Risk Factors and Pathophysiological Mechanisms in Drug-Induced Interstitial Lung Disease Associated With Novel Anticancer Agents: A Scoping Review (2016-2026)

Drug-induced interstitial lung disease (DI-ILD) associated with novel anticancer agents, such as immune checkpoint inhibitors (ICIs), tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs), is a severe adverse event that can lead to fatal outcomes.Effective clinical management requires integrating host-specific risk factors with drug-specific biological mechanisms.This scoping review, conducted following the PRISMA Extension for Scoping Reviews (PRISMA-ScR) guidelines, systematically searched PubMed and Ichushi-Web databases for peer-reviewed articles published between January 2016 and April 2026.Data from 65 included articles were synthesized into a conceptual framework.Pre-existing ILD or subclinical interstitial lung abnormalities (ILA) emerged as highly prevalent and potent class-transcending risk factors, particularly across novel anticancer drug classes.Distinct temporal patterns of injury were identified: TKIs typically induced DI-ILD within the first one to two months via diffuse alveolar damage (DAD) resulting from epithelial repair blockade, whereas ICI-induced pneumonitis peaked between two and four months due to a breakdown of self-tolerance.To transition from reactive drug interruption to a proactive "Precision Clinical Safety" strategy, we propose a risk-adaptive monitoring protocol centered on mandatory pre-treatment screening with thin-section high-resolution computed tomography (HRCT) to detect subclinical ILA.While low-to-intermediate-risk patients follow standard protocols, high-risk patients require enhanced surveillance, including clinical consultations every two weeks during the initial treatment phase.