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The transcription factor runt-related protein 2 (RUNX2) has an important impact on the transformation of bone marrow mesenchymal stem cells to osteoblasts. Further studies have shown that RUNX2 plays a key role in the invasion and metastasis of cancers. RUNX2 is a "key" molecule in the regulatory network comprised of multiple signaling pathways upstream and its target downstream molecules. Due to the complex regulatory mechanisms of RUNX2, the specific mechanism underlying the occurrence, development and prognosis of malignant tumors has not been fully understood. Currently, RUNX2 as a promising therapeutic target for cancers has become a research hotspot. Herein, we reviewed the current literature on the modulatory functions and mechanisms of RUNX2 in the development of malignant tumors, aiming to explore its potential clinical application in the diagnosis, prognosis and treatment of tumors.<br /><br /> Taspase 1 (TASP1) is a highly conserved protease involved in site-specific proteolysis. Existing researches have revealed a link between TASP1 expression and carcinogenesis. However, limited data are available regarding the prognosis and functions of TASP1 in hepatocellular carcinoma (HCC).<br /><br /> Western Blotting and qRT-PCR were employed to evaluate the level of TASP1 in HCC cell lines and clinical specimens. TASP1 expression was further calculated in clinical specimens by immunohistochemistry and the mRNA level of TASP1 in HCC was analyzed using Oncomine and UALCAN databases. The TASP1 promoter methylation modification was shown via MEXPRESS and UALCAN. The association between TASP1 expression and postoperative prognosis was evaluated using Kaplan-Meier and Cox regression analysis in clinical patients. The effect of TASP1 on HCC prognosis was analyzed via Kaplan-Meier plotter, GEPIA and UALCAN. Additionally, the regulators, kinases, miRNA and transcription factor targets of TASP1 were identified using LinkedOHCC and regulate HCC via multiple mechanisms.Despite the clinical development of new adjuvant and neoadjuvant chemotherapy drugs, colorectal cancer is still one of the leading causes of cancer-related death in human beings. WNT5a, an autocrine and paracrine β-catenin independent ligand, has been shown to induce tumor inhibition and carcinogenic signals, depending on the type of cancer. In patients with colorectal cancer, WNT5a triggers a variety of downstream signaling pathways, which mainly affect the migration and invasion of tumor cells. This article reviews the mechanism and therapeutic potential of WNT5a in colorectal cancer. In short, an in-depth understanding of the role of WNT5a in colorectal cancer is very helpful to better deal with this disease.The ability of FasL/CD95L to induce apoptosis in various Fas/CD95-expressing cells has been described in the context of hematopoiesis or thymic elimination of self-reactive T cells and resolution of an acute immune response under physiological conditions. At the same time, non-apoptotic CD95 activation is widely described in cancer and shown to stimulate invasiveness of cancer cells, promote cancer progression as well as stemness of cancer cells. This paper puts emphasis on the evolving understanding of expression and the non-apoptotic activities of the CD95/CD95L signaling pathway on the function of tumor cells, tumor microenvironment and immune cells. The emerging evidence to support the role of CD95/CD95L signaling in the anti-tumor immune response will be presented in the context of various malignancies and the modalities of potential therapeutic interventions via selective CD95L inhibition in combination with traditional interventions such as RT, chemotherapy and immune checkpoint inhibitors.Animal models refers to the animal experimental objects and related materials that can simulate human body established in medical research. As the second-largest disease in terms of morbidity and mortality after cardiovascular disease, cancer has always been the focus of human attention all over the world, which makes it a research hotspot in the medical field. At the same time, more and more animal models have been constructed and used in cancer research. With the deepening of research, the construction methods of cancer animal models are becoming more and more diverse, including chemical induction, xenotransplantation, gene programming, and so on. In recent years, patient-derived xenotransplantation (PDX) model has become a research hotspot because it can retain the microenvironment of the primary tumor and the basic characteristics of cells. Animal models can be used not only to study the biochemical and physiological processes of the occurrence and development of cancer in objects but also for the screening of cancer drugs and the exploration of gene therapy. In this paper, several main tumor animal models and the application progress of animal models in tumor research are systematically reviewed. Finally, combined with the latest progress and development trend in this field, the future research of tumor animal model was prospected.<br /><br /> mutation is one of important driver genes in non-small-cell lung cancer (NSCLC) and the patients with <br /><br /> <br /><br /> mutations benefit from the inhibitor AMG510. [https://www.selleckchem.com/products/uk5099.html see more] However, the frequency, concurrent pathogenic mutations, and clinical characteristic of <br /><br /> <br /><br /> is unknown in the NSCLC population of Northeast China.<br /><br /> The retrospective analysis was derived from 431 NSCLC patients in Jilin Cancer Hospital between January 2018 and June 2019. The mutation frequency and concurrent mutations of <br /><br /> <br /><br /> in tumor or peripheral blood was detected by next-generation sequencing (NGS).<br /><br /> The <br /><br /> mutant rate was observed in 10.7% (46/431) of this cohort. All <br /><br /> -driver cancers are caused by mutations in the <br /><br /> isoform, while the <br /><br /> and <br /><br /> isoforms were not detected. Among <br /><br /> mutant patients, 42 (91.3%) showed exon 2 mutation in 12 codon and 13 codon. <br /><br /> <br /><br /> showed a 4.6% (20/431) mutation rate in this cohort and the highest frequency (43.5%, 20/46) in <br /><br /> -mutant-positive patients. There was no difference between tumor tissue and plasma in ty harbored TP53/PTEN mutations, and providing more genome profile for targeted therapy in local clinical practice.