ArticlePloS one2012
Integrative genomic analysis reveals extended germline homozygosity with lung cancer risk in the PLCO cohort.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review of genetic ancestry as a risk factor for incidence of non-small cell lung cancer in the US.Frontiers in genetics · 2023Pooled it
- When cells rebel: a comparative genomics investigation into marsupial cancer susceptibility.Molecular biology and evolution · 2026Article
- Inbreeding, Native American ancestry and child mortality: linking human selection and paediatric medicine.Human molecular genetics · 2022Article
- Identification of selection signatures involved in performance traits in a paternal broiler line.BMC genomics · 2019Article
- Genome-wide tracts of homozygosity and exome analyses reveal repetitive elements with Barrets esophagus/esophageal adenocarcinoma risk.BMC bioinformatics · 2019Article
- Runs of homozygosity: windows into population history and trait architecture.Nature reviews. Genetics · 2018Review
- Genetic diversity, inbreeding and cancer.Proceedings. Biological sciences · 2018Review
- Assessing runs of Homozygosity: a comparison of SNP Array and whole genome sequence low coverage data.BMC genomics · 2018Article
- PARP1 Is Up-Regulated in Non-small Cell Lung Cancer Tissues in the Presence of the Cyanobacterial Toxin Microcystin.Frontiers in microbiology · 2018Article
- Breast cancer protection by genomic imprinting in close kin families.BMC medical genetics · 2017Review
- Inbreeding and homozygosity in breast cancer survival.Scientific reports · 2015Article
- Genome-wide analysis of runs of homozygosity identifies new susceptibility regions of lung cancer in Han Chinese.Journal of biomedical research · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Susceptibility to common cancers is multigenic resulting from low-to-high penetrance predisposition-factors and environmental exposure. Genomic studies suggest germline homozygosity as a novel low-penetrance factor contributing to common cancers. We hypothesized that long homozygous regions (tracts-of-homozygosity [TOH]) harbor tobacco-dependent and independent lung-cancer predisposition (or protection) genes. We performed in silico genome-wide SNP-array-based analysis of lung-cancer patients of European-ancestry from the PLCO screening-trial cohort to identify TOH regions amongst 788 cancer-cases and 830 ancestry-matched controls. Association analyses was then performed between presence of lung cancer and common(c)TOHs (operationally defined as 10 or more subjects sharing ≥100 identical homozygous calls), aTOHs (allelically-matched groups within a cTOH), demographics and tobacco-exposure. Finally, integration of significant c/aTOH with transcriptome was performed to functionally-map lung-cancer risk-genes. After controlling for demographics and smoking, we identified 7 cTOHs and 5 aTOHs associated with lung cancer (adjusted p<0.01). Three cTOHs were over-represented in cases over controls (OR = 1.75-2.06, p = 0.007-0.001), whereas 4 were under-represented (OR = 0.28-0.69, p = 0.006-0.001). Interaction between smoking status and cTOH3/aTOH2 (2p16.3-2p16.1) was observed (adjusted p<0.03). The remaining significant aTOHs have ORs 0.23-0.50 (p = 0.004-0.006) and 2.95-3.97 (p = 0.008-0.001). After integrating significant cTOH/aTOHs with publicly-available lung-cancer transcriptome datasets followed by filtering based on lung cancer and its relevant pathways revealed 9 putative predisposing genes (p<0.0001). In conclusion, differentially-distributed cTOH/aTOH genomic variants between cases and controls harbor sets of plausible differentially-expressed genes accounting for the complexity of lung-cancer predisposition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.