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Situs inversus totalis (SIT) is a relatively rare congenital anomaly, occurring at an incidence of 1 in 10 000-50 000 live births. Although there are some case reports of SIT with the presence of cancer, there are few reports on the relationship between SIT and cancer. However, the recent phylogenetic investigations of this condition suggest that this may be linked to the development and progression of cancer on the molecular level. The key elements are one of the intracellular motor proteins, the KIF3 complex, and the cell-adhesion factors N-cadherin and beta-catenin. We herein present the cases of advanced gastric cancer and lung cancer with SIT, and review the relationship between SIT and the development and progression of cancer.

Minichromosome maintenance (MCM) proteins, essential molecules in the initiation and elongation of DNA replication, have been considered to be good indicators of cell proliferation. We examined the expressions of MCM7 and Ki-67 in lung adenocarcinomas (ACs) with a diameter less than 3cm (pT1), to clarify their pathobiological significance. Immunohistochemistry was conducted to obtain labeling indices (LIs%) for MCM7, MCM2 and Ki-67 in 100 surgically removed pT1 ACs. The LIs were compared with clinicopathological profiles and overall survival rates. The mean LIs of MCM7 and Ki-67 were 20.2+/-15.2% and 13.7+/-11.2%, the value being higher in the former than in the latter (P0.01). MCM7 LIs were significantly correlated with sex, histological grade, histological subtype, tumor size, LIs of Ki-67, MCM2 and P53 (P0.05). LIs of MCM7 and Ki-67 were significantly higher in the 84 non-bronchioloalveolar carcinomas than in the 16 bronchioloalveolar carcinomas (P0.01). Kaplan-Meier survival curves showed that patients with higher MCM7 LIs had poorer prognosis in the 100 pT1 ACs as well as in the 73 stage I ACs. Multivariate Cox regression analysis confirmed that the LIs of MCM7, but not the LIs of MCM2 and Ki-67, was an independent prognostic marker in the 73 stage I ACs. These results suggest that MCM7 is an independent prognostic marker, being more reliable than MCM2 or Ki-67 in human pT1 ACs as well as in human stage I ACs.

Alveolar adenoma (AA) is a rare lung benign tumor originated from type II pneumocytes. It presents as a well-defined nodule in clinical images, but is difficult to differentiate from early-stage lung cancer. We treated a 58-year-old woman with a small-sized AA measuring 8 × 6 mm in the upper lobe of the left lung by performing a thoracoscopic resection. The AA does not cause any symptoms and it is often incidentally detected as an abnormal shadow. There have been no reported cases of recurrence after a resection of AA, but a subsequent increase in such cases is expected, and we believe that it is necessary to understand the characteristics of this typical benign lung tumor.

A 67-year-old male was admitted to our hospital because of pulmonary metastasis from colo-rectal cancer. Chest computed tomography revealed three tumor shadows just under the pleura. Because the tumors were adjacent to each other, we performed an en bloc pulmonary resection. Pathologically, two of the tumors were diagnosed as pulmonary metastases; the remaining tumor, however, was diagnosed as a subpleural intrapulmonary lymph node (IPLN) metastasis. Metastasis to the IPLN is rare, but when the IPLN is located adjacent to a pulmonary metastasis, as observed in this case, it may be possible.

We report a case of pleomorphic carcinoma of the lung that showed a rapid growth. The patient was a 77-year-old female with an abnormality detected in her chest radiograph during a screening examination, but a definite diagnosis could not be obtained based on a needle biopsy guided by CT. After one month, the tumor had continued to grown rapidly and lung cancer was strongly suspected, so the patient underwent surgery. The intraoperative diagnosis demonstrated it to be a pleomorphic carcinoma of the lung in which a squamous element and a sarcomatous element were mixed; and a right lower lobectomy and lymphadenectomy were performed. In a pathological examination after surgery, the tumor was found to be composed of a sarcomatous element that had a high MIB-1 index of 30%, and this was believed to be the cause of the rapid growth.

We herein describe the case of a 20-year-old woman who was diagnosed as having tuberous sclerosis complex (TSC) at the age of 10 years. The patient had a history of right pneumothorax at the age of 19. This time, a right pneumothorax recurrence was detected, and video-assisted thoracoscopic surgery (VATS) was performed. In the intraoperative findings, an infinitesimal lung cyst was detected on the lung lobe, and partial resection was performed. Pathologically, antibody-positive smooth muscle cells of the human melanoma block (HMB)-45 had grown and been diagnosed as pulmonary lymphangioleiomyomatosis (LAM). About half a year later, left pneumothorax occurred, and VATS was performed again. Pathologically, antibody-positive smooth muscle cells of HMB-45 were not detected. Occasionally, TSC is known to cause LAM complications, but in some cases it is difficult to make an accurate pathological diagnosis. Making a pathological diagnosis based on the VATS findings and taking a sufficient amount of tissue specimen are considered useful for making the diagnosis.

We performed thoracoscopic resection of a middle mediastinal noninvasive thymoma in a 69-year-old woman. Chest computed tomography on admission showed a tumor, 75 × 48 × 32 mm in size, and pathological examination revealed a spindle-cell, noninvasive thymoma, of type A according to the World Health Organization classification, and stage I according to the Masaoka staging system. Thymomas are prone to ectopic occurrence, and should be considered in the differential diagnosis of middle mediastinum tumors.

We experienced a case in which a pulmonary arteriovenous fistula was found due to the occurrence of cerebral infarction. The patient was a 65-year-old female who had seen a local doctor for lightheadedness occurring upon rising in the morning. She underwent a cerebral MRI and was diagnosed to have a cerebral infarction. Upon closer examination, a chest radiograph revealed an abnormal shadow and a three-dimensional computed tomography (3D-CT) chest angiography detected a pulmonary arteriovenous fistula 32x30 mm in size with the feeder blood vessel A10 and drainer blood vessel V10 in the left inferior lobe S10, which was considered to be the cause of the cerebral infarction. Video-assisted thoracic surgery (VATS) was conducted for a segmental resection of the basal segment of the left lung. The patient's postoperative progress was good and there was no reoccurrence of the cerebral infarction. The rate of occurrence of cerebral infarction along with pulmonary arteriovenous fistula is considered to be 11.4%; however, cerebral infarction may be an early indicator of pulmonary arteriovenous fistula, and therefore, due attention must be paid.

7557 Background: In 2011, invasive adenocarcinomas were newly classified into the five predominant subtypes by IASLC/ATS/ERS: lepidic, papillary, acinar, micropapillary, and solid. The purpose of this study is to investigate the correlation between EGFRmutation and the histological predominant subtype of lung adenocarcinoma. Methods: Among a total of 1,736 patients with lung adenocarcinoma who underwent surgical resection from 2002 to 2011 in National Cancer Center Hospital East, 1,507 were classified into invasive adenocarcinoma. 526 of whom were examined EGFR mutation status. Histological predominant subtypes were evaluated at the maximum cut surface of tumors. The EGFR mutation analysis was performed by PCR-invader method. Treatment efficacy of EGFR-tyrosine kinase inhibitors (TKIs) in 73 relapsed patients with EGFRmajor mutations were also examined. Results: 526 adenocarcinomas were consisted of 95 lepidic (18%), 221 papillary (42%), 80 acinar (15%), 9 micropapillary (2%), and 121 solid predominant subtype (23%). EGFR mutations were detected in 227 adenocarcinomas (43%), and its frequency in the solid subtype (22%) was significantly less than that of other histological subtypes (lepidic 47%, papillary 53%, and acinar 44%; P < 0.01). The proportion of minor mutations, other than exon 21 L858R and exon 19 deletions, were significantly higher in the solid subtype (22%) than that of the others (lepidic 4%, and papillary 12%; P < 0.01). In 73 patients with EGFR major mutations treated by EGFR-TKIs, the response rate was not different between histological subtypes (lepidic 86%, papillary 76%, acinar 89%, and solid 60%). Conclusions: The correlation between histological predominant subtypes of lung adenocarcinoma and the presence of EGFR mutations or the efficacy of EGFR-TKI were not identified in this study. Little is known about the reason why EGFR minor mutations were highly detected in the solid subtype of adenocarcinoma, however it is possibly due to the high frequency of heavy smokers in solid subtype (heavy smoker: solid 67% vs. others 27-44%).