Abstract 433P
Background
Previous researches have reported on the protective effect of aspirin on different types of cancers. However, evidence from observational studies can be biased by multiple confounding factors. Also, it remains unclear whether aspirin use is casually related to a decreased cancer risk. Consequently, we conducted Mendelian randomization analyses, using single nucleotide polymorphisms (SNPs) as instrumental variables to investigate the casual effect of aspirin on different types of cancers.
Methods
Mendelian randomization analyses were conducted using pooled statistics from corresponding researches and several large-scale consortia. Inverse-variance weighted, MR-Egger and weighted median methods were utilized to evaluate the possible causal relationship between aspirin and the observed reduction in cancer risk. Results were shown by odds ratios (OR) and their corresponding 95% CIs. Analyses were conducted using the package “TwoSampleMR” in R.
Results
A total of 19 cancers corresponding to 344,392 cases and 5,424,758 controls were included in the final analysis. In contrast to the lower risk for various cancer types reported in conventional observational studies, our MR results only showed a decreased risk in lung cancer [odds ratio (OR) 0.0418; 95% confidence interval (CI) 0.0031-0.5638; P=0.0168] and squamous cell lung cancer [OR=0.002; 95% CI 1.2145×10-5-0.3009; P=0.0153]. Insignificant results were observed in other types of cancers including lung adenocarcinoma, breast cancer, ovarian cancer, colon cancer, kidney cancer, liver cancer, esophageal cancer, oral cancer, pancreas cancer, rectal cancer, malignant melanoma, non-melanoma skin cancer, Hodgkin’s lymphoma as well as non-Hodgkin’s lymphoma.
Conclusions
The potential effect of aspirin in cancer prevention still needs to be interpreted with cautions and aspirin is still too early to be recommended as a universal chemoprotective agent for primary cancer prevention. Further randomized controlled trials with a more rigorous design are warranted in the future.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
312P - Identification of neoantigen-specific T cell response and anti-tumour immunity in pancreatic cancer
Presenter: Xiaoxiao Du
Session: e-Poster Display Session
313P - Diagnostic value of micro RNA (miRNA) in renal cell cancer: A meta-analysis and systemic review
Presenter: Jestoni Aranilla
Session: e-Poster Display Session
314P - Comprehensive microbial signatures and genomic profiling in tumour samples using next generation sequencing
Presenter: Mei Qi Yee
Session: e-Poster Display Session
315P - High-penetrance breast and/or ovarian cancer susceptibility genes in Filipinos
Presenter: Frances Victoria Que
Session: e-Poster Display Session
316P - Implementation of Vela Analytics to accelerate comprehensive interpretation and reporting of next-generation sequencing-based oncology testing in clinical diagnostic laboratories
Presenter: Yingnan Yu
Session: e-Poster Display Session
317P - Genomic profiling and molecular pathology of Chinese glioma patients
Presenter: yuanli Zhao
Session: e-Poster Display Session
320P - Psychometric interplay of the perception of the real-life impact of COVID-19 pandemic: A cross-sectional survey of patients with newly diagnosed malignancies
Presenter: Kelvin Bao
Session: e-Poster Display Session
321P - Impact of COVID-19 and lockdown on adherence to treatment schedule among cancer patients
Presenter: Krishnamani Kalpathi
Session: e-Poster Display Session
322P - Challenged faced by cancer patients during the COVID-19 pandemic
Presenter: mithra Krishnamani
Session: e-Poster Display Session
323P - Oncology care in the Republic of Kazakhstan during COVID-19
Presenter: Dilyara Kaidarova
Session: e-Poster Display Session