To improve reproducibility and worldwide applicability, future work will focus on standardizing biomarker validation, employing adaptive clinical trial designs, and integrating multi-omic data.
Abstract
Cancer is one of the major causes of morbidity and mortality globally, and treatment resistance and disease heterogeneity are ongoing problems. Over the past five years, cancer treatment has
undergone a substantial transformation thanks to precision medicine, molecular profiling, and the application of artificial intelligence (AI) in diagnostics. Next-generation immune checkpoint inhibitors,
CAR T-cell treatments targeting solid tumours, and bispecific antibodies are examples of advances in
immunotherapy. RNA-based treatments, oncolytic viruses, and tailored cancer vaccinations all made a
big difference. The discovery of novel biomarkers, including ctDNA, tumour mutational burden
(TMB), and spatial transcriptomic signatures, has enhanced real-time monitoring, patient stratification,
and resistance prediction. Early intervention and flexible treatment adjustments are now possible
thanks to developments in single-cell sequencing, liquid biopsy, and AI-assisted imaging. The assessment of minimal residual disease (MRD) and the detection of non-invasive cancer have also changed
as a result. However, due to issues such as tumour heterogeneity, unequal access to state-of-the-art
technology, insufficient biomarker validation, and implementation costs, these developments are not
widely adopted in clinical practice. Moreover, immune-related side effects and the emergence of resistance mechanisms continue to hinder treatment efficacy. To improve reproducibility and worldwide
applicability, future work will focus on standardizing biomarker validation, employing adaptive clinical trial designs, and integrating multi-omic data. Enhancing collaboration between genomics, computational biology, and immuno-oncology will be crucial to accelerating the shift to personalized, accurate, and accessible cancer care.
Recent advances in NSCLC with established alterations are summarized, including EGFR, ALK, ROS1, KRAS, BRAF, RET, HER2, MET, and NTRK, and emerging targets are discussed, and emerging targets, such as NRG1 fusions, MTAP loss, and SMARCA4 deficiency are discussed.
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