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Purpose <p>Recent studies have shown that nutritional factors may contribute to <i>KRAS</i> gene mutation. This study aims to explore the association between dietary total antioxidant capacity (DTAC) and <i>KRAS</i> mutant status in patients with metastatic colorectal cancer (mCRC).</p> Methods <p>This case-control study was conducted on 90 patients with mCRC. Participants’ dietary intake was assessed using a validated food frequency questionnaire (FFQ) of 147 items. The ferric-reducing antioxidant potential (FRAP) method was used to determine DTAC. Multivariate analysis evaluated diet by DTAC categories, and Logistic regression examined the relationship between DTAC and <i>KRAS</i> gene mutation, adjusting for confounders.</p> Results <p>The mean DTAC was 14.10 ± 6.10 and 15.95 ± 8.52 for case and controls, respectively, with no significant difference (<i>p</i> = 0.300). An inverse, but non-significant, association was observed between a higher score of DTAC and odds of <i>KRAS</i> mutation [(crude; OR = 0.640, 95%CI = 0.279–1.47, <i>P</i> = 0.293) (adjusted; OR: 0.309, 95% CI: 0.077–1.236, <i>P</i> = 0.097)]. The mean fat intake of participants among the case and control groups was significantly different in the higher scores category of DTAC [(93.91 ± 30.77) vs. (114 ± 42.15), <i>P</i> = 0.010].</p> Conclusion <p>The findings suggest a non-significant relationship between DTAC and <i>KRAS</i> gene mutation. Future well-designed longitudinal observational studies with higher populations are warranted to investigate the comprehensive relationship between the DTAC and <i>KRAS</i> mutant gene.</p>

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Association of dietary total antioxidant capacity with KRAS gene mutation in metastatic colorectal cancer patients: a case-control study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月22日

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  • Fahmideh Bagrezaei,
  • Bahram Pourghassem Gargari,
  • Sorayya Kheirouri,
  • Reza Eghdam Zamiri,
  • Sedigheh Yusefinejad,
  • Roghayeh Molani-Gol,
  • Mohammad Alizadeh

摘要

Purpose

Recent studies have shown that nutritional factors may contribute to KRAS gene mutation. This study aims to explore the association between dietary total antioxidant capacity (DTAC) and KRAS mutant status in patients with metastatic colorectal cancer (mCRC).

Methods

This case-control study was conducted on 90 patients with mCRC. Participants’ dietary intake was assessed using a validated food frequency questionnaire (FFQ) of 147 items. The ferric-reducing antioxidant potential (FRAP) method was used to determine DTAC. Multivariate analysis evaluated diet by DTAC categories, and Logistic regression examined the relationship between DTAC and KRAS gene mutation, adjusting for confounders.

Results

The mean DTAC was 14.10 ± 6.10 and 15.95 ± 8.52 for case and controls, respectively, with no significant difference (p = 0.300). An inverse, but non-significant, association was observed between a higher score of DTAC and odds of KRAS mutation [(crude; OR = 0.640, 95%CI = 0.279–1.47, P = 0.293) (adjusted; OR: 0.309, 95% CI: 0.077–1.236, P = 0.097)]. The mean fat intake of participants among the case and control groups was significantly different in the higher scores category of DTAC [(93.91 ± 30.77) vs. (114 ± 42.15), P = 0.010].

Conclusion

The findings suggest a non-significant relationship between DTAC and KRAS gene mutation. Future well-designed longitudinal observational studies with higher populations are warranted to investigate the comprehensive relationship between the DTAC and KRAS mutant gene.