Inhibitory effect of vitamin D-binding protein-derived macrophage activating factor on DMBA-induced hamster cheek pouch carcinogenesis and its derived carcinoma cell line.

This study investigated the inhibitory effect of vitamin D-binding protein-derived macrophage-activating factor (GcMAF) on carcinogenesis and tumor growth, using a 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced hamster cheek pouch carcinogenesis model, as well as the cytocidal effect of activated macrophages against HCPC-1, a cell line established from DMBA-induced cheek pouch carcinoma. DMBA application induced squamous cell carcinoma in all 15 hamsters of the control group at approximately 10 weeks, and all 15 hamsters died of tumor burden within 20 weeks. By contrast, 2 out of the 14 hamsters with GcMAF administration did not develop tumors and the remaining 12 hamsters showed a significant delay of tumor development for approximately 3.5 weeks. The growth of tumors formed was significantly suppressed and none of the hamsters died within the 20 weeks during which they were observed. When GcMAF administration was stopped at the 13th week of the experiment in 4 out of the 14 hamsters in the GcMAF-treated group, tumor growth was promoted, but none of the mice died within the 20-week period. On the other hand, when GcMAF administration was commenced after the 13th week in 5 out of the 15 hamsters in the control group, tumor growth was slightly suppressed and all 15 hamsters died of tumor burden. However, the mean survival time was significantly extended. GcMAF treatment activated peritoneal macrophages in vitro and in vivo, and these activated macrophages exhibited a marked cytocidal effect on HCPC-1 cells. Furthermore, the cytocidal effect of activated macrophages was enhanced by the addition of tumor-bearing hamster serum. These findings indicated that GcMAF possesses an inhibitory effect on tumor development and growth in a DMBA-induced hamster cheek pouch carcinogenesis model.

Migration of a foreign body (staple) from the oral floor to the submandibular space: case report.

We report a case of foreign bodies, staples, accidentally put in the oral cavity. One of the staples had migrated from the oral floor through the submandibular space and penetrated the submandibular gland. The staple was removed successfully using CT scan and fluoroscope imaging.

Inhibitory effect of sulindac on DMBA-induced hamster cheek pouch carcinogenesis and its derived cell line.

In order to investigate the involvement of cyclooxygenase (COX)-2 in oral carcinogenesis and chemoprevention for it, we examined the COX-2 expression during dimethylbenzanthracene (DMBA)-induced hamster cheek pouch carcinogenesis and the inhibitory effect of sulindac, a non-steroidal anti-inflammatory drug (NSAID), on the carcinogenesis and its derived squamous carcinoma cell line HCPC-1. From the beginning of DMBA application, basal diet or diets containing sulindac 200 or 400 ppm were given to hamsters, and observation of tumor development and measurement of body weight were performed. Immunohistochemical analysis revealed that COX-2 expression was increased toward carcinogenesis from epithelial dysplasia to squamous cell carcinoma (SCC). All hamsters developed SCC, but the onset of carcinoma formation was significantly delayed up to 14.8 and 11.8 weeks in the 200 ppm, and 400 ppm sulindac group, respectively, as compared to 8.7 weeks in the control group. In addition, tumor growth was retarded in the group of sulindac treatment, and mean survival time was 23.7 weeks in the control group and 36.3 and 33.8 weeks in the 200 and 400 ppm sulindac group, respectively. Body weight loss was not observed during the experimental period. Histologically, administration of sulindac inhibited angiogenesis in the tumor stroma. Treatment with sulindac sulfide, an active metabolite of sulindac, caused inhibition of cell growth, PGE2 production and VEGF production in HCPC-1 cells in vitro. Expression of COX-2 protein in HCPC-1 cells was also decreased 2-fold by treatment with sulindac sulfide. It was thus indicated that inhibitory effects were partly due to inhibition of tumor angiogenesis by sulindac. These findings suggested the involvement of COX-2 in DMBA-induced hamster cheek pouch carcinogenesis and the chemopreventive potential of sulindac.

Keratotic basal cell carcinoma of the tongue: case report.

Basal cell carcinoma (BCC) is the most common skin cancer. Its occurrence in the oral mucosa is extremely rare. We report the clinical course of BCC arising in the inferior surface of the tongue. We performed a super selective intra-arterial chemotherapy combined with radiotherapy for this case. Local tumor response showed CR, and no recurrence was seen after the treatment.

Relations among expression of CXCR4, histological patterns, and metastatic potential in adenoid cystic carcinoma of the head and neck.

Adenoid cystic carcinoma (ACC) may acquire a chemokine-mediated mechanism during the process of metastasis. To investigate the involvement of chemokines in metastasis from ACC, expression of CXCR4 in surgical specimens of ACC and two tumor lines transplantable to nude mice was examined immunohistochemically. In addition, the expression levels of CXCR4 protein and mRNA were examined by Western blotting and reverse-transcription polymerase chain reaction. Our results showed that patients whose tumors expressed high levels of CXCR4 had metastases to the regional lymph nodes and the lung, resulting in poor outcomes. ACCs showing a solid or cribriform pattern with distant metastasis were strongly positive for CXCR4, while those showing a tubular or cribriform pattern without metastasis were weakly positive for CXCR4. In the in vivo model, ACCY tumor showed increasing expression levels of CXCR4 with tumor growth, and the histological pattern changed from cribriform to solid. The histological pattern of ACCI, associated with spontaneous metastasis to the neck, changed from cribriform to undifferentiated carcinoma and was highly metastatic to the lung. This tumor showed high levels of CXCR4 protein and mRNA. These results suggest that CXCR4 expression, histological patterns, and metastatic potential are closely related in ACC.