Our study addressed novel mechanisms for overcoming failures of immune checkpoint inhibitor (ICI) therapy for non-small-cell lung cancer (NSCLC) through endogenous regulation of NLRP4 on type I interferon. This is realized mostly through reshaping the tumor microenvironment to a “hot” tumor status, which is beneficial to the treatment of anti-programmed cell death protein-1. Furthermore, we provided new evidence on type I interferon (regulated by NLRP4 in our study) as a potential immune adjuvant to improve the efficacy of NSCLC patients ineffective to ICI treatment.

It is critical to explore additional immunosuppressive mechanisms different from PD-L1/PD1 in UTUC. Our study highlights IDO1 expression on tumor cells as a key regulator of the immunosuppressive microenvironment that resulted in poor prognosis in UTUC. Furthermore, we developed and validated an IDO1-based prognostic classifier with clear immunological relevance and superior prognostic accuracy, so that it could help clinicians make complete and accurate prognostic estimates and ultimately guide treatment.

In this study, we developed a new type of artificial adjuvant vector cell (aAVC-NY-ESO-1) expressing a CD1d-NKT cell ligand complex and a tumor-associated antigen, NY-ESO-1. Although the induction of CTLs by vaccines for NY-ESO-1 is believed to be difficult, we successfully showed the NY-ESO-1-specific CTLs by aAVC-NY-ESO-1 therapy. As a key mechanism, we also determined that the NY-ESO-1 antigen from aAVC-NY-ESO-1 was delivered to the DCs in situ.

C1QBP knockdown renders T cells prone to apoptosis due to less accumulation of the anti–apoptotic proteins, including Bcl-2 and Bcl-XL, thus facilitating caspase-3 activation and PARP cleavage. C1QBP knockdown impairs T cells’ proliferation through dampening of the AKT-mTORC1 signaling pathway. C1QBP deficiency retards T cell tumor infiltration and aggravates tumor infiltrating T cell exhaustion, thereby decreasing their anti–tumor immunity.

Aging-related signature predicts favorable outcome and immunogenicity in lung adenocarcinoma.

FOXA2 plays a pivotal role in directing adenocarcinoma development of human papillomavirus-driven cervical cancer.

Schematic representation of the phenotypic shift from Wnt addiction to Wnt independence of KRAS-mutated tumor cells and hypoxia-promoted metastasis.

The current research data suggest that HIF-1α/CXCR4 may serve as potential therapeutic target for ESCC patients. HIF-1α enhances transcriptional activity of CXCR4 through binding to its promoter hypoxia response element sites.

Activation of RIG-I-like receptor (RLR) signaling in cancer cells is widely recognized as a critical cancer therapy method. New facets of the protumorigenic function of transforming growth factor-β that suppresses both pyroptotic cancer cell death and interferon-β-induced cytostasis are suggested when RLR-mediated cancer treatment is used in triple-negative breast cancer.

Vasculogenic mimicry (VM), a phenomenon in which cancer cells form capillary-like structures without endothelial cells, has been recognized to be a cause of malignant phenotypes in some solid tumors. This report demonstrated the significance of ErbB4-mediated VM formation, and suggested the possibility of ErbB4 mutations as effective targets in breast cancer.

This is the first report to show that DYRK2 overexpression by intravascularly administered adenoviruses produces an antitumor effect on a mouse model of colorectal cancer liver metastasis. Currently, systemic chemotherapy is the only treatment available for unresectable liver metastases from colorectal cancer. This study could open up a novel therapeutic approach.

Squalene synthase (FDFT1) induces accumulation of reactive oxygen species and promotes colon cancer cell proliferation through upregulation of D-pantethine and NAT8. In addition, FDFT1 synergizes squalene epoxidase to facilitate colon adenocarcinoma progression.

The finding that MiR-181a-5p in exosomes from M1-polarized macrophages inhibits STK16 by targeting ETS1 to regulate cell viability and apoptosis in LUAD provides guidance for the treatment of LUAD and deserves attention in the clinical practice of precision medicine.

ACTN4 gene amplification contributed to the decision regarding adjuvant chemotherapy for stage I lung adenocarcinomas. There is not enough of an improvement with adjuvant chemotherapy with tegafur/uracil. Only 33% of patients received postoperative adjuvant chemotherapy in general practice.

This phase 1 study assessed the safety and anti-tumor activity of xentuzumab in 21 Japanese patients with solid tumors. Treatment was generally well tolerated with no significant changes in blood glucose levels and no drug-related grade ≥3 adverse events. Two patients (9.5%) had a partial response and disease control was achieved in a total of 6 patients (28.6%); both patients with partial responses and 2 patients with stable disease had sarcomas.

According to whole-exome sequencing of patients with stage I esophageal squamous cell carcinoma, amplification of FGF19 showed the strongest association with progression-free survival.

This study aimed to optimize the epithelial cell adhesion molecule (EpCAM)-chip and clarify the prognostic impact of circulating tumor cells (CTCs) in lung cancer patients. The EpCAM-chip is a highly sensitive system for detecting CTCs. The EpCAM-chip contributes to the prediction of recurrence and progression and enables genetic analysis of captured CTCs, which could open new diagnostic, therapeutic, and prognostic options for lung cancer patients.

Patients with metastases limited to the supraclavicular lymph nodes had a better survival time compared with patients with a cT4b tumor (without metastases) and patients with distant metastases. Survival of patients with advanced unresectable ESCC in clinical practice was poor, even in patients treated with curative intent.

Designated cancer care hospitals are required to perform 400 surgeries annually in Japan, which is not necessarily defined based on patient outcomes. This study estimated the annual surgical volume thresholds based on the association between annual surgical volume and adjusted 3-year survival probability, and found that the existing surgical volume requirement is higher than our estimated thresholds. The existing requirement is considered optimal to ensure patient survival, and estimating surgical volume thresholds based on the association with patient survival can be used as an evidence-based reference.

In this study, we developed a novel diagnostic method that could classify mCRC cases as highly methylated colorectal cancer (HMCC) or low-methylated colorectal cancer (LMCC) based on the methylation status of 16 CpG sites. We then compared the clinical outcomes of patients in the validation cohort between HMCC and LMCC groups. The primary results of our study are (1) HMCC was associated with a significantly worse response rate, progression-free survival, and overall survival than LMCC for RAS wild-type mCRC; (2) even in the right-sided or left-sided colon, LMCC had a better progression-free survival (PFS) than HMCC; (3) DNA methylation status was an independent predictive factor of anti-EGFR treatment and a more accurate biomarker than the primary tumor site. The novel DNA methylation assay we developed in this study was useful for predicting the clinical outcomes of anti-EGFR treatment regardless of the primary tumor site, suggesting it can be used as a complementary diagnostic in a clinical setting.

Previous genetic analyses of pancreatic cancer mostly used resected tissues, and commercially based NGS for precision medicine requires at least 50 ng of DNA. In this study, endoscopically obtained tissue samples acquired in real clinical practice were used for NGS analysis, and a low number of gene alterations was associated with poor prognosis in localized pancreatic cancer. In addition, NGS could be used in samples containing ≤10 ng of DNA.

In this study, we investigated the 2 types of telomere maintenance mechanisms in a large cohort of MLPS cases and examined the relationship between the telomere maintenance mechanism and disease prognosis or clinicopathological parameters in patients with MLPS. Their findings suggest that TERT aberrations are not prognostic factors, but might occur at an early stage and play key roles in tumorigenesis.