Multiple cancers frequently occur in the upper aerodigestive tract. The high incidence rate of multiple carcinomas in this region is often explained in terms of involvement of the same underlying risk factors. It has been reported that the oral bacterium Streptococcus anginosus (S. anginosus) is associated with esophageal, gastric, and pharyngeal cancer tissues. In this study, a highly specific quantification method for S. anginosus DNA using real-time PCR was established. We employed this assay to determine whether S. anginosus is also associated with oral cancer tissues. This precise quantification method revealed different degrees of infection with S. anginosus in esophageal cancer and oral cancer. We assayed 10 ng of genomic DNA from cancer tissues, and found that eight of 18 samples (44%) from the esophagus contained a detectable level ( > > > >10 fg) of S. anginosus DNA, whereas this was the case for only five of 38 samples (13%) of oral cancer. The quantity of S. anginosus DNA in the esophageal cancer tissues was significantly higher than in oral cancer. The maximum amount of S. anginosus DNA was approximately ten times higher in esophageal than in oral cancer tissues. In addition, none of the five different oral cancer sites (floor of the mouth, mandibular gingival, maxillary gingival, buccal mucosal, and tongue) showed significant signs of S. anginosus infection. On the other hand, most non-cancerous tissues of the esophagus and tongue showed an undetectable level of S. anginosus. These results suggest that S. anginosus is associated with esophageal cancer, but is not closely related with oral cancer. (Cancer Sci 2003; 94: 492-496) acterial and viral infections are important factors in cancer development.1) It has been reported that Helicobacter pylori (H. pylori) is associated with gastritis, gastric atrophy, and gastric cancer.2-4) The presence of microorganisms in several kinds of human cancers was recently investigated, and Streptococcus anginosus (S. anginosus) DNA fragments were frequently found in DNA samples from esophageal cancer tissues, gastric cancer tissues, and dysplasia of the esophagus.5, 6) Viable S. anginosus was also recovered from esophageal cancer tissues (unpublished data). These results suggest that S. anginosus infection occurs at an early stage of esophageal cancer and is related to esophageal and gastric carcinogenesis. S. anginosus is classified as an oral bacterium and can be isolated from several parts of the body such as the oral cavity, gastrointestinal tract, and genitourinary tract. It is often associated with pyogenic infections, including endocarditis. 7-9) S. anginosus DNA has also been found in head and neck squamous cell carcinomas 10) ; it was found much less frequently in non-cancerous tissues of the esophagus and was absent from the colon, lung, bladder, renal, and cervical cancer tissues. 6) Therefore, it was suggested that S. anginosus DNA is associated with cancers in the upper digestive tract, although the involvement of S. anginosus infection in the carc...

These complex changes, which concomitantly occur in the injured mucosal epithelium, could contribute to the development and maintenance of characteristic mucosal epithelial architectures seen in OLP.

Ito T, Kawabe R, Kurasono Y, Hara M, Kitamura H, Fujita K, Kanisawa M: Expression of heat shock proteins in squamous cell carcinoma of the tongue: an immunohistochemical study. J Oral Pathol Med 1998; 27: 18–22. © Munksgaard, 1998. Twenty‐four specimens of squamous cell carcinoma of the tongue were immuno‐stained for heat shock proteins (HSPs) to reveal differences in stainability among normal epithelium, dysplasia and carcinoma and to clarify the prognostic significance of HSPs in comparison with survival period, clinical stage, lymph node metastasis, histological grade, and p53 immunostaining. Normal epithelium was positively stained in the suprabasal layer for HSP60 and HSP70, but was negative for HSP27 and HSP90. Dysplastic lesions were positive for HSP27, HSP70 and HSP90, but stained variously for HSP60. In squamous cell carcinoma, the cytoplasm of suprabasal tumor cells was often positive for HSP27 and HSP90 (18/24, 17/24, respectively). Although HSP immunohistochemistry has revealed changes in HSP expression during tumorigenesis of squamous epithelium of the tongue, there was no correlation between HSP staining and survival period, stage, lymph node metastasis, histological grade or p53 immunostaining.

In the present study the significance of nuclear/cytoplasmic expression of beta-catenin (CTNNB1) and mutation of the CTNNB1 gene (CTNNB1) in odontogenic tumors was examined. Six ameloblastomas (five follicular ameloblastomas and one plexiform ameloblastoma) and three malignant odontogenic tumors (one metastasizing ameloblastoma, one ameloblastic carcinoma, and one primary intraosseous odontogenic carcinoma) were investigated for CTNNB1 expression and CTNNB1 mutation. Immunohistochemically, all follicular ameloblastomas and one primary intraosseous odontogenic carcinoma exhibited focal and moderate nuclear/cytoplasmic expression of CTNNB1, whereas the plexiform ameloblastoma and the remaining two malignant odontogenic tumors had entirely membranous expression. CTNNB1 mutation at codon 40 of exon 3 was found in one of the six follicular ameloblastomas. The other five follicular ameloblastomas, the plexiform ameloblastoma, and the three malignant odontogenic tumors did not show mutation in exon 3 of CTNNB1. These findings further confirmed that CTNNB1 mutation is not frequent in ameloblastoma and malignant odontogenic tumors, although the abnormality of Wnt signaling may be associated with some of these tumors.

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