RESUMEN
Previous case-control studies having investigated the relationship between the X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp polymorphism and thyroid cancer (TC) have drawn inconsistent conclusions. The current study aimed to clarify the role of this polymorphism in susceptibility to TC. An up-to-date search of PubMed and Web of Science databases was conducted, including articles published up to August 2015. Crude odds ratios (ORs) with 95%CIs were calculated to establish the association between the XRCC1 Arg194Trp polymorphism and TC risk. Five studies were used, comprising 911 patients and 1476 controls. Our meta-analysis indicated that this polymorphism is associated with TC risk in Caucasians (TrpTrp vs ArgArg: OR = 5.72, 95%CI = 1.39-23.54; ArgTrp vs ArgArg: OR = 1.20, 95%CI = 0.87-1.66; dominant model: OR = 1.31, 95%CI = 0.96-1.79; recessive model: OR = 0.18, 95%CI = 0.04-0.73). This investigation demonstrates that the XRCC1 Arg194Trp polymorphism constitutes a risk factor for TC in Caucasian individuals.
Asunto(s)
Proteínas de Unión al ADN/genética , Predisposición Genética a la Enfermedad , Polimorfismo Genético , Neoplasias de la Tiroides/genética , Estudios de Asociación Genética , Humanos , Oportunidad Relativa , Proteína 1 de Reparación por Escisión del Grupo de Complementación Cruzada de las Lesiones por Rayos XRESUMEN
We examined the effects and molecular mechanism of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib on NKG2D ligand expression in human lung adenocarcinoma A549 cells and the cytotoxicity of cytokine-induced killer cells. Flow cytometry was used to detect NKG2D ligand expression in A549 cells under effects of erlotinib and EGFR downstream molecules, including LY294002 (phosphoinositide 3-kinase inhibitor), SB203580 (mitogen-activated protein kinase inhibitor), and STAT21 (signal transduction and transcription 3 inhibitor) after 24 h. A lactate dehydrogenase release assay was used to detect, at different effector-to-target ratios, the A549 cell killing activity of cytokine-induced killer cells before and after treatment with 10 mM erlotinib. Erlotinib suppressed MICA expression in A549 cells and upregulated MICB and UL16 binding protein 1 expression. EGFR downstream molecules mitogen-activated protein kinase and signal transduction and transcription 3 inhibitor did not affect the expression of NKG2D ligands in A549 cells. The phosphoinositide 3-kinase inhibitor reduced MICA expression in A549 cells, while erlotinib enhanced the killing sensitivity of cytokine-induced killer cells in A549 cells. The anti-lung carcinoma effects of EGFR tyrosine kinase inhibitor were associated with the sensitivity of lung cancer cells to enhanced immune cell killing.
Asunto(s)
Adenocarcinoma/terapia , Células Asesinas Inducidas por Citocinas/efectos de los fármacos , Clorhidrato de Erlotinib/farmacología , Neoplasias Pulmonares/terapia , Adenocarcinoma/tratamiento farmacológico , Adenocarcinoma/inmunología , Adenocarcinoma del Pulmón , Línea Celular Tumoral , Terapia Combinada , Células Asesinas Inducidas por Citocinas/inmunología , Receptores ErbB/antagonistas & inhibidores , Citometría de Flujo , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/inmunología , Subfamilia K de Receptores Similares a Lectina de Células NK/biosíntesisRESUMEN
Six to nine populations of the diamondback moth, Plutella xylostella (L.), were collected annually from fields of crucifer vegetables in the United States and Mexico from 2001 to 2004 for baseline susceptibility tests and resistance monitoring to spinosad, indoxacarb, and emamectin benzoate. A discriminating concentration for resistance monitoring to indoxacarb and emamectin benzoate was determined based on baseline data in 2001 and was used in the diagnostic assay for each population in 2002-2004 together with a discriminating concentration for spinosad determined previously. Most populations were susceptible to all three insecticides, but a population from Hawaii in 2003 showed high levels of resistance to indoxacarb. Instances of resistance to spinosad occurred in Hawaii (2000), Georgia (2001), and California (2002) as a consequence of a few years of extensive applications in each region. The collaborative monitoring program between university and industry scientists we discuss in this article has provided useful information to both parties as well as growers who use the products. These studies provide a baseline for developing a more effective resistance management program for diamondback moth.