The frequency of circulating CD15⁺ MDSC in patients with head and neck squamous cell carcinoma correlated with peripheral T cells, but not iNKT cells, and associated with the prognosis. T cell activation was suppressed by CD15⁺ MDSC. However, iNKT cell activation upon α-galactosylceramide stimulation was not affected, suggesting that iNKT cells are more resistant to hydrogen peroxide than T cells.

The combination of intratumoral nanobubble injection and ultrasound (US) exposure caused extensive tissue necrosis.

Intranodal pressures in metastasized lymph nodes.

We investigated the feasibility of combination therapy using iNKT cells and an anti-GD2 antibody. Not only cytokines produced by activated iNKT cells, but also NK-NKT cell contact or NK cell-dendritic cell contact contributed to the increase in NK cell cytotoxicity and further IFNγ production by iNKT cells and NK cells. iNKT cell-based immunotherapy could be an appropriate candidate for anti-GD2 antibody therapy for neuroblastoma.

KLF4/HMGB1 interaction may mediated osteosarcoma chemotherapy resistance, targeting KLF4/HMGB1 may be a therapeutic strategy for osteosarcoma chemotherapy.

Carcinogenic multi-wall carbon nanotubes selectively adsorb hemoglobin and transferrin, which increase catalytic Fe(II) leading to DNA damage, upon exposure to mesothelial cells.

In this study, we demonstrated miR-127-5p, one of the miRNAs indirectly targeting NF-κB pathway, suppressed NF-κB activity and the transcription of downstream targets of NF-κB signaling pathway through inhibiting p65 nuclear translocation.This newly found miR-127-5p/BLVRB axis provides another link between miRNA, inflammation and cancer.

The downregulation of RAP80 activating EMT through reciprocal regulators, ZEB1 and miR200c, promoting pulmonary metastasis of cancer cells. Of consistent note, the level of RAP80 was found to negatively correlate with survival rate in lung adenocarcinoma and breast cancer patients. These findings indicate that RAP80 is a critical gatekeeper to impede metastasis of cancer as well as to secure DNA integrity.

SDPR suppresses cell proliferation and invasion in breast cancer cells. SDPR depletion induces epithelial-mesenchymal transition by activation of TGF-β signaling.

Our findings proved the first time that CSC population in luminal BC induces ectopic expression of FOXA1. The precise analysis of the function of FOXA1 would provide new data to establish a novel strategy to treat luminal BC and its late recurrence.

We examined the role of Wnt5a-Ror2 signaling in bone marrow-derived mesenchymal stem cells (MSCs) in regulating proliferation of undifferentiated gastric cancer cell line, MKN45 cells. Our findings show that Wnt5a-Ror2 signaling enhances expression of CXCL16 in MSCs and as a result enhanced secretion of CXCL16 from MSCs might act on CXCR6 expressed on MKN45, leading to the promotion of its proliferation.

Association of decreased cystatin C expression with p53 mutation.

This novel CTC system performed superior sensitivity in CTC detection compared with CellSearch in various cancer patients. EGFR and PIK3CA mutation are detected from captured CTC in lung and breast cancer patients, respectively.

A combination of amrubicin plus cisplatin following chemoradiotherapy for limited-disease small-cell lung cancer was well-tolerated, although a large number of patients required G-CSF support. Survival data were promising with the median progression-free survival of 41.9 months and 5-year overall survival rate of 57.8%. This regimen is under investigation in a randomized phase II trial (JCOG1011).

We investigated genome-wide DNA methylation status of 28 tumor and 13 normal lung tissues, and gene expression profiling of 25 SCLC tissues. Clustering of SCLC led to the important identification of a CpG island methylator phenotype (CIMP) of the tumor with a significantly poorer prognosis (P = 0.002). Multivariate analyses revealed that postoperative chemotherapy and the non-CIMP were significantly good prognostic factors.

Cancer specificity of the diagnostic index using the combination of miR-1246, miR-1307-3p, miR-4634, miR-6861-5p, and miR-6875-5p in the test cohort.

We studied anti-TF antibody, clone 1859, which had no effect on blood coagulation and prepared anti-TF antibody (clone1859)-conjugated epirubicin-incorporating micelles (NC-6300). In addition, to determine the optimum size of the antibody fragment to conjugate with NC-6300, three forms of the 1859 antibody (whole IgG, F[ab’]₂, and Fab’) were conjugated to NC-6300. All three different forms of anti-TF1859-NC-6300 as follows: (i) anti-TF1859-IgG-; (ii) anti-TF1859-F(ab’)₂-; and (iii) anti-TF1859-Fab’-NC-6300 significantly suppressed tumor growth when compared to NC-6300 in the xenograft model of TF-high-expressing human pancreatic cancer cell lines, BxPC3.

Effective anticancer agents and treatment protocols are necessary to improve outcomes in patients of peritoneal dissemination. We used the luciferase assay to evaluate peritoneal micrometastasis and established an accurate mouse model to evaluate tumorigenesis and drug efficacy. This model has advantages over previous models, and is useful to validate peritoneal micrometastasis formation and to evaluate drug efficacy without sacrificing mice.

In this study, to assess the transporter-mediated mechanisms in FAMT uptake by tumors, we have synthesized [14C]FAMT for in vitro transport assay and revealed that FAMT is very specific to cancer type amino-acid transporter LAT1 and not transported by any other amino acid transporters. This explains cancer-specific accumulation of [18F]FAMT in PET.

Circulating tumor DNA (ctDNA) is an emerging field of cancer research. For lung cancer, noninvasive genotyping of EGFR is the foremost application. We examined the dynamics of ctDNA represented by activating and resistant mutations using deep sequencing with a massively parallel DNA sequencer.

The I-branching N-acetylglucosaminyltransferase (GCNT2) is a glycosyltransferase that converts linear i-antigens to I-branching glycans. In the present study, we demonstrated that GCNT2 expression correlates with malignant potential of prostate cancer (PCa). GCNT2-expressing PCa formed I-branching glycan on cell surface glycolipids, and GCNT2-low PCa cells exhibited decreased invasion potential and α5β1 integrin-mediated protein kinase B phosphorylation, suggesting that GCNT2 plays important roles in PCa invasiveness.