider alternative models that have some computational advantages and with different dependence parameters based on odds ratios of the survival function using the Plackett distribution. We also suggest a way of assessing how and if the dependence is changing over time, by considering either truncated or right-censored versions of the data to measure late or early dependence. This can be used for formally testing if the dependence is constant, or decreasing/increasing. The proposed procedures are applied to Danish twin data to describe dependence in the lifetimes of the twins. Here we show that the early deaths are more correlated than the later deaths, and by comparing MZ and DZ associations we suggest that early deaths might be more driven by genetic factors. This conclusion requires models that are able to look at more local dependence measures. We further show that the dependence differs for MZ and DZ twins and appears to be the same for males and females, and that there are indications that the dependence increases over calendar time.},
  owner     = {first},
  publisher = {Springer New York LLC},
}

@Article{Eriksen2015,
  author    = {Eriksen, Marie and Jensen, David H and Tribler, Siri and Holst, Jens J and Madsbad, Sten and Krarup, Thure},
  title     = {Reduction of insulinotropic properties of GLP-1 and GIP after glucocorticoid-induced insulin resistance},
  journal   = {Diabetologia},
  year      = {2015},
  volume    = {58},
  number    = {5},
  pages     = {920--928},
  publisher = {Springer},
}

@InProceedings{Hvistendahl2015,
  author    = {Hvistendahl, Mark and Brandt, Christopher F and Tribler, Siri and Naimi, Rahim and Hartmann, Bolette and Holst, Jens Juul and Rehfeld, Jens Frederik and Hornum, Mads and Andersen, Jens Rikardt and Mortensen, Per B and others},
  title     = {The glucagon-like peptide-1 receptor agonist liraglutide reduces jejunostomy output and improves intestinal absorption in short bowel syndrome patients with intestinal failure: A pilot study},
  booktitle = {{\AA}rsm{\o}de i Dansk Selskab for Klinisk Ern{\ae}ring},
  year      = {2015},
}

@Article{hjelmborg-prostate-et-al-2013,
  author     = {Hjelmborg, Jacob B. and Scheike, Thomas and Holst, Klaus and Skytthe, Axel and Penney, Kathryn L. and Graff, Rebecca E. and Pukkala, Eero and Christensen, Kaare and Adami, Hans-Olov and Holm, Niels V. and Nuttall, Elizabeth and Hansen, Steinbjorn and Hartman, Mikael and Czene, Kamila and Harris, Jennifer R. and Kaprio, Jaakko and Mucci, Lorelei A.},
  title      = {The Heritability of Prostate Cancer in the Nordic Twin Study of Cancer},
  journal    = {Cancer Epidemiology Biomarkers \& Prevention},
  year       = {2014},
  doi        = {10.1158/1055-9965.EPI-13-0568},
  eprint     = {http://cebp.aacrjournals.org/content/early/2014/05/08/1055-9965.EPI-13-0568.full.pdf+html},
  url        = {http://cebp.aacrjournals.org/content/early/2014/05/08/1055-9965.EPI-13-0568.abstract},
  abstract   = {Background: Prostate cancer is thought to be the most heritable cancer, although little is known about how this genetic contribution varies across age. Methods: To address this question, we undertook the world's largest prospective study in the Nordic Twin Study of Cancer cohort, including 18,680 monozygotic and 30,054 dizygotic same sex male twin pairs. We incorporated time-to-event analyses to estimate the risk concordance and heritability while accounting for censoring and competing risks of death, essential sources of biases that have not been accounted for in previous twin studies modeling cancer risk and liability. Results: The cumulative risk of prostate cancer was similar to that of the background population. The cumulative risk for twins whose co-twin was diagnosed with prostate cancer was greater for MZ than for DZ twins across all ages. Among concordantly affected pairs, the time between diagnoses was significantly shorter for MZ than DZ pairs (median 3.8 versus 6.5 years, respectively). Genetic differences contributed substantially to variation in both the risk and the liability (heritability=58% (95% CI 52%-63%) of developing prostate cancer. The relative contribution of genetic factors was constant across age through late life with substantial genetic heterogeneity even when diagnosis and screening procedures vary. Conclusions: Results from the population based twin cohort, indicate a greater genetic contribution to the risk of developing prostate cancer when addressing sources of bias. The role of genetic factors is consistently high across age Impact: Findings impact the search for genetic and epigenetic markers and frame prevention efforts.},
  bdsk-url-1 = {http://cebp.aacrjournals.org/content/early/2014/05/08/1055-9965.EPI-13-0568.abstract},
  bdsk-url-2 = {http://dx.doi.org/10.1158/1055-9965.EPI-13-0568},
}

@Manual{metsR,
  author     = {Klaus K. Holst and Thomas Scheike},
  title      = {mets: Analysis of Multivariate Event Times},
  year       = {2014},
  note       = {R package version 1.2.4},
  url        = {http://lava.r-forge.r-project.org/},
  bdsk-url-1 = {http://lava.r-forge.r-project.org/},
}

@Article{scheike-holst-hjelmborg-2010,
  author        = {Scheike, T. H. and Holst, K. and Hjelmborg, J. V.},
  title         = {Estimating heritability for cause specific mortality based on twin studies},
  journal       = {Lifetime Data Anal.},
  year          = {2014},
  volume        = {20},
  number        = {2},
  pages         = {210-233},
  bdsk-file-1   = { },
  booktitle     = {Estimating heritability for cause specific mortality based on twin studies},
  date-added    = {2013-04-24 11:08:06 +0000},
  date-modified = {2013-04-24 11:08:06 +0000},
  keywords      = {teoretisk statistik peer review},
  own           = {first},
  owner         = {first},
}

@Article{scheike-holst-hjelmborg-2011,
  author        = {Scheike, Thomas H and Holst, Klaus K and Hjelmborg, Jacob B},
  title         = {Estimating twin concordance for bivariate competing risks twin data},
  journal       = {Statistics in Medicine},
  year          = {2014},
  volume        = {33},
  pages         = {1193-204},
  date-added    = {2013-10-27 18:17:17 +0000},
  date-modified = {2013-10-27 18:18:14 +0000},
  keywords      = {teoretisk statistik peer review},
  own           = {first},
  owner         = {first},
  publisher     = {Wiley Online Library},
}

@Article{Hjelmborg2014,
  author    = {Hjelmborg, {Jacob B} and Thomas Scheike and Klaus Holst and Axel Skytthe and Penney, {Kathryn L} and Graff, {Rebecca E} and Eero Pukkala and Kaare Christensen and Hans-Olov Adami and Holm, {Niels V} and Elizabeth Nuttall and Steinbjorn Hansen and Mikael Hartman and Kamila Czene and Harris, {Jennifer R} and Jaakko Kaprio and Mucci, {Lorelei a}},
  title     = {The Heritability of Prostate Cancer in the Nordic Twin Study of Cancer.},
  journal   = {Cancer Epidemiology, Biomarkers \& Prevention},
  year      = {2014},
  volume    = {23},
  number    = {11},
  month     = {11},
  pages     = {2303--2310},
  issn      = {1055-9965},
  doi       = {10.1158/1055-9965.EPI-13-0568},
  abstract  = {Background: Prostate cancer is thought to be the most heritable cancer, although little is known about how this genetic contribution varies across age. Methods: To address this question, we undertook the world's largest prospective study in the Nordic Twin Study of Cancer cohort, including 18,680 monozygotic and 30,054 dizygotic same sex male twin pairs. We incorporated time-to-event analyses to estimate the risk concordance and heritability while accounting for censoring and competing risks of death, essential sources of biases that have not been accounted for in previous twin studies modeling cancer risk and liability. Results: The cumulative risk of prostate cancer was similar to that of the background population. The cumulative risk for twins whose co-twin was diagnosed with prostate cancer was greater for MZ than for DZ twins across all ages. Among concordantly affected pairs, the time between diagnoses was significantly shorter for MZ than DZ pairs (median 3.8 versus 6.5 years, respectively). Genetic differences contributed substantially to variation in both the risk and the liability (heritability=58% (95% CI 52%-63%) of developing prostate cancer. The relative contribution of genetic factors was constant across age through late life with substantial genetic heterogeneity even when diagnosis and screening procedures vary. Conclusions: Results from the population based twin cohort, indicate a greater genetic contribution to the risk of developing prostate cancer when addressing sources of bias. The role of genetic factors is consistently high across age Impact: Findings impact the search for genetic and epigenetic markers and frame prevention efforts.},
  publisher = {American Association for Cancer Research (A A C R)},
}

@Article{Scheike2014,
  author    = {Thomas Scheike and Holst, {Klaus K.} and Hjelmborg, {Jacob B.}},
  title     = {Estimating heritability for cause specific mortality based on twin studies},
  journal   = {Lifetime Data Analysis},
  year      = {2014},
  volume    = {20},
  number    = {2},
  month     = {4},
  pages     = {210--233},
  issn      = {1380-7870},
  doi       = {10.1007/s10985-013-9244-x},
  keywords  = {Cause specific hazards, Competing risks, Delayed entry, Left truncation, Heritability, Survival analysis},
  owner     = {first},
  publisher = {Springer New York LLC},
}

@Comment{jabref-meta: databaseType:biblatex;}

@Article{,
  title={The Liability Threshold Model for Censored Twin Data},
  author={Holst, Klaus K. and Scheike, Thomas H. and Hjelmborg, Jacob B.},
  year={2015},
  doi={10.1016/j.csda.2015.01.014},
  url={http://dx.doi.org/10.1016/j.csda.2015.01.014},
  journal={Computational Statistics and Data Analysis}
}


@Article{,
  title={Estimating heritability for cause specific mortality based on twin studies},
  author={Scheike, Thomas H. and Holst, Klaus K. and Hjelmborg, Jacob B.},
  year={2013},
  issn={1380-7870},
  journal={Lifetime Data Analysis},
  doi={10.1007/s10985-013-9244-x},
  url={http://dx.doi.org/10.1007/s10985-013-9244-x},
  publisher={Springer US},
  keywords={Cause specific hazards; Competing risks; Delayed entry; 
            Left truncation; Heritability; Survival analysis},
  pages={1-24},
  language={English}
}


