BACKGROUND Tumor budding is a readily detectable histopathological feature and has been recognized as an adverse prognostic factor in several human cancers. However, the prognostic value of tumor budding in tongue squamous cell carcinoma (TSCC) has not been reported. The purpose of this study is to assess the correlation of tumor budding with the clinicopathologic features, and the known molecular biomarkers (E-cadherin and Vimentin), as well as to evaluate its prognostic significance for TSCC. METHODS Archival clinical samples of 230 patients with TSCC were examined for tumor budding. Immunohistochemistry analyses were performed to examine the expression of E-cadherin and Vimentin. Statistical analyses were carried out to assess the correlation of tumor budding with clinicopathologic parameters and patient survival. The potential association between tumor budding and alterations of E-cadherin and Vimentin expression was also assessed. RESULTS Of the 230 TSCC cases examined, tumor budding was observed in 165 cases (71.7%), with a mean tumor bud count of 7.5 (range from 1 to 48 buds). High-intensity budding (≥ 5 tumor buds) was observed in 111 cases (48.3%). Statistical analysis revealed that tumor budding was associated with tumor size (P<0.05), differentiation (P<0.05), clinical stage (P<0.05), lymph node metastasis (P<0.01), and correlated with reduced overall survival. In addition, significant associations were observed among tumor budding and the deregulation of E-cadherin (P<0.001) and Vimentin (P<0.001). CONCLUSIONS Tumor budding, which associates with epithelial-mesenchymal transition, is a frequent event and appears to be an independent prognostic factor in TSCC.
Tumor budding is a frequent event in tongue squamous cell carcinoma. It independently predicted prognosis of patients with T1/2 stage tongue squamous cell carcinoma and may be used for routing pathological diagnosis and the decision of elective lymph node dissection.
Recent studies have revealed that angiotensin II (Ang II) interacts with two pharmacologically different types of seven-transmembrane domain receptors, hence named Ang II type 1 and type 2 (AT, and AT 2 ) receptors. cDNAs for the AT, receptor have been cloned, and the existence of two receptor subtypes, AT, A and AT 1B , has been revealed in rat and mouse. This study presents a new approach for the specific quantification of AT, A and AT, B receptor mRNAs by reverse transcription and polymerase chain reaction amplification in the presence of an AT, receptor mutant cRNA as internal standard. Absolute quantities of mRNA are then determined by extrapolation using the standard curve generated with the internal standard. Moreover, addition of this internal standard to each tube controls for both reverse transcription and polymerase chain reaction amplification in each sample. In male Wistar rats, the highest absolute AT, A receptor mRNA levels were found in liver and kidney and those for AT 1B receptor mRNA in the pituitary. Expressed as a percentage of total AT, A +AT, B A ngiotensin II (Ang II) is a biologically active peptide of the renin-angiotensin system that produces vasoconstriction, aldosterone secretion, catecholamine release, thirst, and prolactin and corticotropin secretions as well as stimulates hypertrophy of vascular smooth muscle cells. © 1994 American Heart Association, Inc.receptor mRNA content, AT, A receptor mRNA content was 100% in liver, 85% in lung, 73% in kidney, 65% in aorta, 48% in adrenals, and 15% in the hypophysis. Since this approach can determine absolute AT, A and AT, B receptor mRNA quantities in different organs, it allows the study of the regulation of their expression under different pathophysiological conditions. After sodium depletion, known to induce hyperactivity of the reninangiotensin system, adrenal AT, A and AT 1B receptor mRNA levels were increased by 60% and 110%, respectively. In contrast, in renovascular hypertension (two-kidney, one clip), also associated with elevated circulating plasma renin activity, adrenal AT 1B receptor mRNA levels decreased by 50%, whereas there was no change in those of AT, A . Therefore, the differential distribution and regulation of these two receptor subtypes suggest that each of them might be involved in the mediation of different biological effects of Ang II. (Hypertension. 1994^4:538-548.)
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