Alcohol Consumption and Breast Cancer Risk Factors: New Findings on p16 (INK4a) Methylation and Protein Expression

Strategic Insights -

Research on breast cancer risk factors has led investigators to discover new associations between alcohol consumption, breast folate concentration, and variation in one-carbon metabolism genes with p16 (INK4a) promoter methylation and P16 protein expression in histologically normal breast tissues. These findings suggest that alcohol consumption may impede folate metabolism, leading to altered gene methylation. The study, conducted on 138 women with no history of breast cancer, found significant correlations between alcohol consumption, breast folate levels, and p16 (INK4a) methylation.

Key Takeaways:

  • The study investigated the associations between alcohol consumption, breast folate concentration, and variation in one-carbon metabolism genes with p16 (INK4a) promoter methylation and P16 protein expression in histologically normal breast tissues.
  • Alcohol consumption was found to be associated with lower breast folate levels, higher p16 (INK4a) promoter methylation, and less P16 expression in breast tissues.
  • Higher breast folate concentrations were associated with lower p16 (INK4a) promoter methylation.
  • Genetic variation in MTRR (rs1801394), MTHFD1 (rs1950902), and TYMS (rs502396) genes were associated with higher p16 (INK4a) promoter methylation and less P16 protein expression, respectively.

Statistics:

  • 138 women with no history of breast cancer were studied in the cross-sectional investigation.
  • Logistic regression analysis estimated the multivariable-adjusted odds ratios (OR) and 95% confidence intervals (CI) for the associations between alcohol consumption, breast folate levels, and p16 (INK4a) promoter methylation and protein expression.
  • The associations between alcohol consumption and breast folate levels were significant, with coffee consumption being associated with lower breast folate levels (P = 0.03).
  • The correlations between p16 (INK4a) promoter methylation and P16 expression were significant, with a negative correlation (r = -0.28; P = 0.002).
  • The odds ratios for the associations between genetic variation in MTRR, MTHFD1, and TYMS genes with p16 (INK4a) promoter methylation and less P16 protein expression were 2.66, 2.72, and 0.22, respectively.

Sources:

  • Carcinogenesis, 2015;36(1):60-67
  • Oxford University Press
  • Carcinogenesis
  • A.A. Llanos, SUNY Buffalo, Sch Public Hlth & Hlth Profess, Dept. of Epidemiol & Environm Hlth, Buffalo, NY 14214, United States