MET FISH-positive status predicts short progression-free survival and overall survival after gefitinib treatment in lung adenocarcinoma with EGFR mutation.

Background: Lung adenocarcinoma patients with EGFR gene mutations have shown a dramatic response to gefitinib. However, drug resistance eventually emerges which limits the mean duration of response. With that in view, we examined the correlations between MET gene status as assessed by fluorescence in situ hybridization (FISH) with overall survival (OS) and progression-free survival (PFS) in adenocarcinoma patients with EGFR gene mutations who had received gefitinib therapy.

Control of the MYC-eIF4E axis plus mTOR inhibitor treatment in small cell lung cancer.

Background: Mammalian target of rapamycin (mTOR) inhibitors have anti-tumor effects against renal cell carcinoma, pancreatic neuroendocrine cancer and breast cancer. In this study, we analyzed the antitumor effects of mTOR inhibitors in small cell lung cancer (SCLC) cells and sought to clarify the mechanism of resistance to mTOR inhibitors.

Methods: We analyzed the antitumor effects of three mTOR inhibitors including everolimus in 7 SCLC cell lines by MTS assay.

MiR-134/487b/655 cluster regulates TGF-β-induced epithelial-mesenchymal transition and drug resistance to gefitinib by targeting MAGI2 in lung adenocarcinoma cells.

Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA)-related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in NSCLC. miRNA expression profiles were examined before and after transforming growth factor β1 (TGF-β1) exposure in four human adenocarcinoma cell lines with or without EMT.

Activity of EGFR-tyrosine kinase and ALK inhibitors for EML4-ALK-rearranged non-small-cell lung cancer harbored coexisting EGFR mutation.

Background: The EML4-ALK (echinoderm microtubule-associated protein-like 4 gene and the anaplastic lymphoma kinase gene) fusion oncogene represents a novel molecular target in a small subset of non-small-cell lung cancers (NSCLCs). The EML4-ALK fusion gene occurs generally in NSCLC without mutations in epidermal growth factor receptor (EGFR) and KRAS.

Case Presentation: We report that a case of EML4-ALK-positive NSCLC with EGFR mutation had a response of stable disease to both an EGFR tyrosine kinase inhibitor (EGFR-TKI) and ALK inhibitor.

Apoptosis-inducing activity of the actin-depolymerizing agent aplyronine A and its side-chain derivatives.

Aplyronine A (1) and mycalolide B (2), which are cytotoxic actin-depolymerizing marine macrolides, were revealed to induce apoptosis in human leukemia HL60 cells and human epithelial carcinoma HeLa S(3) cells. Based on these results, actin-depolymerizing compounds were expected to exhibit apoptosis-inducing activity in cancer cells. Compounds 3-6, which were synthesized based on the side-chain structure of aplyronine A, were evaluated for their actin-depolymerizing activities in vitro and cytotoxicities against HL60 cells.

Bevacizumab plus chemotherapy for advanced non-squamous non-small-cell lung cancer with malignant pleural effusion.

Purpose: The presence of malignant pleural effusion (MPE) indicates a poorer prognosis for patients with non-small-cell lung cancer (NSCLC) and impairs their quality of life. Because vascular endothelial growth factor (VEGF) is the key mediator MPE production, we evaluated the efficacy and safety of chemotherapy plus bevacizumab, an anti-VEGF antibody, in non-squamous NSCLC patients with MPE, especially regarding the control of pleural effusions.

Methods: From November 1, 2009 to September 30, 2011, medical charts of 13 consecutive patients with MPE who received bevacizumab plus chemotherapy as the initial or secondary treatment were retrospectively analyzed.

MiR-23a regulates TGF-β-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells.

Transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) has been shown to be related to the pathogenesis of various diseases including lung cancer. Recently, microRNAs (miRNA) have been recognized as a new class of genes involved in human tumorigenesis. MiR-23a/24/27a is a miRNA cluster located in chromosome 19p13.

The feasibility study of Carboplatin plus Etoposide for advanced small cell lung cancer with idiopathic interstitial pneumonias.

Background: Idiopathic interstitial pneumonias (IIPs) are among the most common complications in patients with lung cancer. In such patients with cancer, the most serious expression of toxicity in Japan is acute exacerbation of IIPs caused by anticancer treatment. Nevertheless, there has been no consensus and no evidence presented, regarding optimal treatment for advanced lung cancer with IIP.

HSP27 modulates epithelial to mesenchymal transition of lung cancer cells in a Smad-independent manner.

Epithelial to mesenchymal transition (EMT) is induced by transforming growth factor-β1 (TGF-β1) and is a crucial event for cancer cells to acquire invasive and metastatic phenotypes. However, the signals that induce EMT in cancer cells have yet to be adequately defined. In this study, a proteomic investigation was performed to understand the signaling pathway of the EMT of lung cancer using two-dimensional difference gel electrophoresis (2D-DIGE) and mass spectrometry.

Choroidal metastasis in a patient with small cell lung cancer discovered during treatment with chemotherapy.

A 56-year-old male patient complaining of productive cough, hoarseness, and fatigue was found to have extensive disease of small cell lung cancer (ED-SCLC), with staging of cT4N3M1(PUL). He was treated with chemotherapy. While undergoing treatment with chemotherapy, he complained of a right visual disturbance, and choroidal metastasis was diagnosed.

Biselyngbyaside, a macrolide glycoside from the marine cyanobacterium Lyngbya sp.

Bioassay-guided fractionation of the cytotoxic constituents of the marine cyanobacterium Lyngbya sp. led to the isolation of biselyngbyaside (1), a new 18-membered macrolide glycoside. The structure of 1 was established by spectroscopic analysis including 2D-NMR techniques and by synthetic studies.

Synthesis of actin-depolymerizing compounds.

The artificial actin-depolymerizing compounds 3-6, based on aplyronine A, an actin-depolymerizing antitumor marine macrolide, were synthesized, and their actin-depolymerizing activities and cytotoxicities were evaluated.

Retrospective analysis of efficacy and safety of amrubicin in refractory and relapsed small-cell lung cancer.

Background: Amrubicin, a totally synthetic 9-aminoanthracycline, was evaluated retrospectively for the treatment of refractory and relapsed small-cell lung cancer (SCLC).

Methods: Retrospective analysis was performed in 32 patients. Amrubicin was infused over 5 min on days 1-3, with courses repeated at 3- or 4-week intervals.

Estimation of postoperative fat absorption using the 13C mixed-triglyceride breath test in children with choledochal cyst.

No previous studies have focused on postoperative fat malabsorption in children with choledochal cyst (CC) who undergo cyst excision and Roux-en-Y (RY) hepatico-jejunostomy (HJ), a combination of procedures that can lead to the non-physiological mixture of food and bile juice. To examine the effect of RYHJ with cholecystectomy on the fat absorption ability of children with CC, we estimated postoperative fat-absorption ability using the carbon 13-labeled mixed triglyceride (13C-MTG) breath test. Twelve postoperative children with CC and 12 normal control children were administered 13C-MTG orally and asked to give breath samples at six time points: once before the 13C-MTG ingestion and at five 60-min intervals postingestion.