Laufey T. Ámundadóttir
A5042493218- Pancreatic and Hepatic Oncology Research
- Epigenetics and DNA Methylation
- Genetic Associations and Epidemiology
- Liver Disease Diagnosis and Treatment
- Cancer Genomics and Diagnostics
- Endoplasmic Reticulum Stress and Disease
- Blood groups and transfusion
- RNA modifications and cancer
- Pancreatic function and diabetes
- Pancreatitis Pathology and Treatment
- BRCA gene mutations in cancer
- RNA Interference and Gene Delivery
- Nutrition, Genetics, and Disease
- Colorectal Cancer Screening and Detection
- Genomic variations and chromosomal abnormalities
- Prostate Cancer Treatment and Research
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- MicroRNA in disease regulation
- Genetic factors in colorectal cancer
- Genomics and Chromatin Dynamics
- Adipose Tissue and Metabolism
- Telomeres, Telomerase, and Senescence
- SARS-CoV-2 and COVID-19 Research
- Cancer-related molecular mechanisms research
- Single-cell and spatial transcriptomics
National Cancer Institute
2016-2025
National Institutes of Health
2016-2025
Division of Cancer Epidemiology and Genetics
2015-2025
Cancer Genetics (United States)
2014-2023
Cancer Institute (WIA)
2019
Harvard University
1998-2016
Dana-Farber Cancer Institute
2010-2016
Brigham and Women's Hospital
2010-2016
Chinese Academy of Medical Sciences & Peking Union Medical College
2016
Massachusetts Institute of Technology
2016
The causal direction and magnitude of the association between telomere length incidence cancer non-neoplastic diseases is uncertain owing to susceptibility observational studies confounding reverse causation.
Obesity has been proposed as a risk factor for pancreatic cancer.
Smoking is an established risk factor for pancreatic cancer; however, detailed examination of the association smoking intensity, duration, and cumulative dose with cancer limited. The authors analyzed pooled data from international Pancreatic Cancer Cohort Consortium nested case-control study (1,481 cases, 1,539 controls). Odds ratios 95% confidence intervals were calculated by using unconditional logistic regression. intensity effects examined excess odds ratio model that was linear in...
Background The contribution of low-penetrant susceptibility variants to cancer is not clear. With the aim searching for genetic factors that contribute at one or more sites in body, we have analyzed familial aggregation extended families based on all cases diagnosed Iceland over almost half a century. Methods and Findings We estimated risk ratios (RRs) first- up fifth-degree relatives both within between types cancers from 1955 2002 by linking patient information Icelandic Cancer Registry an...
Abstract A recent genome-wide association study (PanScan) identified significant associations at the ABO gene locus with risk of pancreatic cancer, but influence specific genotypes remains unknown. We determined (OO, AO, AA, AB, BO, and BB) in 1,534 cases 1,583 controls from 12 prospective cohorts PanScan, grouping participants by genotype-derived serologic blood type (O, A, B). Adjusted odds ratios (ORs) for cancer alleles were calculated using logistic regression. Compared O, ORs subjects...
The activity of the kinase Aurora-A (Aur-A) peaks during mitosis and depends on phosphorylation by one or more unknown kinases. Mitotic sites were mapped mass spec sequencing recombinant Aur-A protein that had been activated incubation in extracts metaphase-arrested Xenopus eggs. Three identified: serine 53 (Ser-53), threonine 295 (Thr-295), 349 (Ser-349), which are equivalent to Ser-51, Thr-288, Ser-342, respectively, human Aur-A. To ask how these residues might affect activity, each was...
Studies of related individuals have consistently demonstrated notable familial aggregation cancer. We aim to estimate the heritability and genetic correlation attributable additive effects common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.
Recent heritability analyses have indicated that genome-wide association studies (GWAS) the potential to improve genetic risk prediction for complex diseases based on polygenic score (PRS), a simple modelling technique can be implemented using summary-level data from discovery samples. We herein propose modifications performance of PRS. introduce threshold-dependent winner's-curse adjustments marginal coefficients are used weight single-nucleotide polymorphisms (SNPs) in Further, as way...
A family history of pancreatic cancer has consistently been associated with increased risk cancer. However, uncertainty remains about the strength this association. Results from previous studies suggest a select cancers (i.e., ovarian, breast and colorectal) could also be associated, although not as strongly, We examined association between 5 types (pancreas, prostate, using data collaborative nested case-control study conducted by Pancreatic Cancer Cohort Consortium. Cases controls were...
Purpose We developed an absolute risk model to identify individuals in the general population at elevated of pancreatic cancer. Patients and Methods Using data on 3,349 cases 3,654 controls from PanScan Consortium, we a relative for men women European ancestry based non-genetic genetic factors estimated risks these incidence rates. Results Our included current smoking (multivariable adjusted odds ratio (OR) 95% confidence interval: 2.20 [1.84–2.62]), heavy alcohol use (>3 drinks/day) (OR:...
Abstract To investigate large structural clonal mosaicism of chromosome X, we analysed the SNP microarray intensity data 38,303 women from cancer genome-wide association studies (20,878 cases and 17,425 controls) detected 124 mosaic X events >2 Mb in 97 (0.25%) women. Here show rates for X-chromosome are four times higher than mean autosomal rates; more often include entire participants with likely harbour events. frequency increases age (0.11% 50-year olds; 0.45% 75-year olds), as...
Four loci have been associated with pancreatic cancer through genome-wide association studies (GWAS). Pathway-based analysis of GWAS data is a complementary approach to identify groups genes or biological pathways enriched disease-associated single-nucleotide polymorphisms (SNPs) whose individual effect sizes may be too small detected by standard single-locus methods. We used the adaptive rank truncated product method in pathway-based from 3851 cases and 3934 control participants pooled 12...
Abstract Genome-wide association studies (GWAS) have led to the identification of hundreds susceptibility loci across cancers, but impact further remains uncertain. Here we analyse summary-level data from GWAS European ancestry fourteen cancer sites estimate number common variants (polygenicity) and underlying effect-size distribution. All cancers show a high degree polygenicity, involving at minimum thousands loci. We project that sample sizes required explain 80% heritability vary 60,000...