Although mesiodentes are not caused by malocclusion, they may cause it. A long period of impaction of mesiodentes may bring about dentigerous cyst formation or movement of the mesiodentes.

The ATP-binding cassette transporter G1 (ABCG1) is a cholesterol lipid efflux pump whose role in tumor growth has been largely unknown. Our transcriptomics revealed that ABCG1 was powerfully expressed in rapidly metastatic, aggregative colon cancer cells, in all the ABC transporter family members. Coincidently, genetic amplification of ABCG1 is found in 10–35% of clinical samples of metastatic cancer cases. Expression of ABCG1 was further elevated in three-dimensional tumoroids (tumor organoids) within stemness-enhancing tumor milieu, whereas depletion of ABCG1 lowered cellular aggregation and tumoroid growth in vitro as well as hypoxia-inducible factor 1α in cancer cells around the central necrotic areas in tumors in vivo. Notably, depletion of ABCG1 triggered the intracellular accumulation of extracellular vesicles (EVs) and regression of tumoroids. Collectively, these data suggest that ABCG1 plays a crucial role in tumorigenesis in metastatic cancer and that depletion of ABCG1 triggers tumor regression with the accumulation of EVs and their derivatives and cargos, implicating a novel ABCG1-targeting therapeutic strategy by which redundant and toxic substances may be accumulated in tumors leading to their regression.

No abstract

Genetic amplification, overexpression, and increased signaling from the epidermal growth factor receptor (EGFR) are often found in oral squamous cell carcinoma (OSCC) and thus EGFR is frequently targeted molecularly by the therapeutic antibody cetuximab. We assessed effects of cetuximab in control of EGF-driven malignant traits of OSCC cells. EGF stimulation promoted progression level of mesenchymal traits in OSCC cells, which were attenuated by cetuximab but incompletely. We pursued a potential mechanism underlying such incomplete attenuation of OSCC malignant traits. Cetuximab promoted secretion of EGFR-EVs by OSCC cells and failed to inhibit EGF-driven secretion of EGFR-EVs. Cetuximab was also found to be robustly secreted with the EGFR-EVs by the OSCC cells. Thus, EGF promotes the level of mesenchymal traits of OSCC cells and secretion of EGFR-EVs, which involve cetuximab resistance.

To evaluate the diagnostic value of dynamic contrast-enhanced MRI (DCE-MRI) in salivary gland tumors, thirty-five patients (47 lesions) who underwent MR examinations and were histopathologically diagnosed with salivary gland tumors in Okayama University Hospital, between April 1998 and March 2005, were entered in the present study. The parameters included CI(max300) or CI(max600), which was the contrast index (CI) at maximal contrast enhancement upon 300 s or 600 s, and Tmax, which was the time that corresponded to the CI(max300). Washout ratio (WR(300) or WR(600)) was defined as follows: CI(max300)-CI(300s)/CI(max300) or CI(max600)-CI(600s)/CI(max600)x100 (%), where CI(300) or CI(600) was the CI at 300s or 600s after contrast medium administration. We obtained the following results from the analysis of DCE-MRI parameters; (a) The salivary gland tumors were categorized into three CI curve types according to Tmax and WR300; Pleomorphic adenoma; Tmax > 210 s and WR300 < 10%, Warthin tumor; Tmax < 60 s and WR300 > 40%, and malignant tumor; 60s < Tmax < 210 s and 10% < WR300 < 30%; (b) On the basis of the relationship between Tmax and CImax or WR, all pleomorphic adenomas were successfully differentiated from Warthin tumor lesions. Of the 20 pleomorphic adenomas, 18 (90.0%) were successfully differentiated from malignant tumors. All Warthin tumor lesions were successfully differentiated from pleomorphic adenomas and malignant tumors. Of 12 the malignant tumors, 11 (91.7%) were successfully differentiated from pleomorphic adenomas. All malignant tumors were successfully differentiated from Warthin tumors. Thus, DCE-MRI parameters are useful in diagnosing salivary gland tumors on the basis of the combined assessment of Tmax and CImax or WR.