在正常的上皮组织中，原癌基因调控着细胞内或细胞间的关键功能，包括细胞生长与增殖、凋亡和通过不同途径介导从细胞周边（胞外空间）到细胞核的信号转导。癌基因是相应原癌基因的突变或放大形式，在细胞发生肿瘤发展和恶性转化过程中起着至关重要的作用。唾液腺癌（SGCs）展示了多种组织发生类型，并且其具有广泛的染色体和基因改变谱。特别是在某些基因中的放大【人表皮生长因子受体2（HER2）、人表皮生长因子受体4（HER4）、表皮生长因子受体（EGFR）、间变性淋巴瘤激酶（ALK）、鼠双分钟2同源物（MDM2）、雄激素受体（AR）、程序性细胞死亡配体1（PD-L1）、神经分化因子2（NEUROD2）、磷脂酰肌醇3，4,5-三磷酸依赖的RAC交换蛋白1（PREX1）、细胞周期依赖性蛋白激酶4/6（CDK4/6）、富含脯氨酸酸性蛋白1（PRAP1）、凯尔抗原系统（KEL）、谷氨酸受体亚单位ε2（GRIN2D）、Ewing肉瘤RNA结合蛋白1（EWSR1）、MYC原癌基因（MYC）】与染色体数目失衡（非整倍体/多体/单体）的结合或不结合构成了不同的基因特征，影响了其对单克隆抗体为基础的癌症靶向治疗方案的反应。不同的SGC组织类型表现出特定的突变/放大基因组合，从而改变其临床组织学特征。在当前的分子综述中，我们介绍了最重要的放大癌基因及其对SGCS生物学行为的影响。版权所有2023年，国际抗癌研究学会。

In normal epithelia, proto-oncogenes regulate critical intra- or intercellular functions, including cell growth and proliferation, apoptosis, and signaling transduction from the cell periphery (extracellular space) to the nucleus mediated by different pathways. Oncogenes are the mutated or amplified forms of the corresponding proto-oncogenes that are crucially involved in cell neoplastic and malignant transformation during carcinogenesis. Salivary gland carcinomas (SGCs) demonstrate a variety of histogenetic types. They are characterized by a broad spectrum of chromosomal and gene alterations. In particular, amplifications in specific genes [human epidermal growth factor receptor 2 (HER2), human epidermal growth factor receptor 4 (HER4), epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), Mouse double minute 2 homolog (MDM2), androgen receptor (AR), programmed death (ligand 1 (PD-L1), neurogenic differentiation factor 2 (NEUROD2), phosphatidylinositol 3,4,5-trisphosphate-dependent RAC exchanger 1 protein (PREX1), cyclin-dependent kinase4/6 (CDK4/6), proline-rich acidic protein 1 (PRAP1), kell antigen system (KEL), glutamate receptor subunit epsilon 2 (GRIN2D), Ewing sarcoma RNA-binding protein 1 (EWSR1), MYC proto-oncogene (MYC)] combined or not with chromosomal numerical imbalances (aneuploidy/ polysomy/monosomy) form different genetic signatures affecting the response to monoclonal antibody-based, oncologicaly targeted regimens. Different SGC histotypes demonstrate specific combinations of mutated/amplified genes that modify their clinicohistological features. In the current molecular review, we present the most important amplified oncogenes and their impact on the biological behavior of SGCS.Copyright 2023, International Institute of Anticancer Research.