AimThis study aimed to evaluate the association between thyroid neoplasms (TN) and the risk of developing breast neoplasms (BN) by assessing data on single nucleotide polymorphisms (SNPs) obtained from the Deutsches Krebsforschungszentrum (DKFZ) and Breast Cancer Association (BCAC).MethodsData on SNPs associated with TN and BN were obtained from DKFZ and BCAC, respectively. Secondary data analysis of all pooled data from genome-wide association studies (GWAS) was performed to identify the genetic loci closely associated with TN or BN as instrumental variables (IVs). To evaluate the causal relationship between TN and BN, a bidirectional Mendelian randomization (MR) analysis was performed using MR Egger regression, weighted median, inverse variance weighted (IVW) random effects model, simple mode, weighted mode, maximum likelihood, penalized weighted median, IVW radial, IVW fixed effects, and robust adjusted profile scores (RAPS) method.ResultsThe MR in this study demonstrated a modest reverse causal relationship between TN and BN but a significant positive causal relationship between BN and TN.ConclusionsThe MR of this study provided genetic evidence suggesting an association between BN and TN; however, further research is warranted to explore the potential mechanism of interaction between these two malignancies. Moreover, general breast screening should be performed in individuals with TN, but TN screening should be reinforced in individuals with BN.

AimTo explore whether C-reactive protein (CRP) mediates the risk of body mass index (BMI) in pancreatic cancer (PC) and calculate the mediate proportion of CRP in this possible mechanism.MethodsBased on two-sample Mendelian randomization (TSMR), a two-step Mendelian randomization (TM) model was conducted to determine whether CRP was a mediator of the causal relationship between BMI and PC. The multivariable Mendelian randomization (MVMR) study was designed for mediating analysis and to calculate the mediating proportion mediated by CRP.ResultsBMI has a positive causal relationship with PC (n = 393 SNPs, OR = 1.484, 95% CI: 1.021–2.157, p< 0.05). BMI has a positive causal relationship with CRP (n = 179 SNPs, OR = 1.393, 95% CI: 1.320–1.469, p< 0.05). CRP has a positive causal relationship with PC (n = 54 SNPs, OR = 1.348, 95% CI: 1.004–1.809, p< 0.05). After adjusting CRP, BMI has no causal relationship with PC (n = 334 SNPs, OR = 1.341, 95% CI: 0.884–2.037, p< 0.05). After adjusting BMI, there was still a positive causal relationship between CRP and PC (n = 334 SNPs, OR = 1.441, 95% CI: 1.064–1.950, p< 0.05). The mediating effect of CRP was 29%.ConclusionsIn clinical practice, while actively advocating for weight loss among obese patients, we should focus on chronic inflammation levels in obese patients as well. In addition, anti-inflammatory dietary patterns and appropriate physical activity are important in preventing PC.

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