Yiping Han

Over-expression of deubiquitinating enzyme USP14 in lung adenocarcinoma promotes proliferation through the accumulation of β-catenin.

The deubiquitinating enzyme USP14 has been identified and biochemically studied, but its role in lung cancer remains to be elucidated. The aim of this study was to evaluate the prognostic significance of USP14 in patients with lung adenocarcinoma and to define its role in lung cancer cell proliferation. USP14 mRNA levels in different non-small cell lung cancer (NSCLC) cell lines were detected by real-time qPCR. USP14 protein levels in surgically resected samples from NSCLC patients, and in NSCLC cell lines, were detected by immunohistochemistry or Western blot. The correlation of USP14 expression with clinical characteristics and prognosis was determined by survival analysis. After silencing USP14, cell proliferation was assessed by MTT assay and the cell cycle was measured by FACS assay. It was found that USP14 expression was upregulated in NSCLC cells, especially in adenocarcinoma cells. Over-expression of USP14 was associated with shorter overall survival of patients. Downregulation of USP14 expression arrested the cell cycle, which may be related to β-catenin degradation. Over-expression of USP14 was associated with poor prognosis in NSCLC patients and promoted tumor cell proliferation, which suggests that USP14 is a tumor-promoting factor and a promising therapeutic target for NSCLC.

Malignant Pleural Effusion Supernatants Are Substitutes for Metastatic Pleural Tumor Tissues in EGFR Mutation Test in Patients with Advanced Lung Adenocarcinoma

Background Though the possibility of using malignant pleural effusions (MPEs) as alternatives for metastatic pleural tumor tissues (MPTTs) in epidermal growth factor receptor (EGFR) mutation test has been examined, due to the lack of studies comparing the results in matching MPEs and MPTTs, the clinical value of MPEs for advanced adenocarcinoma patients with pleural effusions is not confirmed. Methods EGFR mutation statuses in matching MPTTs, MPE supernatants and cell blocks, of 41 patients with advanced lung adenocarcinoma as diagnosed by thoracoscopy were analyzed using amplification refractory mutation system (ARMS). Results EGFR mutations were detected in 46.3% (19/41) of MPTTs, 43.9% (18/41) of MPE supernatants and 56.3% (18/32) of MPE cell blocks by ARMS analysis. Generally, the same EGFR statuses were identified in both MPTTs and matching MPE cell blocks of 81.3% patients (26/32), whereas MPTTs and matching MPE supernatants of 87.8% (36/41) patients shared the same EGFR status. Compared with EGFR mutation detection in MPTTs, the sensitivity of EGFR mutation detection in MPE-cell blocks was 87.5% (14/16), specificity was 75.0% (12/16), while the sensitivity of EGFR mutation detection in MPE-supernatants was 84.2% (16/19), specificity was 90.9% (20/22). Conclusions The high concordance of EGFR mutation statuses between MPEs and MPTTs in lung adenocarcinoma patients with pleural metastasis as determined by ARMS analysis suggests that MPEs, particularly MPE supernatants, may be substitutes for MPTTs in EGFR mutation test.

Inhalation of TGF-β1 antibody: a new method to inhibit the airway stenosis induced by the endobronchial tuberculosis.

Tuberculous tracheobronchial stenosis is a serious clinical problem because it can cause obstructive pneumonia, dyspnea on exertion even pulmonary atelectasis of the whole lung. More than 90% of the patients with EBTB have some degree of bronchial stenosis. The interventional therapy through bronchoscopy has been used as standard treatment to deal with the scar stenosis of EBTB routinely, which have showed significant effects to keep airway open. However the scar rapid growing and restenosis can often be seen in many patients. TGF-beta1 has been demonstrated to play a very important role in scar formation. Some agents against TGF-beta1 have been proved to inhibit the scar growing effectively. The level of TGF-beta elevated in the BALF of EBTB patients suggests TGF-beta be related to the pathogenesis of stenosis induced by EBTB. We hypothesize that inhalation of TGF-beta1 antibody can neutralize the local TGF-beta and reduce the level of this kind of cytokine so as to prevent the scar formation partially, and find a new pathway to deal with this tough clinical problem.

A case of diffuse pulmonary lymphangiomatosis with unilateral lung invasion

Diffuse pulmonary lymphangiomatosis (DPL) is a rare interstitial lung disease characterized by intrathoracic lymphatic system abnormalities often with involvement of both lungs. Here, we report a 24-year-old male patient with DPL initially located in one lung, presenting only with transient fever. Resection of the right middle and lower lobes was performed for diagnosis and complete removal of the lesions. The pathologic features shown by diffuse smooth thickening of the interlobular septa, bronchovascular bundles, infiltration of patchy ground glass opacities and specific immunohistologic D2-40 and CD34 positive staining confirmed the diagnosis of DPL. The patient did not show signs of relapse during the 2-year follow-up period, which suggests that surgery is an effective and reasonable method for treating DPL with relatively localized lesions.

A case report of tongue metastasis from lung squamous cell carcinoma and literature review

Rationale: Tongue metastasis from lung cancer is extremely rare, and the prognosis of these patients is rather poor. Patient concers: A 56-year-old man was found a 4-cm cavity lesion in the left upper lobe, which was initially misdiagnosed as tuberculosis. Diagnoses: A case of lung squamous cell carcinoma that metastasized to the base of a patients tongue. Intervations: We send the biopsy of the lung and the tongue lesions for gene sequencing. Outcomes: He received systemic chemotherapy, but continued to have pain at the base of his tongue and died 7 months later. Lessons: From sequencing data, mutations in KRAS proto-oncogene, GTPase (KRAS), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), and tumor protein p53 (TP53) were found in the tumor biopsy of the patient. All of these were indicators of poor prognosis.