Intrathoracic Needle Migration from the Mediastinum into the Thoracic Cavity.

Intrathoracic needles are rarely used in clinical practice. They can migrate within the body, injure large blood vessels and other organs, and cause severe complications. We report an interesting case of intrathoracic needle removal using video-assisted thoracoscopic surgery. The needle was inserted under the left clavicle, penetrated the mediastinum, and migrated into the right thoracic cavity. Although pneumothorax developed during the disease course, no severe complications were observed. This rare case illustrates the course of needle migration from the mediastinum into the thoracic cavity. Prompt imaging and surgical removal of foreign bodies are necessary in cases of intrathoracic foreign bodies.

[Long-term Survival Giant Cell Carcinoma of the Lung with Chest Wall Invasion by Multidisciplinary Therapy:Report of a Case].

Giant cell carcinoma of the lung is a rare tumor with poor prognosis. A 70-year-old male was referred to our hospital because of chest pain and abnormal shadow on the chest X-ray. He had a lung tumor invading the chest wall. The tumor was surgically removed, and since the diagnosis of giant cell carcinoma with p-N2 was obtained pathologically, adjuvant chemotherapy was performed. However, the local recurrence was found at eight months after surgery and was treated with radiotherapy( total 70 Gy/28 Fr). The patient has been well for over 10 years with no clinically evident recurrence after treatment.

Intrathoracic lipoma in the horizontal fissure of the right lung: a case report.

Lipomas are benign tumors that originate from mesenchymal tissue, such as subcutaneous tissue. Intrathoracic lipomas are rare, and they can occur in the chest wall, mediastinum and bronchi. In the present case, the patient had an intrathoracic lipoma that was located in the horizontal fissure of the right lung. Retrospective review of chest radiographs taken at a previous health checkup confirmed that the tumor was growing. The patient had no symptoms, and computed tomography and magnetic resonance imaging suggested that the tumor was a hamartoma. The tumor was resected by video-assisted thoracic surgery, and was diagnosed by pathological analysis as an intrathoracic lipoma consisting of no atypical fats.

[Thymoma Showing Elevating Anti-acetylcholine Receptor Antibody without Clinical Symptoms of Myasthenia Gravis;Report of a Case].

A 46-year-old man was referred to our hospital with a suspicion of pericardial cyst. Chest computed tomography (CT) revealed an anterior mediastinal tumor. He had no symptoms, but laboratory data showed positive titer to acetylcholine receptor antibody (Anti-AchR Ab). Under a clinical diagnosis of thymoma, extended thymectomy was performed. This case may represent subclinical myasthenia gravis, so we suggest extended thymectomy is crucial for thymoma with elevated level of Anti-AchR Ab without any symptoms.

Nicotine enhances hepatocyte growth factor-mediated lung cancer cell migration by activating the α7 nicotine acetylcholine receptor and phosphoinositide kinase-3-dependent pathway.

Cigarette smoking not only promotes lung carcinogenesis, but it has also been demonstrated to promote the progression of lung cancer. Despite nicotine being a major component of cigarette smoke, it is not carcinogenic when acting alone. Instead, it is believed to function as a tumor promoter. Due to the fatal consequences of lung cancer being primarily associated with the processes of invasion and metastasis, the present study aimed to determine the effect of nicotine on the migratory activity of lung cancer cells. The effect of nicotine on the migration of lung cancer A549 cells was evaluated by a wound healing assay. Hepatocyte growth factor (HGF) was used as a pro-migratory stimulus. During several of the experiments, specific inhibitors of α7-nicotine acetylcholine receptor (α7-nAchR), phosphoinositide kinase-3 (PI3K) and extracellular signal-related kinase (ERK)1/2 were included. The phosphorylation levels of Akt and ERK1/2 were examined using a cell-based protein phosphorylation assay. It was observed that nicotine did not induce cell migration by itself, but that it instead promoted HGF-induced cell migration. The effects of nicotine were inhibited by the pretreatment of the cells with the α7-nAchR inhibitor, methyllycaconitine, and the PI3K inhibitor, LY294002. The mitogen-activated protein kinase/ERK kinase kinase inhibitor exerted modest, but non-significant inhibitory activity on the effect of nicotine. Nicotine did not induce Akt phosphorylation by itself, but instead promoted the HGF-induced phosphorylation of Akt. It was also observed that nicotine had no effect on ERK1/2 phosphorylation. The results from the present study indicate that nicotine, when alone, does not have a pro-migratory function, but instead enhances responsiveness to the pro-migratory stimulus emitted by HGF. The current study provides an insight into the mechanism of tumor promotion by demonstrating that nicotine and α7-nAchRs act in synergy with the HGF-induced PI3K/Akt signaling pathway, increasing the sensitivity of lung cancer cells to HGF, and thereby promoting cell migration, a vital step in invasion and metastasis.

An intrapericardial foregut cyst: report of a thoracoscopically resected case.

Intrapericardial foregut cysts are rare, and are usually found serendipitously. An abnormal shadow was incidentally found on a chest X-ray film of a 45-year-old asymptomatic female undergoing a regular check-up. Computed tomography revealed a smooth-walled, left mediastinal cyst (70 × 46 mm) immediately adjacent to the pericardium and left ventricle. We performed video-assisted thoracic surgery, which suggested that the lesion had macroscopically originated from the epicardium. However, the resected cyst was histologically determined to be an intrapericardial foregut cyst. This experience taught us that, while intrapericardial cysts possess the latent possibility of causing sudden death, cardiac failure, or eventual malignant changes, carefully planned and meticulously executed resection, avoiding damage to adjacent organs or vessels, is recommended.

Coexpression of actin-related protein 2 and Wiskott-Aldrich syndrome family verproline-homologous protein 2 in adenocarcinoma of the lung.

PURPOSE: Highly invasive and metastatic cancer cells, such as adenocarcinoma of the lung cells, form irregular protrusions by assembling a branched network of actin filaments. In mammalian cells, the actin-related protein 2 and 3 (Arp2/3) complex initiates actin assembly to form lamellipodial protrusions by binding to Wiskott-Aldrich syndrome (WASP)/WASP family verproline-homologous protein 2 (WAVE2). In this study, colocalization of Arp2 and WAVE2 in adenocarcinoma of the lung was investigated to elucidate its prognostic value. EXPERIMENTAL DESIGN: Immunohistochemical staining of Arp2 and WAVE2 was done on mirror sections of 115 adenocarcinomas of the lung from pathologic stage IA to IIIA classes. Kaplan-Meier disease-free survival and overall survival curves were analyzed to determine the prognostic significance of the coexpression of Arp2 and WAVE2. RESULTS: Immunoreactivity for both Arp2 and WAVE2 was detected in the same cancer cells in 78 (67.8%) of the 115 lung cancer specimens. The proportion of cancer cells expressing both Arp2 and WAVE2 was significantly higher in cases with lymph-node metastasis (P = 0.0046), and significantly lower in bronchioloalveolar carcinomas (P < 0.0001). The patients whose cancer cells coexpressed them had a shorter disease-free survival time (P < 0.0001) and overall survival time (P < 0.0001). Multivariate Cox regression analysis revealed that coexpression of Arp2 and WAVE2 is an independent risk factor for tumor recurrence. CONCLUSIONS: Coexpression of Arp2 and WAVE2 is correlated with poorer patient outcome, and may be involved in the mechanism of cancer metastasis.

[Non-platinum induction chemotherapy for stage III non-small cell lung cancer].

We conducted combination chemotherapy with gemcitabine (GEM) and paclitaxel (TXL) for stage III non-small cell lung cancer. The chemotherapy schedule consisted of GEM 800 mg/m2 and TXL 70 mg/m2 once a week for 6 consecutive weeks. The patients were 7 males and 3 females with a median age of 66 years. There were 5 adenocarcinomas and 5 squamous cell carcinomas, 7 stage IIIA and 3 IIIB. Eight patients completed 6 cycles of planned administration. Of 9 patients who were evaluable for response, 6 patients achieved PR (66.7%), 2 patients had SD, and 1 patient had PD. The cancers were resectable in 7 out of 9 patients, and were resected completely in 5 patients. Grade 3 anemia and leucopenia were observed in 1 patient and 2 patients, respectively, but they were mild. In our experience, a non-platinum weekly regimen with GEM and TXL is well tolerated and effective, which suggests the possibility of induction chemotherapy and outpatient treatment.