Hai-Ping Pang

Qing Yang

IntechOpen

Crossref

English

Optimal Sliding Mode Control for a Class of Uncertain Nonlinear Systems Based on Feedback Linearization

The title compound, C13H8BrI2NO, was prepared by the reaction of 3,5-diiodo­salicyl­aldehyde with 4-bromo­phenyl­amine in ethanol. There is an intra­molecular O—H⋯N hydrogen bond in the mol­ecule, which generates an S(6) ring. The dihedral angle between the benzene rings is 2.6 (3)°

Ji, Hao

Ma, Hua-Ping

Yang, Yong-An

Zhu, Hai-Liang

Directory of Open Access Journals

PubMed Central

Fractional atomic coordinates and isotropic or equivalent isotropic displacement parameters (Å2) xy zU iso*/Ueq I1

organic compounds o788 Ji et al. doi:10.1107/S160053681200551X Acta Cryst.

SMART and SAINT.

2-[(4-Bromo­phenyl­imino)­meth­yl]-4,6-di­iodo­phenol

The asymmetric unit of the title compound, C13H8ClI2NO, contains half of the mol­ecule situated on a mirror plane. The hy­droxy group is involved in the formation of an intra­molecular O—H⋯N hydrogen bond. π–π inter­actions between the benzene rings of neighbouring mol­ecules [centroid–centroid distance = 3.629 (3) Å] form stacks along the b axis. In the crystal, weak C—H⋯O and C—H⋯Cl inter­actions are observed

Fractional atomic coordinates and isotropic or equivalent isotropic displacement parameters (Å2) xy z U iso*/Ueq I1

organic compounds Acta Cryst.

2-[(2-Chloro­phen­yl)imino­meth­yl]-4,6-di­iodo­phenol

Abstract Background/Aim Fas/FasL system is a major regulator of apoptosis. The mechanisms by which Fas mediates cisplatin resistance remain unclear. The aim of this study is to explore the effect of Fas over-expression on cisplatin resistance of small cell lung cancer cells and its possible mechanisms. Materials and methods Fas was over-expressed in H446/CDDP cells by infection with the adenoviruses containing Fas. Sensitivity of Fas-overexpressed H446/CDDP cells to cisplatin was evaluated using MTT assay. Expressions of Fas, GST-π and ERCC1 were detected by RT-PCR and Western blot analysis. Apoptosis rate was examined by FACS. Results Over-expression of Fas in H446/CDDP cells significantly decreased the expressions of GST-π and ERCC1 at mRNA and protein levels, and increased the cell apoptosis. Furthermore, up-regulation of Fas significantly decreased the tolerance of H446/CDDP cells to cisplatin. Conclusion Over-expression of Fas reverses drug resistance of H446/CDDP cells, possibly due to the increased cell sensitivity to apoptosis and the decreased expressions of GST-π and ERCC1.</p

Guo, Wei

He, Ping

Jiang, Yao-guang

Wang, Hai-dong

Wu, Wei

Yang, Kang

Zhao, Yun-ping

Springer - Publisher Connector

Activation of programmed cell death by anticancer agents: cisplatin as a model system. Cancer Cell

Augmented expression of metallothionein and glutathione Stransferase pi as unfavourable prognostic factors in cisplatin-treated ovarian cancer patients. Virchows Arch

BR: Glutathione S-transferase pi amplification is associated with cisplatin Received:

Cell biological mechanism of multidrug resistance in tumors.

Chemoimmunosensitization of the T24 human bladder cancer line to Fas-mediated cytotoxicity and apoptosis by cisplatin and 5-fluorouracil. Oncol Rep

Cisplatin induces fas expression in esophageal cancer cell lines and enhanced cytotoxicity in combination with LAK cells [J]. Oncology

Cisplatin: mode of cytotoxic action and molecular basis of resistance. Oncogene

Correlation analysis among expression of ERCC-1, metallothionein, p53 and platinum resistance and prognosis in advanced non-small cell lung cancer. Ai Zheng

Debatin K-M: Crossresistance of CD95- and drug-induced apoptosis as a consequence of deficient activation of caspases (ICE/ced-3 proteases). Blood

Debatin KM: Involvement of the CD95 (APO-1/FAS) receptor/ligand system in drug-induced apoptosis in leukemia cells. Nat Med

Dempfle L: Relative expression software tool (REST) for group-wise comparison and statistical analysis of relative expression results in real-time PCR. Nucleic Acids Res

Dimanche-Boitrel MT: Sensitization of cancer cells treated with cytotoxic drugs to Fasmediated cytotoxicity.

Eberlein TJ: Pancreatic cancer cells can evade immune surveillance via nonfunctional Fas (APO-1/CD95) receptors and aberrant expression of functional Fas ligand. Surgery

Etxaniz O: Applications of genomics in NSCLC. Lung Cancer

Fas and Fas ligand: a death factor and its receptor. Adv Immunol

Fesik SW: NMR structure and mutagenesis of the Fas (APO-1/CD95) death domain. Nature

FL: Construction and propagation of human adenovirus vectors.

Glutathione S-transferase pi immunostaining of cisplatin-resistant ovarian cancer cells in ascites. Acta Cytol

HJ: Small interfering RNAinduced suppression of ERCC1 enhances sensitivity of human cancer cells to cisplatin. Biochem Biophys Res Commun

Human pancreatic adenocarcinomas express Fas and Fas ligand yet are resistant to Fas mediated apoptosis. Cancer Res

ID: Glutathioneassociated enzymes in head and neck squamous cell carcinoma and response to cisplatin-based neoadjuvant chemotherapy.

Insights into mechanisms of cisplatin resistance and potential for its clinical reversal. Pharmacotherapy

Köberle B: Reduced levels of XPA, ERCC1 and XPF DNA repair proteins in testis tumor cell lines.

Legembre Patrick: Redistribution of CD95 into the Lipid Rafts to Treat Cancer Cells? Recent Patents on Anti-Cancer Drug Discovery

Loss of caspase-8 activation pathway is a possible mechanism for CDDP resistance in human laryngeal squamous cell carcinoma, HEp-2 cells[J].

Messenger RNA levels of XPAC and ERCC1 in ovarian cancer tissue correlate with response to platinum-based chemotherapy.

Ng IO: Induction of apoptosis by cisplatin and its effect on cell cycle-related proteins and cell cycle changes in hepatoma cells. Cancer Letters

Nucleotide excision repair pathways involved in Cisplatin resistance in non-smallcell lung cancer. Cancer Control

Paul: Cisplatin Enhances Protein Kinase R-Like Endoplasmic Reticulum Kinase- and CD95-Dependent Melanoma DifferentiationAssociated Gene-7/Interleukin-24-Induced Killing in Ovarian Carcinoma Cells. Mol Pharmacol

PH: p53 activates the CD95 (APO-1/Fas) gene in response to DNA damage by anticancer drugs.

Platinum-DNA adduct, nucleotide excision repair and platinum based anti-cancer chemotherapy. Cancer Treat Rev

PR: Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53.

Ramp Uwe, Bier Henning: Is there a role for the Fas-/Fas-Ligand pathway in chemoresistance of human squamous cell carcinomas of the head and neck (SCCHN)? Oral Oncology

RD: An intrastrand d(GpG) platinum crosslink in duplex M13 DNA is refractory to repair by human cell extracts. Proc Natl Acad Sci USA

Reed E: Association between the level of ERCC-1 expression and the repair of cisplatin-induced DNA damage in human ovarian cancer cells. Anticancer Res

Rittgen W: Cellular predictive factors for the drug response of lung cancer. Anticancer Res

S: The cDNA structure, expression, and chromosomal assignment of the mouse Fas antigen.

Stahnke K: Regulation of apoptosis through CD95 (APO-I/Fas) receptor-ligand interaction. Biochem Soc Trans

Tsukuda M: The relationship of the human glutathione S-transferase PI polymorphism and chemotherapeutic sensitivity in head and neck squamous carcinoma.

VA: Increased gene-specific repair of cisplatin interstrand cross-links in cisplatin-resistant human ovarian cancer cell lines. Mol Cell Biol

Up-regulation of fas reverses cisplatin resistance of human small cell lung cancer cells

Optimal Sliding Mode Control for a Class of Uncertain Nonlinear Systems Based on Feedback Linearization

2-[(4-Bromophenylimino)methyl]-4,6-diiodophenol

2-[(2-Chlorophenyl)iminomethyl]-4,6-diiodophenol

Up-regulation of fas reverses cisplatin resistance of human small cell lung cancer cells