Genetic and Epigenetic Biomarkers for Lung Cancer: Molecular Mechanisms and Detailed Insights

Lung cancer is one of the leading causes of cancer deaths worldwide, resulting in extensive research into its molecular mechanisms. Also in Iran, lung cancer is one of the five common cancers and its incidence is increasing. Genetic mutations found in lung cancer are stressed in this investigation. The main aim of this study was to show how important genetic and epigenetic markers are in diagnosing, treating, and from a prognosis perspective managing lung cancers. As you know Genomic biomarkers refer to changes in DNA sequences which are specific for cancer. In lung cancer, some mutations are vital including: EGFR Mutations: these occur frequently in non-small cell lung cancers whereby they result in perpetual receptor activation as well as uncontrolled cellular proliferation and thus help predict responses to EGFR tyrosine kinase inhibitors (TKIs) hence aiding personalized therapy. KRAS Mutations: These drive tumor growth through continuous activation of RAS/MAPK signaling pathway and often lead to resistance against certain therapies suggesting alternative therapeutic measures. ALK Rearrangements: These generate oncogenic proteins that initiate the process of malignancy. ALK inhibitors work well for such patients thereby underscoring their importance as targets for therapy. TP۵۳ Mutations: TP۵۳ is an acronym used to mean “guardian of the genome” since it plays a role of suppressing tumors but when mutated becomes defective causing genomic instability and progression into malignancies. They affect how well a person will recover and what treatments they should get. Epigenetic modification affects gene expression without changing the DNA sequence, which is crucial in lung cancer. Some of these alterations are: DNA Methylation: Aberrant methylation of CpG islands in promoter regions of tumor suppressor genes leads to their silencing, which can silence genes such as CDKN۲A and RASSF۱A that normally suppress tumor growth. These patterns help with early detection and risk assessment. Histone Modifications: Changes like acetylation and methylation regulate gene expression. Misregulated enzymes can lead to cancer, with interest in inhibitors emerging as possible therapies. Non-Coding RNAs: MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) control the activity of genes. Their disruption is linked to lung cancer, which makes them potential diagnostic and prognostic markers. These interactions between genetic and epigenetic biomarkers are discussed. Genetic mutations often activate oncogenic pathways while epigenetic changes inhibit tumor-suppressive genes, leading to progression of cancer. Knowing these biomarkers helps tailor treatment resulting into improved response rates among patients having specific genetic mutations such as ALK inhibitors for EGFR or EGFR inhibitors on cancers caused by EGFR gene alterations specifically. Epigenetic-based therapies including demethylating agents (DNMTis) and HDACis hold promise for reversing aberrations seen. Genetic and epigenetic biomarkers provide essential insights into lung cancer management including diagnosis, prognosis prediction, therapeutic approaches, etc. In addition, ongoing research will drive our understanding forward along with the improvement of patient outcomes aimed at making treatment more personalized.

کلیدواژه ها:

Lung-cancer ، EGFR ، TP۵۳ ، ALK ، RAS/MARP