The dysregulation of cyclin-dependent kinase 12 (CDK12), which may result from genomic alterations or modulation by upstream effectors, is implicated in cancer oncogenesis and progression. CDK12 overexpression or activation is sufficient to induce tumor initiation, recurrence, and therapeutic resistance. However, CDK12 may also exert tumor-suppressive functions in a context-dependent manner. Therefore, caution is warranted when targeting CDK12 in future clinical trials. A comprehensive elucidation of the dual roles and underlying mechanisms of CDK12 in carcinogenesis is urgently needed to advance precision oncology. This review provides an overview of the current understanding of the dysregulation and biological roles of CDK12 in cancer. Subsequently, we systematically summarize the functions and mechanisms of the oncogenic and tumor-suppressive roles of CDK12 in different contexts. Finally, we discuss the potential of CDK12 as a novel therapeutic target and its implications in clinical oncology, offering insights into future directions for innovative cancer treatment strategies.

OBJECTIVE:To observe the haemostasis outcome of treating radical gastrectomy for gastric cancer with Rep-tilase.METHODS:A total of30patients underwent radical gastrectomy for gastric cancer were randomly divided into reptilase group and control group,the preoperative and postoperative blood clotting functional parameter changes of the2groups were observed and the volumes of intraoperative blood loss and blood infusion were recorded.RESULTS:There was no significant difference in the blood clotting functional parameters before and after operation in the reptilase group,the intraoperative blood loss volume and blood infusion volume in this group were all lower than in the control group(P