rs10056700 - TH2LCRR, RAD50

Magnitude 2.2 · 2 studies on file

Reported associations

• Genome-Wide Integration of Genetic and Genomic Studies of Atopic Dermatitis: Insights into Genetic Architecture and Pathogenesis. - The Journal of investigative dermatology (2022) · Chen Y, Chen W · PubMed 35577104

  Atopic dermatitis (AD) is a common heterogeneous, chronic, itching, and inflammatory skin disease. Genetic studies have identified multiple AD susceptibility genes. However, the genetic architecture of AD has not been elucidated. In this study, we conducted a large-scale meta-analysis of AD (35,647 cases and 1,013,885 controls) to characterize the genetic basis of AD. The heritability of AD in different datasets varied from 0.6 to 7.1%. We identified 31 previously unreported genes by integrating multiomics data. Among the 31 genes, MCL1 was identified as a potential treatment target for AD by mediating gene‒drug interactions. Tissue enrichment analyses and phenome-wide association study provided strong support for the role of the hemic and immune systems in AD. Across 1,207 complex trait

• Global multi-ancestry genome-wide analyses identify genes and biological pathways associated with thyroid cancer and benign thyroid diseases - Unknown journal (n.d.) · Unknown authors · PubMed 41644669

  ABSTRACT: Thyroid diseases are common and highly heritable. We performed a meta-analysis of genome-wide association studies from 19 biobanks for five thyroid diseases: thyroid cancer (ThC), benign nodular goiter, Graves' disease, lymphocytic thyroiditis and primary hypothyroidism. We analyzed genetic association data from ~2.9 million genomes and identified 313 known and 570 new independent loci linked to thyroid diseases. We discovered genetic correlations between ThC, benign nodular goiter and autoimmune thyroid diseases (rg = 0.16-0.97). Telomere maintenance genes contributed to benign and malignant thyroid nodular disease risk, whereas cell cycle, DNA repair and damage response genes were associated with ThC. We propose a paradigm that explains genetic predisposition to benign

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