We report distinct characteristics of TCR repertoires in lung adenocarcinomas with and without EGFR mutations.

In the current study, we describe a strategy entailing particulate antigen-encapsulating PEG-modified large sized liposomes as an antigen protein delivery device. In the nanoparticle delivery approach, the function of encapsulated particulate antigen-capturing dendritic cells in vivo would be a key to demonstrate an efficient antitumor response.

Treatment with NLF-sup and GOTO-sup induces the secretion of IL-6 and IL-10 by monocytes and generates tolerogenic DCs. Tolerogenic DCs secrete little IL-12 and TNF-α after maturation stimuli and have a decreased ability to activate iNKT cells. Furthermore, NLF-sup-treated DCs elevate CD40 expression and increase IL-12 production by addition of IFN-γ, and the interactions between iNKT cells and αGalCer-pulsed DCs have the potential to recover the immunosuppression of tolerogenic DCs.

We established the murine pancreatic ductal adenocarcinoma (PDAC) models to understand the host immune responses of PDAC affected by chemotherapy. In PDAC murine models, GEM treatment was associated with an immune response consistent with an anti-cancer effect. Furthermore, depletion of myeloid-lineage cells played an important role in enhancing anti-cancer immunity associated with GEM treatment.

Our study elucidated a novel pathway in lnc-DANCR-mediated miR-665 targeting transforming growth factor beta receptor 1 (TGFBR1) on growth and metastasis, which suggests new therapeutic targets, including the ERK/SMAD signaling pathway, in the prevention and treatment of cervical cancer.

The platform readily achieved efficient conditional genome editing with minimal leak both in vitro and in vivo. We succeeded to model Wilms’ tumor and the progression of intestinal adenomas with multiple mutations including an activating mutation with a large genomic deletion. The platform should make complicated disease modeling in the mouse easily attainable, extending the range of in vivo experiments.

In the present study, we analyzed the association and clinical significance of wt-p53 and LDHA expression in breast cancer with wt-p53 expression and explored the mechanism of p53 regulation of LDHA at the transcription level. Furthermore, we carried out rescue experiments to identify the functional role and molecular mechanism of wt-p53 and LDHA in breast cancer in vitro and in vivo. In summary, our findings show that p53 can directly regulate the expression of LDHA at the transcriptional level to control aerobic glycolysis, cell growth and invasion in breast cancer.

Bazedoxifene exerted significant inhibitory effects on STAT3 phosphorylation, nuclear translocation and expression of STAT3-mediated downstream genes in human liver cancer cell lines. Bazedoxifene also showed significant anti-tumor activity in nude mice implanted with HEPG2 cells.

We confirmed that REV7 confers radioresistance in ESCC cells and tumor xenograft models. REV7-PRDX2 binding functions pronouncedly in radioresistance of ESCC, bridging DNA repair and the anti–oxidation process.

A schematic model depicting the molecular mechanism of MIR22HG in hepatocellular carcinoma.

Leucine-rich alpha-2 glycoprotein enforced transforming growth factor-inducing epithelial-mesenchymal transition.

PIK3CD is significantly overexpressed in colorectal cancer (CRC) and can induce CRC cell growth and invasion. PIK3CD exerts its functions through activating AKT/GSK-3β/β-catenin signaling. PIK3CD might be a novel independent prognostic biomarker and a potential therapeutic target for CRC.

In the phase 1b KEYNOTE-025 study, pembrolizumab was generally well tolerated and showed promising antitumor activity in Japanese patients with previously treated PD-L1–expressing NSCLC. Outcomes were consistent with those from the phase 3 KEYNOTE-010 study.

This phase I study showed that alpelisib, an α-specific PI3K inhibitor, as a single agent showed a favorable safety profile and encouraging preliminary efficacy in Japanese patients with advanced solid tumors.

Of the 60 evaluable patients, 5 had partial response and none had complete response, resulting in an ORR of 8.3% (95% CI: 1.3%-15.3%). In addition, 43 (71.7%) had stable disease, for an overall DCR of 80.0% (95% CI: 69.9%-90.1%).

We found that knockout of MCM9 or knockdown of MCM8 selectively hypersensitized transformed cells to cisplatin and olaparib, suggesting that conceptual MCM8-9 inhibitors will be powerful cancer-specific chemosensitizers for platinum compounds and poly(ADP-ribose) polymerase inhibitors.

Nitric oxide level was significantly higher in HBV-related HCC. The source of NO at least partially attributed to the expression of iNOS and eNOS, but not nNOS in liver tissue. By disrupting Beclin 1/hVps34 association and increasing Bcl-2/Beclin 1 interaction, NO regulates autophagy and apoptotic cell death during HCC.

Fluzoparib, a novel and potent PARP inhibitor undergoing phase II clinical trials, displays favorable pharmacokinetic properties and superior in vivo antitumor activity compared with olaparib. For the first time, we discover that fluzoparib in combination with apatinib and paclitaxel elicits significantly improved antitumor responses without extra toxicity. Based on this finding, a phase I study has been initiated.

Our paper provides an investigation on the cause-specific mortality among the residents in a unique urban area where asbestos-related factories were concentrated in Japan. The excess mortality due to mesothelioma suggests the impact of occupational asbestos exposure in men and nonoccupational asbestos exposure in women in the cohort.

Estrogen-mediated E2F6 competing endogenous network epigenetically and competitively inhibits microRNA-193a activity, promoting ovarian cancer stemness and tumorigenesis.

In this study, we revealed that the extent of promoter methylation was different depending on the arrangement of genes using DNA methylation data of 119 colorectal cancer specimens. Divergent promoters were hypomethylated compared to unidirectional promoters. The provide data is essential for the understanding of the carcinogenic mechanism.

The lack of relevant molecular biomarkers for the early recurrence of serous ovarian cancers is linked to the poor prognosis of this disease. This study identified ZNF671 as a prognostic and predictive biomarker for the early recurrence of serous ovarian cancer.

TNFA and the TNF receptor modulator SPATA2 are high in ovarian cancer supporting the inflammatory character of this disease. High SPATA2, which was markedly induced by inflammatory stimuli in vitro, independently reflected poor clinical outcome of ovarian cancer patients.