Oral cavity cancer incidence rates in Osaka, Japan between 2000 and 2014.

BACKGROUND: We investigated trends in oral cavity cancer incidence from 2000 to 2014 in Osaka, Japan. METHODS: Using Osaka Cancer Registry (OCR) data, oral cavity cancer incidence number and age-standardized incidence rates were calculated according to three 5-year-time-periods: 2000-2004, 2005-2009 and 2010-2014. We calculated the distribution of clinical stage for each 5-year period and the proportion of oral cavity cancer among all cancers. RESULTS: A total of 6,086 oral cavity cancers were registered in OCR in 2000-2014. Across the period, between 55.6% and 65.0% were 65 years+ and approximately 60% were men. Tongue cancer accounted for 30.4% to 43.8% of the registrations, while gum accounted for 30.7% to 34.7%. 36.3% to 37.3% were regional, while 1.8% to 2.8% were distant. The age-standardized incidence rate of oral cavity cancer increased from 2.1/100,000 in 2000 to 3.8/100,000 in 2014, although the proportion of oral cavity cancer among all cancers only increased slightly from 0.71% in 2000 to 0.92% in 2014. Proportion of localized stage cancer was 60.8%-67.5% for tongue and 31.0%-49.5% for gum or floor of mouth. Proportion of distant stage cancer was 0.3%-1.0% for tongue and 2.5%-4.2% for gum or floor of mouth. CONCLUSIONS: Age-standardized incidence rate of oral cavity cancer increased, but was not higher than other countries. The proportion of localized stage tongue cancer was higher, while that of distant stage cancer was lower than other sites. Tongue cancer might be easier to detect in its earlier stages than other sites.

Preventable Sternocleidomastoid Muscular Atrophy after Neck Dissection.

BACKGROUND: Modified radical neck dissection (mRND) [preserving the sternocleidomastoid muscle (SCM) and the spinal accessory nerve] and supraomohyoid neck dissection have become common surgical procedures for treating head and neck cancer. Postoperative severe asymmetry of the neck and severe atrophy of the SCM, however, have been demonstrated. METHODS: Using computed tomographic images, cross-sectional areas of the SCMs were measured in 99 patients with carcinoma of the oral cavity who underwent unilateral mRND or supraomohyoid neck dissection. An asymmetry index was used. RESULTS: Innervation to the SCM was preserved in 91 patients. The spinal accessory nerve and the innervation were sacrificed in 3 patients; the innervation was repaired in 5 patients. Sacrifice of innervation to the SCM resulted in extremely severe asymmetry. Repair of the innervation prevented severe asymmetry in 40%. Preservation of the innervation prevented severe asymmetry in 75% at the middle portion of the neck and in 56% at the lower portion after mRND. CONCLUSION: Preserving innervation to the SCM and gentle handling of the nerve during neck dissection could prevent severe asymmetry after neck dissection.

Differential expression of aquaporin 5 and aquaporin 3 in squamous cell carcinoma and adenoid cystic carcinoma.

Aquaporins (AQPs) are a membrane protein family involved in the selective transport of water across cell membranes. Recent studies have reported the expression of AQP5 in several tumor types such as gastric, pulmonary, ovarian, pancreatic and colorectal cancer. We have previously reported the expression on tumor cells and the important role of AQP3 on cell growth in tongue cancer. However, little is known about the expression and precise role of AQP5 on squamous cell carcinoma (SCC) of the tongue. We investigated the expression of AQP5 and AQP3 in human oral SCC and adenoid cystic carcinoma (ACC). Overexpression of both AQP5 and AQP3 were immunohistochemically observed on tumor cells in SCC, whereas ACC cells were faintly stained with those antibodies against AQPs. Treatment with pan-AQP inhibitor or specific AQP5-siRNA showed inhibition of cell growth in SCC cell lines via the inhibition of integrins and the mitogen-activated protein kinase pathway. AQPs play important roles in cell growth in SCC rather than ACC.

Role of endothelin receptor signalling in squamous cell carcinoma.

Endothelin plays important roles in various physiological functions including vascular constriction. Recent studies reported that the endothelin receptors ETA and ETB are highly expressed in lung and skin tumor tissues. In contrast, there are few reports on endothelin signalling in the proliferation of head and neck cancer. We found that both ETA and ETB endothelin receptors were overexpressed in tumor cells of tongue cancer samples by immunohistochemistry. ETA and ETB were expressed in cultured lingual and esophageal squamous cell carcinoma (SCCs) cell lines. When both cultured cell lines were treated with an ETA selective antagonist (BQ123) or an ETB selective antagonist (BQ788), inhibition of cell growth was observed. Similar results were observed when SCCs were treated with specific siRNA for the suppression of ETA or ETB. Furthermore, inhibition of the mitogen-activated protein (MAP) kinase pathway by the treatments with ET receptor antagonists and siRNA was also observed. These results indicate that endothelin signalling may, in part, play important roles in cell growth in SCCs through the MAP kinase pathway.

Critical role of aquaporin 3 on growth of human esophageal and oral squamous cell carcinoma.

Aquaporins (AQP) play important roles in water and glycerol transport. We examined whether AQP3 is expressed in primary squamous cell carcinoma (SCC) such as esophageal and oral cancer and lymph node metastasis, and whether AQP3 is a potential target for tumor therapy. A high level expression of AQP3 was observed in tumor areas of human primary SCC such as esophageal and lingual cancers, and lymph node metastasis, but was not observed in normal areas. Treatment with pan-AQP inhibitor caused apoptotic cell death on the SCC cell lines in a concentration-dependent manner. Small interfering RNA (siRNA) specific for AQP3 also inhibited cell adhesion and growth of SCC, but not those of adenocarcinoma cell lines and fibroblasts. Expression of integrin α5 and ß1, counter adhesion molecules for fibronectin, was inhibited by treatment with AQP3-siRNA. The phosphorylation of focal adhesion kinase (FAK) was decreased by treatment with AQP3-siRNA, which then caused decreases in phosphorylation of Erk and MAPK. These results indicate that the decreases in integrins and the inhibition of cell adhesion might cause inhibition of the FAK signaling pathways. Combination of AQP3-siRNA with cisplatin, a major anti-cancer drug, strongly inhibited the growth of SCC. Cell death caused by the inhibition of AQP3 was a result of direct interference with cell adhesion involving intracellular FAK-MAPK signaling pathways. These results imply a potentially important and novel role for the inhibition of AQP3 function via the use of specific siRNA in the treatment of SCC.