Publications by authors named "Ryoichi Kawabe"

Salivary duct carcinoma (SDC) is a distinctive and aggressive neoplasm. The most frequent site of origin is the parotid gland, followed by the submandibular gland. SDC originating in the minor salivary glands, particularly in the ectopic glands within the mandible, is extremely rare.

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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.

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The desmoplastic ameloblastoma is a histological variant of ameloblastoma. The neoplastic epithelial islands seen in desmoplastic ameloblastoma are small and ameloblastic cells are rare. Basal cell ameloblastoma is also a rare variant of ameloblastoma, in which the tumor is composed of more primitive cells and has even fewer features of peripheral palisading.

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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.

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Background: In oral lichen planus (OLP), destruction of the basal cell layer, which is one of the characteristic histological features, is seen and many changes in cell proliferation, cell repair and cell death occur in the injured mucosal epithelium.

Methods: We studied mucosal tissues from 19 patients of OLP and 10 controls, with immunohistochemistry for Ki-67, p53, cyclin dependent kinase inhibitors (CDKI) and cyclins. Mitotic count was calculated.

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