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ORIGINAL RESEARCH article

Front. Oncol.
Sec. Molecular and Cellular Oncology
Volume 14 - 2024 | doi: 10.3389/fonc.2024.1452559
This article is part of the Research Topic Crosstalk between Lung Cancer and Fibrosis: Pathogenesis and Therapeutic Strategies View all articles

Fibrosis to Carcinogenesis: Unveiling the Causal Dynamics Between Pulmonary Fibrosis and Lung Cancer

Provisionally accepted
Yiming Huang Yiming Huang 1Lin Zhi Lin Zhi 2Ting Huang Ting Huang 3Heran Zhou Heran Zhou 3*
  • 1 Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang Province, China
  • 2 Fudan University, Shanghai, Shanghai Municipality, China
  • 3 Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province, China

The final, formatted version of the article will be published soon.

    Background Previous clinical evidence has shown a correlation between pulmonary fibrosis (PF) and lung cancer (LC), but their causal relationship remains unknown.This study utilized a bidirectional two-sample Mendelian randomization (MR) approach to explore the causal relationship between PF and LC, including its subtypes.Genetic data were obtained from the IEU and FinnGen Genome-Wide Association Studies (GWAS). SNPs with genome-wide significance were selected, and analyses were conducted using Inverse-Variance Weighted (IVW), MR Egger, and Weighted Median methods. The IVW results for various subtypes of lung cancer and PF were used in a meta-analysis to investigate the overall causal effect between PF and lung cancer. Sensitivity analysis was used for both MR and meta-analysis to investigate the robustness of the results.The bidirectional MR analysis showed no significant causal relationship between PF and overall LC or its subtypes, except for SCLC, which had a significant positive association (OR = 1.29, 95% CI 1.07-1.57, p = 0.009). The meta-analysis results indicated no overall causal effect (OR = 1.067, 95% CI: 0.952-1.195, P = 0.265, I² = 57.3%). In the reverse MR analysis, NSCLC and LUSC showed significant associations with PF (OR = 1.12, 95% CI 1.01-1.23, p = 0.028 and OR = 1.04, 95% CI 1.01-1.08, p = 0.012, respectively), while the meta-analysis results indicated no significant causal effect (OR = 1.006, 95% CI: 0.973-1.040, P = 0.734, I² = 55.9%).Sensitivity analyses indicated no evidence of horizontal pleiotropy or significant heterogeneity.This study suggests a potential causal relationship between PF and SCLC, as well as between NSCLC and LUSC with PF. However, the overall causal relationship between PF and LC was not statistically significant, possibly due to individual variability and other influencing factors. Further research using data from diverse populations is needed to validate these findings.

    Keywords: Pulmonary Fibrosis, lung cancer, Mendelian randomization, Small Cell Lung Cancer, Non-small cell lung cancer

    Received: 21 Jun 2024; Accepted: 01 Aug 2024.

    Copyright: © 2024 Huang, Zhi, Huang and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Heran Zhou, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang Province, China

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