Cancer-related genes

Cancer-related genes refer to a broad and diverse group of genomic sequences whose alterations—such as mutations, amplifications, or deletions—drive the initiation, progression, and maintenance of malignancy [6, 12]. These genes are fundamentally classified into three functional categories: oncogenes, which promote uncontrolled cell growth when activated; tumor suppressor genes, which normally inhibit cell division or induce apoptosis but lose function in cancer; and DNA repair (or stability) genes, which maintain genomic integrity [1, 2]. Oncogenes like KRAS and MYC often act as 'gas pedals' for cell division, while tumor suppressors like TP53 and RB1 act as 'brakes' [7, 8]. In modern oncology, these genes serve as the foundation for precision medicine, acting as both therapeutic targets for small molecules and monoclonal antibodies and as critical biomarkers for patient stratification [3, 9]. For example, drugs like imatinib target the BCR-ABL fusion protein, while olaparib exploits deficiencies in BRCA1/2 through synthetic lethality [13, 15]. Because the term 'Cancer-related genes' describes a functional class of thousands of distinct molecular entities rather than a single specific protein or receptor, it is categorized as a generic grouping rather than a discrete therapeutic target [10, 11]. Identifying these genes through genomic profiling allows clinicians to tailor treatments to the specific molecular drivers of an individual's tumor [10]. However, challenges such as acquired drug resistance and the difficulty of restoring function to inactivated tumor suppressors remain significant hurdles in the field [9, 11].

Other names

OncogenesTumor suppressor genesCancer driver genesDNA repair genesStability genes

Various mechanisms including kinase inhibition, monoclonal antibody binding, immune checkpoint blockade, and synthetic lethality (e.g., PARP inhibition) depending on the specific gene product [9, 13, 15].