rs11778371 - CHRNA2

Magnitude 2.2 · 3 studies on file

Reported associations

  • Multi-ancestry GWAS meta-analyses of lung cancer reveal susceptibility loci and elucidate smoking-independent genetic risk - Unknown journal (n.d.) · Unknown authors · PubMed 39366959

    ABSTRACT: Lung cancer remains the leading cause of cancer mortality, despite declining smoking rates. Previous lung cancer GWAS have identified numerous loci, but separating the genetic risks of lung cancer and smoking behavioral susceptibility remains challenging. Here, we perform multi-ancestry GWAS meta-analyses of lung cancer using the Million Veteran Program cohort (approximately 95% male cases) and a previous study of European-ancestry individuals, jointly comprising 42,102 cases and 181,270 controls, followed by replication in an independent cohort of 19,404 cases and 17,378 controls. We then carry out conditional meta-analyses on cigarettes per day and identify two novel, replicated loci, including the 19p13.11 pleiotropic cancer locus in squamous cell lung carcinoma. Overall, we

  • Genetic Analysis of Lung Cancer and the Germline Impact on Somatic Mutation Burden - Unknown journal (n.d.) · Unknown authors · PubMed 35511172

    ABSTRACT: Abstract Background Germline genetic variation contributes to lung cancer (LC) susceptibility. Previous genome-wide association studies (GWAS) have implicated susceptibility loci involved in smoking behaviors and DNA repair genes, but further work is required to identify susceptibility variants. Methods To identify LC susceptibility loci, a family history-based genome-wide association by proxy (GWAx) of LC (48 843 European proxy LC patients, 195 387 controls) was combined with a previous LC GWAS (29 266 patients, 56 450 controls) by meta-analysis. Colocalization was used to explore candidate genes and overlap with existing traits at discovered susceptibility loci. Polygenic risk scores (PRS) were tested within an independent validation cohort (1 666 LC patients vs 6 664 contr

  • Sex‐specific genetic architecture of late‐life memory performance - Unknown journal (n.d.) · Unknown authors · PubMed 37984853

    ABSTRACT: Abstract BACKGROUND Women demonstrate a memory advantage when cognitively healthy yet lose this advantage to men in Alzheimer's disease. However, the genetic underpinnings of this sex difference in memory performance remain unclear. METHODS We conducted the largest sex‐aware genetic study on late‐life memory to date (N males = 11,942; N females = 15,641). Leveraging harmonized memory composite scores from four cohorts of cognitive aging and AD, we performed sex‐stratified and sex‐interaction genome‐wide association studies in 24,216 non‐Hispanic White and 3367 non‐Hispanic Black participants. RESULTS We identified three sex‐specific loci (rs67099044-CBLN2, rs719070-SCHIP1/IQCJ‐SCHIP), including an X‐chromosome locus (rs5935633-EGL6/TCEANC/OFD1), that


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Lifestyle context

Concrete actions anchored to the cited research. We do not prescribe, we describe.

Discuss with your doctor

  • Genetic lung cancer predisposition and personalized prevention High

    rs11778371 T allele consistently shows large effect size (OR 0.865 and 0.881) across two large population-based GWAS (n=223,372 and n=329,946, p<1e-10)

    Review personal and family cancer history; develop individualized surveillance and risk-reduction strategy

Lifestyle

  • Tobacco products and secondhand smoke exposure High

    CHRNA2 T allele increases lung cancer risk; tobacco smoke is the primary lung cancer cause; genetic predisposition significantly amplifies smoking-related harm

    Strictly avoid all tobacco products; pursue cessation support if currently using tobacco

Screening

  • Lung cancer risk assessment and screening High

    CHRNA2 rs11778371 T allele strongly associated with lung cancer; carriers have substantially elevated susceptibility requiring clinical evaluation

    Discuss with physician about personal risk stratification and whether screening protocols should be considered