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Background This study aimed to examine the association between overtime work and the frequency of preventive dental visits among workers in Japan. Methods A self-administered questionnaire was completed by 14,847 daytime-workers. We used a logistic regression model stratified by sex and age and adjusted for marital status, occupation, education, and oral status to investigate the association between overtime work hours and the frequency of preventive dental visits. Results In total 1037 men (9.3%) and 511 women (13.9%) attended quarterly preventive dental visits, and 2672 men (23.9%) and 1165 women (31.8%) attended annual preventive dental visits. Overtime work was statistically significantly associated with quarterly preventive dental visits among men aged 50–59 years, with adjusted odds ratios (aOR) and 95% confidence intervals (CI) of 0.73 (0.56–0.95), 0.75 (0.54–1.04), and 0.55 (0.34–0.90) for Conclusions Our study revealed associations between overtime and preventive dental visits among male workers aged in their 40s and 50s.

Aurora kinase B (AURKB) inhibitors are regarded as potential molecular-targeting drugs for cancer therapy. The present study evaluated the cytotoxic effect of a combination of AZD1152-hQPA, an AURKB inhibitor, and various anticancer agents on the HeLa human cervical cancer cell line, as well as its cisplatin-resistant equivalent HCP4 cell line. It was demonstrated that AZD1152-hQPA had an antagonistic effect on the cytotoxicity of cisplatin, etoposide and doxorubicin, but had a synergistic effect on that of all-trans-retinoic acid (ATRA), Am80 and TAC-101, when tested on HeLa cells. Cisplatin, etoposide and doxorubicin were shown to increase the cellular expression of AURKB, while ATRA, Am80 and TAC-101 downregulated its expression. These results suggested that AURKB expression is regulated by these anticancer agents at the transcriptional level, and that the level of expression of AURKB may influence the cytotoxic effect of AZD1152-hQPA. Therefore, when using anticancer agents, decreasing the expression of AURKB using a molecular-targeting drug may be an optimal therapeutic strategy.

The polypeptide N-acetylgalactosaminyltransferase (GalNAc-Ts) family of enzymes regulates the critical initial steps of mucin-type O-glycosylation. Among GalNAc-Ts that may significantly influence cancer biology, thus affecting cell differentiation, adhesion, invasion, and/or metastasis, GalNAc-T3 exhibits a high expression in several human cancers, closely associated with tumor progression and a poor prognosis. However, the expression pattern of GalNAc-T3 in oral squamous cell carcinoma (OSCC) remains obscure. Since postoperative recurrence of even early stage OSCC (ESOSCC) occurs at an early phase, significantly affecting their clinical course and worse outcome, the identification of clinically significant accurate biomarkers is needed. Therefore, we investigated the correlation between the immunohistochemical GalNAc-T3 expression and various clinicopathological characteristics and recurrence using 110 paraffin-embedded tumor samples obtained from patients with surgically resected ESOSCC (T1–2N0). Recurrence was recognized in 37 of 110 (33.6 %) patients. The GalNAc-T3 expression was considered to be strongly positive when 20 % or more of the cancer cells showed positive cytoplasmic staining. Consequently, a strong expression of GalNAc-T3 was observed in 40 patients (36.4 %), showing a close relationship to poor differentiation, the presence of lymphatic and vascular invasion, and recurrence. Univariate and multivariate analyses further demonstrated that the patients with a strong GalNAc-T3+ status had markedly lower disease-free survival (DFS) rates, especially within the first 2 years postoperatively. Therefore, GalNAc-T3 might play a role in the pathogenesis of ESOSCC recurrence, and its immunohistochemical detection potentially predicts a shorter DFS and may be a useful parameter for providing clinical management against ESOSCC in the early postoperative phase. Electronic supplementary material The online version of this article (doi:10.1007/s13277-015-3928-7) contains supplementary material, which is available to authorized users.

Mitochondria are important cellular organelles that function as control centers of the energy supply for highly proliferative cancer cells and regulate apoptosis after cancer chemotherapy. Cisplatin is one of the most important chemotherapeutic agents and a key drug in therapeutic regimens for a broad range of solid tumors. Cisplatin may directly interact with mitochondria, which can induce apoptosis. The direct interactions between cisplatin and mitochondria may account for our understanding of the clinical activity of cisplatin and development of resistance. However, the basis for the roles of mitochondria under treatment with chemotherapy is poorly understood. In this review, we present novel aspects regarding the unique characteristics of the mitochondrial genome in relation to the use of platinum-based chemotherapy and describe our recent work demonstrating the importance of the mitochondrial transcription factor A (mtTFA) expression in cancer cells.

The objectives of this study were to evaluate the effect of insulin-like growth factor I (IGF-I) on the fractional synthesis rate (FSR) of muscle and whole body protein breakdown rate (WPBR) during methionine-free total parenteral nutrition (MTPN). We also determined whether the inhibition of endogenous methionine availability reduced tumor protein synthesis. AH109A hepatoma cells were inoculated onto the backs of Donryu rats on day 0. On day 10, the rats were catheterized for TPN and assigned to one of four groups: 1) standard TPN (STPN), 2) STPN + IGF-I, 3) MTPN, or 4) MTPN + IGF-I. The addition of IGF-I to MTPN reduced the loss of body weight by both increasing muscle FSR and reducing WPBR. The tumor FSR did not differ between MTPN + IGF-I and MTPN. The methionine extraction ratio from the liver was negative with MTPN + IGF-I but positive in the other groups. We concluded that IGF-I blockage of endogenous methionine release from peripheral protein sites was associated with a shift to liver-derived methionine, with no change in tumor growth in MTPN-treated rats.

We have studied the expression of vascular endothelial growth factor (VEGF) in esophageal cancer using immunohistochemistry. A total of 101 specimens of esophageal cancer tissue were fixed by formalin, embedded in paraffin wax, and examined in 3μm sections by avidin-biotin peroxidase complex method. VEGF was noted in the cytoplasm of normal esophageal glandular cells, monocyte-macrophages, squamous carcinoma cells and of the vascular endothelial cells themselves. VEGF expression by monocyte-macrophages was observed in all cases, in contrast the incidence of VEGF expression in the tumor cells was relatively low at 26.7% of all specimens. However, in the cases where the tumor cells were positive for VEGF, it was discovered that the main source of the VEGF production was the tumor cells themselves. In the cases with proper mucosal invasion the incidence of VEGF expression by the tumor cells was quite low at 7.6%. However, when the tumor invaded the submucosal layer the expression increased to 33.3%. There was also a significant correlation in those with the submucosal invasion between the expression of VEGF in the tumor cells and the density of microvessels at the tumor invasive edge. These results suggest that VEGF may play an important role in tumor progression and in the angiogenesis via auto-crine and para-crine mechanisms in esophageal cancer.

We experienced a case of rectal schwannoma which was diagnosed before surgery. In this paper we have described this rare case and have discussed a number of similar cases reported in the literature.

It has increased that we encounter reports concerning a malignant lymphoma which appeared in the chest wall several decades after tuberculous empyemathorax or tuberculous pleuritis. A 54-year-old male, with asymptomatic chronic empyema thorax was admitted to the hospital because of pain from a huge chest tumor. The chest CT and MRI studies revealed that the tumor of the chest wall invaded the ribs, and it seems to arise from the chest wall which adjoined to the peel of the parietal pleura with severe carcifications of the empyemathorax. Biopsy of the tumor revealed a non-epitherial malignant tumor but correct diagnosis of a malignant lymphoma could not be attained. The tumor of the chest wall was widely resected and a radical surgery was also performed for chronic empyemathorax. The resected specimens were pathologically diagnosed as non-Hodgikin's malignant lymphoma which was of B cell lymphocyte origin, diffuse type and medium sized cell type by LSG classification. Two courses of chemotherapy with ACOP were administered after the surgery. There has been no sign of local recurrences and metastasis up to now. We discussed and reviewed this unusual cases which have been previously published in the Japanese literature.

A 55-year-old postmenopausal female presented with genital bleeding and lower abdominal mass. An abdominal MRI revealed a heterogeneously enhanced, 15 × 10 cm mass, completely filling the lumen of the enlarged uterus. The cytologic analysis of the mass showed tumor cells in small clusters and as individual cells showing hyperchromatic round to oval nuclei, and pleomorphic and occasionally unipolar "tadpole"-shaped cytoplasm, in a background of severe necrosis and many degenerated squamous cells. We first interpreted it merely as atypical cells, possibly originated from sarcoma. A total abdominal hysterectomy and salpingo-oophorectomy were performed, and gross examination showed an exophytic polypoid mass with a whitish to white-grayish, necrotic appearance, protruding from the endometrial mucosa. Microscopically, the tumor was composed of a diffuse proliferation of highly atypical spindle-shaped cells, admixed with many characteristic rhabdomyoblasts having abundant densely eosinophilic cytoplasm with sometimes distinct cross-striations, coexisted with cellular primitive small blue round to oval cells foci. However, neither carcinoma nor additional heterologous sarcoma components were completely seen within our thorough investigation. Therefore, we finally made a diagnosis of embryonal rhabdomyosarcoma arising from the uterine corpus. We should be aware that owing to its characteristic features, cytopathologists might be able to determine a genuine diagnosis, based on multiple and adequate cytology samplings.