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IRAG2 has been evaluated as a candidate gene in lung adenocarcinoma through multi‐patient case–control studies (PMID:18299280) and (PMID:16410263). Although these studies encompassed hundreds of lung adenocarcinoma cases, IRAG2-specific variants and familial segregation were not distinctly reported, limiting the genetic precision for this gene. The polymorphism analyses included IRAG2 among other candidate genes, and no reproducible, isolated association was established for IRAG2 in the absence of supporting variant-level data.
Functional assessments provide additional context; an in vitro study demonstrated that the IRAG2 (also known as Jaw1) protein undergoes specific post‑translational processing that is key to its endoplasmic reticulum localization (PMID:8798562). However, these experiments were not conducted in disease‑relevant models and do not directly link IRAG2’s cellular function to oncogenic processes. Overall, the current body of evidence suggests a limited gene–disease association, implying that while IRAG2 might modulate aspects of lung adenocarcinoma susceptibility, further targeted studies are required to validate its clinical utility.
Gene–Disease AssociationLimitedAssociation inferred from candidate gene studies with IRAG2 included in panels; lacking IRAG2-specific segregation data and distinct pathogenic variants (PMID:18299280, PMID:16410263). Genetic EvidenceLimitedCase–control studies analyzing polymorphic associations did not isolate IRAG2-specific variants or demonstrate familial segregation, reducing the overall genetic evidence strength. Functional EvidenceLimitedIn vitro analysis demonstrated a role for IRAG2 in post‑translational processing and ER localization (PMID:8798562), yet the functional evidence does not directly support an oncogenic mechanism in lung adenocarcinoma. |