PD-L1 plays a crucial role in the host immune system in cancer progression. Its gene promoter region contains a binding site for ZEB1. Our report shows that high PD-L1 expression at the invasive front of esophageal squamous cell carcinoma (ESCC) was associated with greater depth of tumor invasion, epithelial-mesenchymal transition (EMT), and less CD8⁺ lymphocyte infiltration.

Tumor cells secrete a large amount of lactic acid due to the Warburg effect. This study suggestss that lactic acid negatively regulates the accumulation of macrophages at a tumor site, but promotes M2-like macrophage polarization in human HNSCC.

IRP-2 is overexpressed in colorectal cancer and that its expression is tightly correlated with transferrin receptor-1 expression. Furthermore, IRP-2 expression is associated with mutation in BRAF. Using MAPK/ERK inhibitors might be another mechanism by which iron sensitive tumours can be targeted.

Our study suggests that cIAP2 is highly expressed in human GBC and correlates with poor prognosis; furthermore, the results showed that cIAP2 can promote gallbladder cancer invasion and lymphangiogenesis by activating the NF-κB pathway. These data indicate that cIAP2 may be a potential treatment target to prevent the invasion and lymphatic metastasis of GBC.

In this study, we showed a trend of gradually decreasing expression of Talin1 from normal liver tissues to hepatocirrhosis, liver hyperplasia, the corresponding adjacent non-tumor, primary hepatocellular carcinoma (HCC) and eventually metastatic foci. Furthermore, low Talin1 expression is significantly associated with tumor recurrence and poor prognosis in HCC patients. More importantly, we provided novel data to show that Talin1 inhibition can act as a positive regulator of EMT, migration and invasion in HCC cells via activation of the ERK1/2 pathway.

NUBPL plays a vital role in CRC migration and invasion by inducing EMT. It might be a novel therapeutic target for CRC.

ErbB receptor proteins and downstream PI3K/AKT and ERK pathways have been reactivated after treatment of Fulvestrant and HSP90 inhibitor AUY922 can reverse these feedback reactivation effect in both ER positive cell lines and fresh tumor samples.

The sensitivity of cells to V-ATPase inhibitors was correlated with low cathepsin D expression. V-ATPase inhibitors are promising therapeutic options for cancers with downregulated cathepsin D.

Combination of the human immunodeficiency virus protease inhibitor ritonavir and the proteasome inhibitor ixazomib kills bladder cancer cells by causing ubiquitinated protein accumulation.

We identified that EML4-ALK as a novel substrate of the protein lysine methyltransferase SMYD2 and this methylation might play a critical role in the phosphorylation of EML4-ALK protein and its oncogenic activity. We also imply that the SMYD2 inhibitor might enhance the growth suppressive effect of ALK inhibitors.

video abstract

Triple negative breast cancer cell line HCC38 composed of epithelial and mesenchymal population at fixed ratio even though mesenchymal cells proliferate significantly slower than epithelial cells. Using this system, we demonstrate that the efficiency of EMT is about a magnitude higher than that of MET and that the two populations significantly enhance the transition of another population to own population. We propose that HCC38 is a suitable model to analyze the EMT-MET dynamics that could affect development of triple negative breast cancer.

We conducted the present single-arm, open-label, multicenter, phase 2 study to evaluate the efficacy and safety of nivolumab in previously untreated Japanese patients with advanced melanoma. Nivolumab administered at a dose of 3 mg/kg once every 2 weeks was tolerable and demonstrated favorable anti-cancer activity. In addition, patients with BRAF wild-type and those with BRAF mutant melanoma both experienced response.

The subgroup analysis of a randomized global phase II study demonstrated the clinical activity of axitinib in treatment-naïve Japanese patients with metastatic renal cell carcinoma, with an acceptable toxicity profile. The estimated 3-year survival (95% confidence interval) was higher among 44 Japanese than 169 non-Japanese patients: 68.2% (54.4–81.9) versus 47.2% (39.3–55.1). The multivariate analysis identified baseline Eastern Cooperative Oncology Group performance status, baseline tumor burden, and time from histopathological diagnosis to treatment as potential predictors of overall survival.

Metformin can exhibit antineoplastic effects on gallbladder cancer cells. Membrane protein Chloride intracellular channel 1(CLIC1) can affect GBC resistance in the presence of metformin.

We built nomograms for CSS/OS and a prognostic score model for risk stratification based on validated socioeconomic factors, such as marital status, median household income and insurance status. Both nomograms had higher efficacies than the 6th edition TNM staging system, and the prognostic score model generated four risk subgroups with separated CSS/OS. Low-risk socioeconomic status and Chinese race/ethnicity confer protective effects on patients with non-matastatic HNSCC.

We identified a germline mutation in MET by the whole-exome sequencing analysis of familial EGFR-mutant lung cancer. The inactivating mutation in MET potentially generates oncogenic stress that induces compensatory EGFR activation for development of EGFR-mutant lung cancer. The identification of MET as the gene associated with familial EGFR-mutant lung cancer will provide valuable insights into the pathogenic mechanisms of not only familial, but also sporadic EGFR-mutant lung cancer by underscoring MET-related signaling molecules.

Many of the DLBCL-type MTX-LPD patients showed spontaneous remission and a better survival rate after methotrexate discontinuation. In contrast, more of the CHL-type MTX-LPD patients did not show spontaneous remission, and required additional chemotherapy. These findings are clinically relevant because the morphological differences in the pathological histology of MTX-LPD might be a prognostic factor after methotrexate discontinuation.