Ali Johar, Sabiha Bibi, Jan Hanif Ullah, Haider Syed Adnan, Khan Abid Ali, Ali Saima S
Center for Genome Sciences, Rehman Medical College, Phase-V, Hayatabad, Peshawar, KP, Pakistan; AlviArmani International, Mississauga, ON, Canada.
Center for Genome Sciences, Rehman Medical College, Phase-V, Hayatabad, Peshawar, KP, Pakistan.
Oral Oncol. 2017 Jul;70:23-28. doi: 10.1016/j.oraloncology.2017.05.004. Epub 2017 May 17.
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. It accounts for 2.5% of all new cancer cases and 1.9% of all cancer deaths annually. More than 90% of oral cancers (occurring in the mouth, lip, and tongue) are oral squamous cell carcinoma. The incidence rate of oral cancer varies widely throughout the world, with an evident prevalence in South Asian countries. This high incidence occurs in correlation with oral cancer-associated behaviors such as alcohol, tobacco use. Researchers have reported that these behaviors lead to genetic variations in tumor suppressor genes (APC, p53), proto-oncogenes (Myc), oncogene (Ras) and genes controlling normal cellular processes (EIF3E, GSTM1). Processes such as segregation of chromosomes, genomic copy number, loss of heterozygosity, telomere stabilities, regulations of cell-cycle checkpoints, DNA damage repairs and defects in notch signaling pathways are involved in causing oral cancer. In order to develop preventive and therapeutic options, it is necessary to comprehend the basic molecular mechanisms forcing oral tumorigenesis. This review examines, in detail, the mechanisms of genetic alteration which are considered to be responsible for the initiation of oral cancer.
头颈部鳞状细胞癌（HNSCC）是全球第六大常见癌症。它占每年所有新发癌症病例的2.5%，以及所有癌症死亡病例的1.9%。超过90%的口腔癌（发生在口腔、嘴唇和舌头）是口腔鳞状细胞癌。口腔癌的发病率在世界各地差异很大，在南亚国家尤为明显。这种高发病率与与口腔癌相关的行为如饮酒、吸烟有关。研究人员报告说，这些行为会导致肿瘤抑制基因（APC、p53）、原癌基因（Myc）、癌基因（Ras）以及控制正常细胞过程的基因（EIF3E、GSTM1）发生基因变异。诸如染色体分离、基因组拷贝数、杂合性缺失、端粒稳定性、细胞周期检查点调控、DNA损伤修复以及Notch信号通路缺陷等过程都与口腔癌的发生有关。为了开发预防和治疗方案，有必要了解促使口腔肿瘤发生的基本分子机制。本综述详细探讨了被认为是导致口腔癌发生的基因改变机制。
