BackgroundVideo-assisted thoracic surgery (VATS) lobectomy is a standard treatment for lung cancer. This study retrospectively compared long-term outcomes after VATS lobectomy versus lobectomy via open thoracotomy for clinical stage IA non-small cell lung cancer (NSCLC).MethodsFrom July 2002 to June 2012, 160 patients were diagnosed with clinical stage IA NSCLC and underwent lobectomy. Of these, 114 underwent VATS lobectomy and 46 underwent lobectomy via open thoracotomy.ResultsThe 5-year disease-free survival (DFS) rate was 88.0% in the VATS group and 77.1% in the thoracotomy group for clinical stage IA NSCLC (p = 0.1504), and 91.5% in the VATS group and 93.8% in the thoracotomy group for pathological stage IA NSCLC (p = 0.2662). The 5-year overall survival (OS) rate was 94.1% in the VATS group and 81.8% in the thoracotomy group for clinical stage IA NSCLC (p = 0.0268), and 94.8% in the VATS group and 96.2% in the thoracotomy group for pathological stage IA NSCLC (p = 0.5545). The rate of accurate preoperative staging was 71.9% in the VATS group and 56.5% in the thoracotomy group (p = 0.2611). Inconsistencies between the clinical and pathological stages were mainly related to tumor size, nodal status, and pleural invasion. Local recurrence occurred for one lesion in the VATS group and six lesions (five patients) in the thoracotomy group (p = 0.0495).ConclusionsThe DFS and OS were not inferior after VATS compared with thoracotomy. Local control was significantly better after VATS than after thoracotomy. Preoperative staging lacked sufficient accuracy.
Decay-accelerating factor (DAF) is one of the complement regulatory proteins. Two isoforms of DAF have been identified in humans. In this study, we isolated novel cDNAs encoding five isoforms of DAF from the human lung, which were generated by insertion of new exonic sequences. RT-PCR revealed that all isoforms were expressed in almost all tissues tested, although the expression patterns and levels differed among the tissues. Transfection of isoform vDAF1, 2, and 3 cDNAs into CHO cells showed that these molecules are soluble forms secreted after glycosylation. Isoform vDAF4 and vDAF5 cDNAs included a part of and the entire intron 7 sequence, respectively, and the transfection of vDAF4 cDNA produced a large, glycosylated, membrane-bound form. These results suggest that more than seven isoforms of human DAF are involved in the regulation of complement activation under physiological conditions through their specific structures and localization.
Secretoglobin (SCGB) 3A2 is a downstream target gene for the thyroid transcription factor-1 (TITF1). SCGB3A2 plays a role as an anti-inflammatory agent, however, its role in primary pulmonary carcinomas has not been examined. We assessed immunohistochemical expression of SCGB3A2 in primary pulmonary carcinomas and evaluated the correlation between the expression and histopathological phenotypes and prognosis. One hundred and fifty-six primary lung cancers undergone for surgical resection were examined. The percentages of SCGB3A2 positive cells were scored and tumors had immunoreactivity in more than 10% of tumor cells were considered positive for SCGB3A2. Overall reactivity for SCGB3A2 was observed in 116 (74.4%) of 156 primary lung cancers. SCGB3A2 was predominantly expressed in adenocarcinomas (86.5%), compared with squamous cell carcinomas (50.0%) and small cell carcinomas (42.9%). The expression in papillary adenocarcinomas was seen at higher frequency than that in tubular adenocarcinomas. There was no significant relationship between SCGB3A2 expression and tumor differentiation, and pathological stage. Positive expression of SCGB3A2 was not associated with better survival rate. SCGB3A2 expression in primary pulmonary carcinomas is high, especially in adenocarcinomas. Our results indicate that SCGB3A2 has a potential to be a specific and useful marker for primary pulmonary adenocarcinomas.
KeywordsSecretoglobin 3A2 (SCGB3A2); UGRP1 (Uteroglobin-related protein 1); Pulmonary carcinoma; Immunohistochemistry; TITF-1 (thyroid transcription factor-1)
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