临床上诱导化疗在口腔鳞癌中还存在一定争议，如何筛选获益人群是整体提高疗效的关键。微管解聚蛋白Stathmin 1参与调解微管稳定性的动态平衡。课题组在建立口腔黏膜上皮细胞体外癌变模型和蛋白质组学研究的基础上，发现Stathmin 1在口腔鳞癌中起重要作用，并可能受p53基因突变调控；通过检测口腔鳞癌TPF诱导化疗临床试验患者组织中Stathmin 1表达，发现低表达Stathmin 1的患者可从TPF诱导化疗中生存获益，而高表达Stathmin 1的患者没有生存获益。本研究旨在结合分子机制研究和临床试验，重点围绕Stathmin 1与p53突变、PI3K/AKT信号通路，以及Stathmin 1在口腔鳞癌抵抗TPF诱导化疗中的作用，阐明Stathmin 1在口腔鳞癌发展和TPF诱导化疗中的分子机制，探索以Stathmin 1作为预测性生物标志物指导口腔鳞癌个体化治疗选择的肿瘤诊治新策略。

Although induction chemotherapy agents could be used to treat malignancies in head and neck cancers, there are still debates on the clinical application of induction chemotherapy in oral squmaous cell carcinoma (OSCC). The keypoint of improving the entire prognosis is to screen the proper patients who might benefit from induction chemotherapy before deciding the treatment protocol. Stathmin 1 is a microtubule-destabilizing phosphoprotein, ubiquitously expressed and involved in regulating the global dynamics of mitotic and interphase microtubules; however, the molecular role of Stathmin 1 in induction chemotherapy is still unclear in OSCC. Based on our previously established in vitro cellular carcinogenesis model of OSCC and proteomic analysis, we found that Stathmin 1 played an important role in progression of OSCC, it was possibly regulated by mutant p53 genes and correlated with the cellular apoptosis in OSCC; detection of stathmin 1 in biopsy samples from 256 OSCC patients in a clincial trial focusing on TPF induction chemotherpay shew that the patients with low Stathmin 1 expression could significantly benefit from TPF indcuction chemotherpay on suvival, the patients with high Stathmin 1 expression could not benefit from TPF induction chemotherapy. However, in the literatures, there are few studies reporting the molecular mechanism of Stathmin 1 expression on cellular apoptosis through mutant 53 and PI3K/AKT pathways, there are either few studies reporting the mechanism of treatment resistance in patients with Stathmin 1 overexpression against TPF induction chemotherapy in OSCC; therefore, there are still a lot of unknown mechanisms to be further investigated. Our present study will use the combination of basic machanism investigations and clincial trials to reveal the molecular mechanism of Stathmin 1 on cellular apoptosis through mutant p53 and PI3K/AKT pathways and the molecular mechanism of treatment resistance of Stathmin 1 overexpression against TPF induction chemotherapy in OSCC; a new clinical trial of Stathmin 1 expression as a predictive biomarker for choosing TPF induction chemotherpay will also be designed and excuted based on the retrospective results of Stathmin 1 anslysis in OSCC patients from the previous TPF trial. The aim of this study is to clarify the molecular mechanism of Stathmin 1 in cellular apoptosis through mutant 53 and PI3K/AKT pathways, and a personalized treatment strategy based on predictive biomarker in OSCC patients.