Tumorigenesis is driven by the gain-of-function mutation or overexpression of oncogenes, as well as by the inactivation of oncosuppresssive (tumor suppressor) genes due to their loss-of-function mutation, genomic loss, or epigenetic silencing. This combination of factors increases the cell-intrinsic fitness of malignant cells, enhances their capacity to obtain trophic support by the tumor microenvironment, and simultaneously subverts cancer immunosurveillance.¹ Since the realization that neoplasia is driven by molecularly defined genetic alterations, cancer is not more conceived as a fatality but as a disease that — at least theoretically — can be targeted by inhibiting oncogenes or reestablishing oncosuppression within the realm of ‘precision oncology’. Indeed, at the oncological ward, deep sequencing of tumor DNA and RNA has become part of the clinical routine to retrieve information on genomic, epigenomic, and transcriptomic alterations and hence to identify patients who may benefit from specific drugs targeting relevant pathways.²

肿瘤发生是由癌基因的功能获得性突变或过度表达以及由于功能丧失突变、基因组丢失或表观遗传沉默而导致的抑癌基因失活驱动的。这些因素的组合增加了恶性细胞的细胞内在适应性，增强了它们获得肿瘤微环境营养支持的能力，同时破坏了癌症免疫监视。 ¹自从认识到瘤形成是由分子定义的基因改变驱动的，癌症不再被视为一种致命的疾病，而是一种至少在理论上可以通过在“精准肿瘤学”领域内抑制癌基因或重建肿瘤抑制来治疗的疾病。事实上，在肿瘤病房，肿瘤 DNA 和 RNA 的深度测序已成为临床常规的一部分，用于检索基因组、表观基因组和转录组改变的信息，从而识别可能受益于针对相关途径的特定药物的患者。 ²