Akademik Veri Yönetim Sistemi
Airway Diseases, Cemal Cingi,Arzu Yorgancıoğlu,Nuray Bayar Muluk,lvaro A. Cruz, Editör, Springer, London/Berlin , Zug, ss.1-21, 2023
he molecular basis of lung cancer is the progressive accumulation of mutations and epigenetic abnormalities leading to the expression of multiple genes with different functions. These changes lead to the weakening of the DNA structure and its greater susceptibility to subsequent mutations. This is caused by irregularities in cell cycle regulation (mutations of protooncogenes and suppressor genes) and disorders in the repair processes in damaged DNA. Several signaling pathways and specific oncogenes are deregulated in lung cancer and are known to influence modifications related to tumorigenesis, including apoptosis, proliferation, cell-cycle progression, and gene expression [1]. These key pathways and oncogenes affect the development and progression of lung cancer as well as prognosis and resistance.