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Lipiodol lOcalization for Ground-glass opacity mInimal Surgery: Rationale and design of the LOGIS trial. - Contemporary clinical trials
The diagnosis and treatment of ground-glass opacity (GGO) lesions have become important issues because subsolid nodules including GGO are known to frequently represent the histologic spectrum of lung adenocarcinoma. Because small GGO lesions cannot usually be palpated or visualized during surgery, several marking techniques have been reported for localization during thoracoscopic surgery, such as lipiodol and hook-wire localization. This study is designed to demonstrate the usefulness and safety of the lipiodol localization technique for individuals undergoing GGO VATS resection compared to the hook-wire localization technique.Two hundred fifty participants will be prospectively enrolled in a 1:1 manner to the lipiodol or hook-wire group according to the inclusion criteria. All study participants will undergo preoperative lung localization using either the lipiodol or hook-wire method. Thoracoscopic surgery will be performed by experienced thoracoscopic surgeons within several hours after marking under general anesthesia. The primary endpoint is the procedure success rate, and the secondary endpoints are the procedure complication rate, procedure time, surgery time and the margin from the lesion in the resected specimen.Patient enrollment will be completed within 2years. We will analyze the procedure success rate and the presence of complications with regard to the CT results. In addition, the procedure and surgery times, and the safety margin will be also compared between the 2 techniques.If the aims of this study are achieved, then the use of lipiodol localization technique will be widespread in the localization of non-palpable pulmonary lesions that are indicated for surgical resection. (ClinicalTrials.gov: NCT02180568).Copyright Â© 2015 Elsevier Inc. All rights reserved.
PINCH-2 presents functional copy number variation and suppresses migration of colon cancer cells by paracrine activity. - International journal of cancer. Journal international du cancer
In recent years, characterization of cancer and its environment has become necessary. However, studies of the cancer microenvironment remain insufficient. Copy number variations (CNVs) occur in 40% of cancer-related genes, but few studies have reported the correlation between CNVs in morphologically normal tissues adjacent to cancer and cancer progression. In this study, we evaluated cancer cell migration and invasion according to the genetic differences between cancer tissues and their surrounding normal tissues. To study the field cancerization effect, we screened 89 systemic metastasis-related CNVs from morphologically normal tissues adjacent to colon cancers. Among these CNVs, LIM and senescent cell antigen-like domain 2 (PINCH-2) showed copy number amplification and upregulation of mRNA in the nonrelapsed group compared to the systemic relapse group. PINCH-2 expression in colon cancer cells was lower than that in normal epithelial colon cells at both the protein and mRNA levels. Suppression of PINCH-2 resulted in decreased formation of the PINCH-2-IPP (PINCH-2, integrin-linked kinase and Î±-parvin) complex and reciprocally increased formation of the PINCH-1-IPP complex. Although PINCH-2 expression of survival pathway-related proteins (Akt and phospho-Akt) did not change upon suppression of PINCH-2 expression, cell migration-related proteins [matrix-metalloproteinase (MMP)-9 and -11] were upregulated through autocrine and paracrine activation. Thus, PINCH-2 participates in decreased systemic recurrence by competitively regulating IPP complex formation with PINCH-1, thereby suppressing autocrine and paracrine effects on motility in colon cancer. This genetic change in morphologically normal tissue suggests a field cancerization effect of the tumor microenvironment in cancer progression.Â© 2014 UICC.
Metal-organic framework@microporous organic network: hydrophobic adsorbents with a crystalline inner porosity. - Journal of the American Chemical Society
This work reports the synthesis and application of metal-organic framework (MOF)@microporous organic network (MON) hybrid materials. Coating a MOF, UiO-66-NH2, with MONs forms hybrid microporous materials with hydrophobic surfaces. The original UiO-66-NH2 shows good wettability in water. In comparison, the MOF@MON hybrid materials float on water and show excellent performance for adsorption of a model organic compound, toluene, in water. Chemical etching of the MOF results in the formation of hollow MON materials.
Pharmacogenetic determinants associated with sunitinib-induced toxicity and ethnic difference in Korean metastatic renal cell carcinoma patients. - Cancer chemotherapy and pharmacology
The aim of this study was to investigate the pharmacogenetic determinants of sunitinib-related toxicity and ethnic difference in metastatic renal cell carcinoma (mRCC) among Korean patients.A pharmacogenetic study was performed in 65 patients with mRCC treated with the standard schedule of sunitinib (50Â mg orally once daily for 4Â weeks-on/2Â weeks-off). Detailed data regarding the toxicity of sunitinib, including thrombocytopenia, neutropenia, anemia, and hand-foot syndrome (HFS), were prospectively collected in a clinical trial program (nÂ =Â 38) or standard oncology practice (nÂ =Â 27). Total of 12 genetic polymorphisms in 8 candidate genes (CYP1A1, CYP3A5, ABCB1, ABCG2, PDGFRÎ±, VEGFR2, RET, and FLT3) were analyzed for an association with treatment-related toxicity from sunitinib using Pearson Ï‡ (2) test.Common grade 3 or grade 4 treatment-related toxicities were thrombocytopenia (36.9Â %, 24/65), neutropenia (18.4Â %, 12/65), anemia (7.7Â %, 5/65), and HFS (12.3Â %, 8/65). Patients carrying an ABCG2 421 AA genotype developed significantly more grade 3 or grade 4 thrombocytopenia, neutropenia, and HFS adjusted for age, sex, and Eastern Cooperative Oncology Group performance status, and body surface area (odds ratio compared with AC/CC genotypes [OR] 9.90, PÂ =Â 0.04, thrombocytopenia; OR 18.20, PÂ =Â 0.02, neutropenia; and OR 28.46, PÂ =Â 0.01, HFS). In addition, total and surface protein ABCG2 protein expression was decreased in ABCG2 421 AA mutant cells compared to wild type.Among 12 genetic polymorphisms, polymorphism in the ABCG2 421C>A gene may be mostly associated with the risk of sunitinib-related toxicity in mRCC patients. Considering the high frequency of 421C>A SNP in Asian, this may be related to differential toxicities among ethnic groups.
New iron-based mixed-polyanion cathodes for lithium and sodium rechargeable batteries: combined first principles calculations and experimental study. - Journal of the American Chemical Society
New iron-based mixed-polyanion compounds Li(x)Na(4-x)Fe(3)(PO(4))(2)(P(2)O(7)) (x = 0-3) were synthesized, and their crystal structures were determined. The new compounds contained three-dimensional (3D)sodium/lithium paths supported by P(2)O(7) pillars in the crystal. First principles calculations identified the complex 3D paths with their activation barriers and revealed them as fast ionic conductors. The reversible electrode operation was found in both Li and Na cells with capacities of one-electron reaction per Fe atom, 140 and 129 mAh g(-1), respectively. The redox potential of each phase was âˆ¼3.4 V (vs Li) for the Li-ion cell and âˆ¼3.2 V (vs Na) for the Na-ion cell. The properties of high power, small volume change, and high thermal stability were also recognized, presenting this new compound as a potential competitor to other iron-based electrodes such as Li(2)FeP(2)O(7), Li(2)FePO(4)F, and LiFePO(4).
Ribonucleotide reductase M1 (RRM1) 2464G>A polymorphism shows an association with gemcitabine chemosensitivity in cancer cell lines. - Pharmacogenetics and genomics
Significant variability in the efficacy and toxicity of an anticancer drug is observed in cancer patients. Currently, there are no standard tools for prediction of a patient's tumor response or his risk of adverse events to chemotherapy.We investigate an association between polymorphisms of gemcitabine metabolism-related genes and its chemosensitivity in vitro using 62 human cancer cell lines of various origins. Polymorphisms of gemcitabine metabolism-related genes of deoxycytidine monophosphate deaminase (DCTD), deoxycytidine kinase (DCK) and ribonucleotide reductase M1 (RRM1) were evaluated using the CEQ8000 Genetic analysis system and GeneDoc software. Chemosensitivity of gemcitabine was expressed as an IC50 using MTT assay.The frequency of the polymorphisms was 21% in DCTD 315T>C, 45.2% in RRM1 1082C>A, 59.7% in RRM1 2455A>G, and 79% in RRM1 2464G>A. When examining the association between these polymorphisms and IC50, only the RRM1 2464G>A showed the tendency to be more chemosensitive to gemcitabine (P=0.011), and haplotypes containing 2464G>A polymorphism also showed the association with chemosensitivity when compared to wild-type RRM1 (G2464G). We could not see the significant differences of mRNA expression level with real-time PCR between cell lines according to G2464A polymorphism. In oligonucleotide microarray 73 GenBank Accession Number (69 genes) were selected which expressed differently between RRM1 wild-type and the G2464A polymorphism.RRM1 2464G>A polymorphism demonstrated an association with gemcitabine sensitivity, which needs functional studies with co-expressing genes and prospective clinical studies for the clinical application as a predictive bio-marker.
IKKgamma inhibits activation of NF-kappaB by NIK. - Molecules and cells
IKKgamma is a component of the IKK complex, which regulates NF-kappaB activity. To investigate the role of IKKgamma, we expressed wild type IKKgamma containing 412 amino acids, and deletion mutants containing residues 1-312 and 101-412, using murine IKKgamma cDNA. In a co-transfection assay with a CAT reporter plasmid, NIK activated NF-kappaB-dependent gene expression approximately two fold and this expression was inhibited by co-transfection of a wild type IKKgamma expression plasmid. In binding assays IKKgamma inhibited the association of IkappaBalpha with IKKbeta and the subsequent phosphorylation of IkappaBalpha that is activated by NIK. Inhibition by IKKgamma also occurred in an assay with a dominant negative mutant of NIK but not with a C-terminal deletion mutant of IKKgamma, indicating that the C-terminal 100 amino acids of IKKgamma are important for negative regulation of NF-kappaB activation. In addition, the interaction of IKKbeta with IKKgamma was inhibited by co-transfection with a NIK expression plasmid. Our results suggest that overexpression of IKKgamma inhibits activation of NF-kappaB by NIK by competing with NIK for interaction with IKKbeta.
The impact of KRAS mutations on prognosis in surgically resected colorectal cancer patients with liver and lung metastases: a retrospective analysis. - BMC cancer
KRAS mutations are common in colorectal cancer (CRC). The role of KRAS mutation status as a prognostic factor remains controversial, and most large population-based cohorts usually consist of patients with non-metastatic CRC. We evaluated the impact of KRAS mutations on the time to recurrence (TTR) and overall survival (OS) in patients with metastatic CRC who underwent curative surgery with perioperative chemotherapy.Patients who underwent curative resection for primary and synchronous metastases were retrospectively collected in a single institution during a 6Â year period between January 2008 and June 2014. Patients with positive surgical margins, those with known BRAF mutation, or those with an unknown KRAS mutation status were excluded, and a total of 82 cases were identified. The pathological and clinical features were evaluated. Patients' outcome with KRAS mutation status for TTR and OS were investigated by univariate and multivariate analysis.KRAS mutations were identified in 37.8Â % of the patients and not associated with TTR or OS between KRAS wild type and KRAS mutation cohorts (log-rank pâ€‰=â€‰0.425 for TTR; log-rank pâ€‰=â€‰0.137 for OS). When patients were further subdivided into three groups according to mutation subtype (wild-type vs. KRAS codon 12 mutation vs. KRAS codon 13 mutation) or amino acid missense mutation type (Gâ€‰>â€‰A vs. Gâ€‰>â€‰T vs. Gâ€‰>â€‰C), there were no significant differences in TTR or OS. Mutational frequencies were significantly higher in patients with lung metastases compared with those with liver and ovary/bladder metastases (pâ€‰=â€‰0.039), however, KRAS mutation status was not associated with an increased risk of relapsed in the lung.KRAS mutation was not associated with TTR or OS in patients with metastatic CRC who underwent curative surgery with perioperative chemotherapy.
Genetic alterations and their clinical implications in gastric cancer peritoneal carcinomatosis revealed by whole-exome sequencing of malignant ascites. - Oncotarget
Peritoneal carcinomatosis accompanied by malignant ascites is a major cause of death of advanced gastric cancer (GC). To comprehensively characterize the underlying genomic events involved in GC peritoneal carcinomatosis, we analyzed whole-exome sequences of normal gastric tissues, primary tumors, and malignant ascites from eight GC patients. We identified a unique mutational signature biased toward C-to-A substitutions in malignant ascites. In contrast, the patients who received treatment of adjuvant chemotherapy showed a high rate of C-to-T substitutions along with hypermutation in malignant ascites. Comparative analysis revealed several candidate mutations for GC peritoneal carcinomatosis: recurrent mutations in COL4A6, INTS2, and PTPN13; mutations in druggable genes including TEP1, PRKCD, BRAF, ERBB4, PIK3CA, HDAC9, FYN, FASN, BIRC2, FLT3, ROCK1, CD22, and PIK3C2B; and mutations in metastasis-associated genes including TNFSF12, L1CAM, DIAPH3, ROCK1, TGFBR1, MYO9B, NR4A1, and RHOA. Notably, gene ontology analysis revealed the significant enrichment of mutations in the Rho-ROCK signaling pathway-associated biological processes in malignant ascites. At least four of the eight patients acquired somatic mutations in the Rho-ROCK pathway components, suggesting the possible relevance of this pathway to GC peritoneal carcinomatosis. These results provide a genome-wide molecular understanding of GC peritoneal carcinomatosis and its clinical implications, thereby facilitating the development of effective therapeutics.
Genomic Alterations in Biliary Tract Cancer Using Targeted Sequencing. - Translational oncology
Biliary tract cancers (BTCs) are rare and heterogeneous group of tumors classified anatomically into intrahepatic and extrahepatic bile ducts and gallbladder adenocarcinomas. Patient-derived tumor cell (PDC) models with genome analysis can be a valuable platform to develop a method to overcome the clinical barrier on BTCs.Between January 2012 and June 2015, 40 BTC patients' samples were collected. PDCs were isolated and cultured from surgical specimens, biopsy tissues, or malignant effusions including ascites and pleural fluid. Genome analysis using targeted panel sequencing as well as digital multiplexed gene analysis was applied to PDCs as well as primary tumors.Extrahepatic cholangiocarcinoma (N=15, 37.5%), intrahepatic cholangiocarcinoma (N=10, 25.0%), gallbladder cancer (N=14, 35.0%), and ampulla of Vater cancer (N=1, 2.5%) were included. We identified 15 mutations with diverse genetic alterations in 19 cases of BTC from primary tumor specimens. The most common molecular alterations were in TP53 (8/19, 42.1%), including missense mutations such as C242Y, E285K, G112S, P19T, R148T, R248Q, and R273L. We also detected two NRAS mutations (G12C and Q61L), two KRAS mutations (G12A and G12S), two ERBB2 mutations (V777L and pM774delinsMA) and amplification, and three PIK3CA mutations (N345K, E545K, and E521K). PDC models were successfully established in 27 of 40 samples (67.5%), including 22/24 from body fluids (91.7%) and 5/16 from tissue specimens (31.3%).PDC models are promising tools for uncovering driver mutations and identifying rational therapeutic strategies in BTC. Application of this model is expected to inform clinical trials of drugs for molecular-based targeted therapy.Copyright Â© 2015. Published by Elsevier Inc.
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