| Correlation |
Summary |
Reference |
| Positive |
Elevated serum iron was associated with increased risk, strongest in the distal colon and significant in females. Mean transferrin saturation was higher in cases compared to controls (30.7 versus 28.7%), but TIBC did not predict the occurrence of colorectal cancer. |
[10] |
| Mean transferrin saturation and differences in TIBC and serum iron were higher in men who developed cancer than those who did not. When divided into 5 groups on the basis of baseline transferrin saturation, the combined risk of cancer occurrence associated with moderate elevations. |
[13] |
| Mean total iron-binding capacity was significantly lower and transferrin saturation was significantly higher than men who remained free of cancer. The risk of cancer in men in each quartile of transferrin-saturation level relative to the lowest quartile rose incrementally. Among women, a post hoc examination associated with very high transferrin saturation. |
[14] |
| Mortality in postmenopausal women was inversely related to TIBC; the relative risk for the highest tertile of TIBC, adjusted for age, smoking and alcohol intake was 0.05 (95% confidence interval (CI): 0.007-0.39). There was association between body iron stores and mortality due to cancer was observed in men. |
[20] |
| Excess risk of colorectal was found in subjects with transferrin saturation level exceeding 60%. The adjusted relative risk was 3.04 for colorectal cancer. High iron stores may increase the risk of colorectal cancer. |
[21] |
| Elevated relative risk was observed in hereditary hemochromatosis heterozygotes in males for colorectal cancer (RR, 1.28; CI, 1.07-1.53), colonic adenoma (RR, 1.29; CI, 1.08-1.53 for females and 1.24; CI, 1.05-1.46 for males), and stomach cancer in females (RR, 1.37; CI, 1.04-1.79). |
[24] |
| Individuals carrying the HFE Tyr282 allele (homo- and heterozygotes) in combination with homozygosity for the TFR Ser142 allele are at increased risk for neoplasia, including colorectal cancer. The odds ratio for three neoplasms (including CRC) increased for HFE Tyr homozygotes and compound heterozygotes in combination with TFR Ser homozygosity. |
[25] |
| |
There was a significantly increased risk of colorectal cancer associated with higher total iron intake [odds ratio (OR) = 2.50; 95% confidence interval (CI) suggesting a role of luminal exposure to excessive iron but does not support a role for increased body iron stores in CRC development. |
[29] |
| Negative |
There were no associations between the risk of colorectal cancer and any serum iron indices except for serum ferritin, which showed a significant inverse association. This suggests a role of luminal exposure to excessive iron but does not support a role for increased body iron stores in CRC development. |
[29] |
| There was an inverse association between serum ferritin, iron and transferrin and colorectal cancer risk and a suggestion of an inverse association between dietary iron and colorectal cancer risk. However, serum unsaturated iron binding capacity was positively associated with colon cancer risk. |
[30] |
| No association |
In men, transferrin saturation was inversely associated with risk of colon and rectal carcinoma. No cases observed with transferrin saturation. There was no evidence that the risk of epithelial cancer (all sites combined) is related to transferrin saturation level or to iron deficiency (≤5%) or overload (≥60%). |
[26] |
