The tracheal tumors were eccentric, well-defined, polypoid masses in all cases. The endobronchial tumors were masses confined within the bronchus in all cases, and atelectasis or pneumonia of the distal parenchyma was frequently associated. Of the six hamartomas, one was a fatty mass, and two were nodules with calcification. The others were soft-tissue-density nodules. The lipomas manifested as fat density on CT scans in both cases. The other benign tumors were low-attenuating, soft-tissue-density masses without characteristic findings on CT scans.

Transforming acidic coiled-coil containing protein 3 (TACC3) is known to be involved in the control of normal cell growth and differentiation and in mechanisms of unregulated growth leading to tumorigenesis. The aim of the present paper was to determine the rate of TACC3 expression in a non-small cell lung cancer (NSCLC) collection and to clarify its correlation with clinicopathological parameters. A total of 163 NSCLC were analyzed immunohistochemically using a polyclonal TACC3 antibody and monoclonal p53 and Ki-67 antibodies on NSCLC tissue microarrays. A high level of TACC3 expression was observed in 14.8% of cases, preferentially squamous cell carcinomas. Patients whose tumors had a high TACC3 expression had a significantly shorter median survival time. In the Cox regression-based multivariate analysis, TACC3 expression proved to be an independent prognostic parameter (P = 0.031). TACC3 expression was correlated with p53 expression, and patient whose tumors highly expressed TACC3 and p53 had a significantly poorer prognosis than patients whose tumors had low-level expression for both immunostainings (P = 0.006). It is suggested that increase in TACC3 may impart a proliferative advantage to NSCLC and contribute to tumor progression, and that TACC3 expression is a strong prognostic indicator of clinical outcome in NSCLC.

Transforming growth factor-β (TGF-β) promotes tumor invasion and metastasis by inducing epithelialmesenchymal transition (EMT). EMT is often related with acquisition of stemness characteristics. The objective of this study was to determine whether EMT and stemness characteristics induced by TGF-β might be associated with epigenetic regulation in lung cancer. A human normal lung epithelial cell line and four lung cancer cell lines were treated with TGF-β. Transcriptome analysis of BEAS-2B and A549 cells incubated with TGF-β were analyzed through next-generation sequencing (NGS). Western blotting was carried out to investigate expression levels of epithelial and mesenchymal markers. Wound healing and Matrigel invasion assay, sphere formation assay, and in vivo mice tumor model were performed to evaluate functional characteristics of EMT and stemness acquisition. To investigate whether activation of EMT and stem cell markers might be involved in epigenetic regulation of lung cancer, experiment using a DNA methyltransferase inhibitor (5-azacytidine, AZA), methylationspecific PCR (MSP) and bisulfite sequencing were performed. NGS revealed changes in expression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, vimentin, slug and snail) and stem cell markers (CD44 and CD87) in both BEAS-2B and A549 cells. Functional analysis revealed increased migration, invasion, sphere formation, and tumor development in mice after TGF-β treatment. Expression of slug and CD87 genes was activated following treatment with AZA and TGF-β. MSP and bisulfite sequencing indicated DNA demethylation of slug and CD87 genes. These results suggest that TGF-β induced EMT and cancer stemness acquisition could be associated with activation of slug and CD87 gene by their promoter demethylation. Although improvements have been made in cancer treatment, lung cancer remains the leading cause of cancer death worldwide. The poor prognosis is due to its diagnosis at advanced stage of the disease 1,2. Failure in treatment is related with cancer recurrence and metastasis. It has been reported that both epithelial-mesenchymal transition (EMT) and acquisition of cancer stemness play important roles in the invasion, metastasis, and chemoresistance of solid tumors 3,4. Transforming growth factor-beta (TGF-β) regulates invasion and metastasis through loss of epithelial markers and gain of mesenchymal markers. TGF-β induced EMT is a major feature of EMT invasiveness and metastasis

In lung adenocarcinoma diagnosed as clinical N0 by chest computed tomography and positron emission tomography scanning, the possibility of occult lymph node metastasis increases with SUVmax greater than 5 and when lymphatic invasion, vascular invasion, and a micropapillary component are present.

Emphysematous gastritis is a rare form of phlegmonous gastritis, characterized by air in the wall of the stomach due to invasion by gas-forming microorganisms. The most commonly involved microorganisms are streptococci, Escherichia coli, Pseudomonas aeruginosa, Clostrodium perfrigens and Staphylococcus aureus. Gastrointestinal mucormycosis is another rare condition, which is most frequently occurs in the stomach. Because emphysematous gastritis associated with invasive gastric mucormycosis is an extremely rare clinical condition and both are life-threatening diseases, early precise diagnosis and early treatment should be done to avoid mortality. Herein we present an extremely rare case of emphysematous gastritis associated with invasive gastric mucormycosis. A 43-yr-old man, suffering from alcoholism and diabetes, has experienced diffuse abdominal pain for 4 days. Abdominal computed tomography scan demonstrated gas within the stomach wall. A histologic examination of the total gastrectomy specimen showed several gas-filled bubbles in the wall, along with numerous fungal hyphae throughout the necrotic stomach wall. He died of multiorgan failure secondary to disseminated mucormycosis, despite the intensive medical therapy.

Mounting evidence suggests that the alterations of Akt/protein kinase B (PKB) play an important role in tumorigenesis. Phosphorylated Akt regulates many of the key effector molecules involved in apoptosis, angiogenesis, and cell cycle progression during tumorigenesis. The expression of phosphorylated Akt has been described in some human malignancies, but not in primary human lung cancer. In this study, to understand the role of Akt in lung tumorigenesis we analyzed the expression of phosphorylated Akt in 43 non-small cell lung cancers (NSCLCs) by immunohistochemistry. Phosphorylated Akt was detected either in the cytoplasm (23 cases) or nucleus (6 cases) in 29 of 43 NSCLCs (67.4%). Squamous cell carcinomas, adenocarcinomas, and bronchioloalveolar carcinomas expressed phosphorylated Akt in 68.2%, 61.5% and 75%, respectively. We also analyzed the phosphorylated Akt expression between primary NSCLCs and their corresponding nodal metastasis; the expression was not, however, different between the primary and metastatic lesions. Taken together, these results indicate that Akt 1 is frequently activated in NSCLCs, irrespective of the histological subtypes, and suggest that phosphorylated Akt may play a role in the development of NSCLC rather than in the progression of NSCLC.

No abstract

Many types of cancer cells are resistant to Fas-mediated apoptosis by several mechanisms, including the mutations of the genes involved in Fas-mediated apoptosis. In this study, to explore the possibility that the mutations of the genes involved in the proximal pathway of Fas-mediated apoptosis (Fas, FADD, caspase 8 and caspase 10) are involved in cancer metastasis, we have analysed somatic mutation and deletion of these genes in 80 non-small cell lung cancers (NSCLCs) with (n=43) and without (n=37) metastasis to the regional lymph nodes. We found 12 mutations (four Fas, four FADD, and four caspase 10 mutations) in 11 of 80 NSCLCs (13.8%). Interestingly, of these mutations, most mutations (10 out of 12) were detected in the NSCLCs with metastasis, and the frequency in the metastasis lesions (23%) was higher than that in the primary lesions of the NSCLCs without metastasis (5.4%). Furthermore, transfection study revealed that the tumor-derived mutants have decreased apoptosis inductions compared to the wild types. These data suggest that the inactivating mutations of the genes in the proximal pathway of Fas-mediated apoptosis may lead to a decreased cancer cell death and play a role in the metastasis of NSCLC.