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PURPOSE: The activities of insulin-like growth factors (IGFs) in regulating cell proliferation,differentiation, and apoptosis are modulated by a family of high-affinity specific IGF-binding proteins (IGFBPs), especially IGFBP-3, the most abundant IGFBP in circulation. Hypermethylation of the promoter represses the expression of the IGFBP-3 gene. The purpose of this study was to determine whether the methylation status of IGFBP-3 promoter influences the prognosis of non-small cell lung cancer (NS

Compound EGFR mutations, defined as double or multiple mutations in the EGFR tyrosine kinase domain, are frequently detected with advances in sequencing technology but its clinical significance is unclear. This study analyzed 61 cases of EGFR mutation positive lung adenocarcinoma using next-generation sequencing (NGS) based repeated deep sequencing panel of 16 genes that contain actionable mutations and investigated clinical implication of compound EGFR mutations. Compound EGFR mutation was dete

The activities of insulin-like growth factors (IGFs), including mitogenic and antiapoptotic properties, are modulated by a family of high-affinity insulin-like growth factor-binding proteins (IGFBPs), of which IGFBP-3 is the major serum carrier protein. Even though it is well known that IGFBP-3 plays an important role in cell proliferation, the expression of IGFBP-3 and its significance in primary non-small cell lung cancer (NSCLC) samples are unknown. This study explored IGFBP-3 expression in t

PURPOSE: Enolase-alpha is a cytoplasmic glycolytic enzyme important in the formation of phosphoenolpyruvate. Enolase-alpha and c-myc binding protein (MBP-1) originate from a single gene through alternative use of translational starting sites. Both enolase-alpha and MBP-1 can bind to the P2 element in the c-myc promoter and compete with TATA-box binding protein (TBP) to suppress transcription of c-myc. EXPERIMENTAL DESIGN: To determine a potential role of enolase-alpha in vivo, we analyzed enolas

mutations. Identification of mechanisms leading to inhibitor resistance has led to new therapeutic modalities, some of which have now been adapted for patients with unsuccessful tyrosine kinase inhibitor treatment. In this review, we describe mechanisms of tyrosine kinase inhibitor resistance and the available strategies to overcoming resistance.

Among carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family proteins, CEACAM6 has received less attention than CEACAM5 and its presence and role in lung cancer are largely unknown. The application of CellphoneDB on the single cell RNA sequencing dataset showed that the homophilic interactions among CEACAM6 molecules, which are overexpressed in lung cancer cells were highly significant. CEACAM6 was overexpressed in 80.1% of lung adenocarcinomas and its overexpression had a signi

Methionyl-tRNA synthetase (MRS) plays a critical role in initiating translation by transferring Met to the initiator tRNA (tRNAi Met) and protection against ROS-mediated damage, suggesting that its overexpression is related to cancer growth and drug resistance. In this study, the clinical implication of MRS expression in non-small cell lung cancer (NSCLC) was evaluated. Immunoblot and immunohistochemical (IHC) analyses were performed using tissue lysates and formalin-fixed paraffin embedded (FFP

BACKGROUND: mTOR, which can form mTOR Complex 1 (mTORC1) or mTOR Complex 2 (mTORC2) depending on its binding partners, is frequently deregulated in the pulmonary neoplastic conditions and interstitial lung diseases of the patients treated with rapalogs. In this study, we investigated the relationship between mTOR signaling and epithelial mesenchymal transition (EMT) by dissecting mTOR pathways. METHODS: Components of mTOR signaling pathway were silenced by shRNA in a panel of non-small cell lung

BACKGROUND: Hyperprogressive disease (HPD) is a paradoxical acceleration of tumor growth after immune checkpoint inhibitor (ICI) treatment. This study aimed to identify the risk factors and to present a predictive model for HPD in patients treated with ICIs. METHODS: A total of 78 non-small cell lung cancer (NSCLC) cases, treated with at least two cycles of ICIs who underwent computed tomography (CT) for response assessment were recruited into the study from January 2016 to August 2019. HPD was

Genetic heterogeneity between the primary and L/N metastatic lesions is not infrequent finding to consider when interpreting genomic data based on the result of one site inspection. A large prospective study may be needed to evaluate the impact of genetic heterogeneity on the clinical outcomes of NSCLC patients.

A subset of non-small cell lung cancer (NSCLC), which does not have a druggable driver mutation, is treated with platinum-based cytotoxic chemotherapy, but it develops resistance triggered by DNA damage responses. Here, we investigated the effect of activation of STAT3 by cisplatin on anti-apoptotic proteins and the effectiveness of a co-treatment with cisplatin and a BH3 mimetic, ABT-737. We analyzed the relationship between cisplatin and STAT3 pathway and effect of ABT-737, when combined with