Assessment of the role of EGF +61A/G and EGFR R497K polymorphism in patients with inflammatory bowel disease: A case-control study
Bibliographic record
Abstract
Aim: Epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) play an important role in the regulation of cell growth, survival, migration, apoptosis, proliferation, and differentiation. We aimed to investigate the presence of EGF (+61A/G) and EGFR R497Kpolymorphisms in patients with inflammatory bowel disease (IBD) and their associations with clinical features of the patients.Methods: This case-control study included 91 IBD patients (45 Crohn’s disease (CD) patients and 46 ulcerative colitis (UC) patients) and 129 healthy controls (HC). EGF and EGFR were genotyped by polymerase chain reaction and restriction fragment length polymorphism techniques to elucidate their association with clinical outcomes. The disease activity for UC and CD were assessed by Truelove-Witts index (TW) and Crohn's disease activity index (CDAI), respectively. The Montreal classification was used for disease involvement and behavior.Results: EGFR497 AA genotype was significantly decreased in patients with UC compared with CD and HC. In addition, the patients with UC who had EGF +61 A allele had increased risk of moderate and severe disease (p=0.28; OR= 3.13; 95% CI=0.34-28.73). The patients with CD who had the EGF61 AG genotype were found to increased risk for the presence of penetrating disease (p=0.14; χ2=5.59; OR=5.00; 95% CI=1.26-19.83). EGF +61 A genotype carriers also had higher CDAI scores (p=0.19; OR=4.00; 95% CI=0.44-36.14). In addition, A+ carriers were also found to have higher requirement for anti-TNF treatment (p=0.11; OR=5.0; 95% CI=0.56-44.4). Conclusion: In this study, EGFR 497 AA genotype was found to decrease significantly in patients with UC compared to HC and CD patients. To enlighten the mechanism, further studies with larger sample groups are needed to clarify the role of the EGF (+61A/G) and EGFR R497K genes polymorphism, and development of the etiology and pathogenesis of IBD.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".