ArticleCancer medicine2026
Stage-Specific Differences in Circulating Resistin From Premalignant to Advanced Colorectal Cancer: A Cross-Sectional Cohort Study.
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundResistin is a macrophage-associated cytokine linked to obesity-driven inflammation, a recognised risk factor for colorectal cancer. Prior studies of circulating resistin in colorectal cancer have reported inconsistent findings, largely because patients were analysed as a single group without accounting for tumour stage. Whether resistin follows a stage-specific pattern across the adenoma-carcinoma sequence, independent of insulin resistance and conventional tumour markers, has not been systematically examined.
methodsIn this single-centre study, serum resistin levels were measured in 179 participants, including 137 patients with colorectal cancer (CRC), 11 with colorectal adenomas and 31 healthy controls. Tumour markers and metabolic variables were analysed. Moreover, stage-stratified comparisons were performed using non-parametric testing and ordinal logistic regression.
resultsCirculating resistin concentrations varied significantly across diagnostic categories and tumour stage. Elevated levels were observed in adenomas and early-stage CRC (stage I-II; median ~7600 pg/mL), whereas significantly lower levels were detected in advanced-stage disease (stage III-IV; median ~2500 pg/mL; p < 0.001). In multivariable ordinal regression analysis, resistin remained independently associated with tumour stage after adjustment for BMI, fasting insulin, CEA and CA19-9. Resistin levels were not associated with insulin resistance as measured by HOMA-IR.
conclusionsCirculating resistin shows a stage-dependent association across colorectal tumorigenesis, with higher levels in premalignant and early-stage disease and lower levels in advanced-stage disease. These cross-sectional findings are consistent with a model in which resistin reflects host inflammatory activation rather than tumour burden, although this interpretation remains hypothesis-generating. This pattern may help explain previously inconsistent associations reported for resistin in colorectal cancer; however, further prospective and mechanistic studies are required to clarify its role in tumour progression and validate our findings.
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