Biomedical subjects

Kaoru Kusama

Publications and source records attributed to Kaoru Kusama.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Vascular endothelial growth factor and dendritic cells in human squamous cell carcinoma of the oral cavity.

Dendritic cells (DCs) play an important role in the host immune defense against tumors, and there is an inverse correlation between DC density and the expression of vascular endothelial growth factor (VEGF). However, the relationship between VEGF expression in tumors and infiltration of CD1a+ or CD83+ DCs, which express the VEGF receptor (VEGFR), remains unclear. Therefore, in vivo and in vitro studies were conducted to investigate the relationship between VEGF expression and DC subsets in oral squamous cell carcinomas (OSCCs). Strong VEGF expression was detected in cancer tissues from patients with regional lymph node metastasis (PN+ cases). In these tissues, the VEGF expression correlated inversely with the number of CD1a + DCs, but positively with the number of CD83+ DCs. Large amounts of VEGF were secreted by OSCCs cell lines, and their culture supernatants significantly inhibited the production of differentiated CD1a+ DCs from peripheral blood mononuclear cells (PBMCs), whereas differentiated CD83+ DCs were increased. VEGFR-1 and -2 were detected in a few PBMCs and CD1a+ DCs. Furthermore, CD1a mRNA disappeared when recombinant human VEGF165 (rhVEGF165) was added to CD1a+ DCs, while CD83 mRNA increased. These results suggest that, in OSCCs, secreted VEGF might promote escape from tumor immunity by inhibiting the differentiation of CD1a + DCs from progenitor cells and increasing the levels of dysfunctional CD83+ DCs.

Adult↗

PubMedDate not supplied

Expression of CYLD, NF-kappaB and NF-kappaB-related factors in salivary gland tumors.

The cylindromatosis (CYLD) gene was originally identified as a tumor suppressor that is mutated in familial cylindromatosis, an autosomal dominant condition that confers a predisposition to multiple tumors of the skin appendages. CYLD has deubiquitinating enzyme activity and inhibits the activation of transcription factor NF-kappaB. Therefore, loss of CYLD function correlates with tumorigenesis. Expression of CYLD has been detected in various organs, but its expression in salivary gland tumor (SGT) is still unknown. Adenoid cystic carcinoma (ACC) is a well known and typical malignant SGT ACC was previously known as cylindroma in view of its marked histological resemblance to dermal cylindroma. In this study, the expressions of CYLD and NF-kappaB mRNA in HSG, a human SGT cell line, were found to be increased by TNF-alpha stimulation. Immunohistochemistry clearly demonstrated the expression of CYLD and NF-kappaB-related factors in ACC tissue.

Carcinoma, Adenoid Cystic↗

PubMedDate not supplied

Concentration-dependent effect of Rikko-san on the prostaglandin E2 production by mouse macrophage-like cells.

Rikko-san (RKS) and its ingredients were investigated for their activity to stimulate prostaglandin E2 (PGE2) production by unstimulated and lipopolysaccharide (LPS)-stimulated mouse macrophage-like Raw 264.7 cells. LPS significantly stimulated the production and extracellular secretion of PGE2 by Raw 264.7 cells. RKS dose-dependently modified the LPS-stimulated PGE2 production. A lower concentration (0.04-0.4 mg/ml) of RKS stimulated PGE2 production without or with LPS, whereas a higher concentration (4 mg/ml) of RKS inhibited the LPS-stimulated PGE2 production, suggesting the presence of both stimulator(s) and inhibitor(s) for PGE2 production. The inhibitory effect of a higher concentration of RKS was slightly neutralized by supplementation of exogenous arachidonic acid. Among five RKS ingredients, Kanzo inhibited the LPS-stimulated PGE2 production to the greatest extent, whereas other ingredients (Shoma, Ryutan, Saishin, Bofu) stimulated PGE2 production. Western blot analysis demonstrated that RKS and all its ingredients enhanced the intracellular concentration of cyclooxygenase-2, whereas RKS did not significantly affect the phospholipase A2 protein level. The present study demonstrates that the concentration-dependent effect of RKS on the PGE2 production by macrophage cannot be explained only by the expression levels of cyclooxygenase-2 or phospholipase A2.

Animals↗