# Scars That Speak: Unraveling the Oncogenic Aftermath of Pulmonary Tuberculosis—A Narrative Review

## TL;DR

This review explores how past tuberculosis infections may increase the risk of developing lung cancer due to long-term lung damage and immune changes.

## Contribution

The paper provides a comprehensive synthesis of recent evidence on the link between pulmonary tuberculosis and lung cancer.

## Key findings

- Population studies show a two- to threefold increased lung cancer risk after PTB, independent of smoking.
- Post-TB lungs exhibit chronic inflammation, fibrosis, and immune checkpoint activation linked to carcinogenesis.
- TB history complicates lung cancer diagnosis and may affect treatment choices, especially with immune therapies.

## Abstract

Background: Pulmonary tuberculosis (PTB) and lung cancer (LC) are major causes of global respiratory morbidity and mortality. Increasing evidence suggests that tuberculosis may induce persistent pulmonary alterations that extend beyond microbiological cure, potentially facilitating lung carcinogenesis. This review synthesizes current epidemiological and mechanistic evidence linking PTB to subsequent LC development. Methods: A structured narrative appraisal of the literature was conducted using PubMed, Web of Science, Scopus, ScienceDirect, MDPI Journals, and Google Scholar, focusing on studies published between 2020 and 2025. Eligible publications included cohort studies, meta-analyses, observational reports, and mechanistic investigations addressing the TB–LC association. Studies were thematically categorized into epidemiological evidence, pathogenic mechanisms, diagnostic challenges, and therapeutic implications. Results: Population-based studies consistently demonstrate a two- to threefold increased risk of LC among individuals with prior PTB, independent of smoking and other major confounders. Mechanistically, the post-tuberculous lung is characterized by chronic inflammation, oxidative stress, fibrotic remodeling, immune checkpoint activation (including PD-1/PD-L1 signaling), dysregulated microRNA expression, and metabolic reprogramming. Clinically, overlapping radiological and histopathological features may delay cancer diagnosis. A history of TB may also influence therapeutic decisions, particularly regarding immune checkpoint inhibitors due to potential infection reactivation. Conclusions: PTB may represent an independent risk factor for LC through sustained structural and immunological remodeling. Structured post-TB surveillance and risk-adapted screening strategies may be warranted in selected high-risk populations.