Ameloblastoma is an odontogenic tumor of the jaw. It most frequently occurs in the mandible, and less often in the maxilla. Mandibular ameloblastoma harbors a BRAF mutation that causes a valine (V) to glutamic acid (E) substitution at codon 600 (BRAF V600E ). We examined specimens from 32 Japanese patients to detect the prevalence of the BRAF V600E mutation, and to evaluate the relationship between immunohistochemical (IHC) expression and genetic results, of BRAF V600E+ ameloblastoma. Among the 32 cases, 22 (69%) were IHC positive for BRAF V600E protein, and 10 (31%) were IHC negative; and polymerase chain reaction showed 16 of 21 tested cases (76%) carried the BRAF V600E mutation. Our findings indicate that that samples that stain IHC positive for BRAF V600E protein are more likely to carry the BRAF V600E mutation. These results support assessments for BRAF mutations, and the use of BRAF inhibitors as targeted therapy for ameloblastoma in Japanese patients. K E Y W O R D Sameloblastoma, BRAF-V600E mutation, immunohistochemistry, Japanese patients, odontogenic tumor

Background S‐1 is an oral anticancer agent containing tegafur, a prodrug of 5‐fluorouracil (5‐FU). Preoperative S‐1 chemotherapy is performed to prevent tumor proliferation before surgery in oral squamous cell carcinoma (OSCC). The aim of this study was to evaluate the effects of preoperative S‐1 chemotherapy on tumor budding. Methods We examined 248 cases of OSCC and evaluated the budding scores in biopsy and resected specimens by keratin immunohistochemistry. Results In S‐1‐untreated patients, the budding scores in resected specimens tended to show a mild increase. S‐1 treatment had the effect of lowering the budding score, although some cases with dramatically increased budding scores in resected specimens were found in the early phase of administration. Relapse‐free survival showed a significant difference (P < .01) according to the presence or absence of S‐1 treatment among patients with high budding scores. Conclusions The present findings indicate that S‐1 administration may be more effective in patients with high budding scores than in those with lower budding scores.

BackgroundIt has been reported in oral squamous cell carcinoma (OSCC) that myeloid‐derived suppressor cells infiltrate tumor tissues. This study examined whether S‐1 chemotherapy changes immune cell populations in the tumor microenvironment.MethodsWe examined 71 patients with of OSCC, including 51 patients who received preoperative S‐1 chemotherapy. Immunohistochemistry for PD‐L1, CD8, forkhead box protein 3 (FOXP3), and CD15 was performed using biopsy and resected specimens.ResultsThe numbers of CD8+, FOXP3+, and CD15+ cells in resected specimens were significantly decreased by S‐1 chemotherapy. The reduction of the proportion of CD15+ cells significantly differed between responders and nonresponders. Most responders were distributed into the group with low PD‐L1 expression and a low density of CD8+ cells before chemotherapy. Furthermore, many patients with recurrence exhibited a high density of CD15+ cells in biopsy specimens.ConclusionPreoperative S‐1 chemotherapy can potentially improve prognosis by reducing CD15+ cells in the tumor microenvironment.

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Introduction: Secretory carcinoma (SC) is a malignancy of the salivary glands, which is similar to SC of the breast regarding its association with neurotrophic tyrosine receptor kinase fusion-positive gene. SC is a recently described salivary gland tumor, and there are a few reports describing oral minor salivary gland-derived SC. We reported two cases of SC in the oral cavity and reviewed the literature. Patient concerns: The patients included a 65-year-old Japanese woman who presented with a mass of the upper lip and an 84-year-old Japanese man who presented with a mass on the buccal mucosa. Diagnosis: Diagnosis was based on histomorphological and immunohistochemical findings and identification of a specific translocation of the ETS variant 6-neurotrophic receptor tyrosine kinase 3 gene fusion. Case 1 was finally diagnosed using reverse transcription-polymerase chain reaction with formalin-fixed paraffin-embedded tissue samples, while case 2 was diagnosed using fluorescence in situ hybridization analysis. Interventions and outcomes: In case 1, excisional biopsy was done and there was no recurrence observed in five-year follow-up. In case 2, tumor resection was done and there was no recurrence observed in two-year follow-up. Conclusion: It is highly likely for many cases of SC to be initially diagnosed as acinic cell carcinoma (AciCC) owing to their similar histological findings. The treatment strategy for minor salivary gland-originated SC is similar to that of AciCC; however, SC is often highly malignant and involves a high risk of cervical lymph node metastasis. Thus, establishing an accurate diagnosis together with pathologists and confirming the presence of the ETS variant 6-neurotrophic receptor tyrosine kinase 3 fusion gene using genetic analysis is important.