[Double-ambient CO concentration affects the growth, development and sucking behavior of non-target brown plant hopper Nilaparvata lugens fed on transgenic Bt rice].

In recent years, the two issues of climate change including elevated CO etc., and resistance of transgenic Bt crops against non-target insect pests have received widespread attention. Elevated CO can affect the herbivorous insects.

High-performance SERS substrate based on hybrid structure of graphene oxide/AgNPs/Cu film@pyramid Si.

We present a novel surface-enhanced Raman scattering (SERS) substrate based on graphene oxide/silver nanoparticles/copper film covered silicon pyramid arrays (GO/AgNPs/PCu@Si) by a low-cost and simple method. The GO/AgNPs/PCu@Si substrate presents high sensitivity, good homogeneity and well stability with R6G molecules as a probe. The detected concentration of Rhodamine 6 G (R6G) is as low as 10 M.

Gold@silver bimetal nanoparticles/pyramidal silicon 3D substrate with high reproducibility for high-performance SERS.

A novel and efficient surface enhanced Raman scattering (SERS) substrate has been presented based on Gold@silver/pyramidal silicon 3D substrate (Au@Ag/3D-Si). By combining the SERS activity of Ag, the chemical stability of Au and the large field enhancement of 3D-Si, the Au@Ag/3D-Si substrate possesses perfect sensitivity, homogeneity, reproducibility and chemical stability. Using R6G as probe molecule, the SERS results imply that the Au@Ag/3D-Si substrate is superior to the 3D-Si, Ag/3D-Si and Au/3D-Si substrate.

β1 integrin mediates an alternative survival pathway in breast cancer cells resistant to lapatinib.

Introduction: The overexpression of human epidermal growth factor receptor (HER)-2 in 20% of human breast cancers and its association with aggressive growth has led to widespread use of HER2-targeted therapies, such as trastuzumab (T) and lapatinib (L). Despite the success of these drugs, their efficacy is limited in patients whose tumors demonstrate de novo or acquired resistance to treatment. The β1 integrin resides on the membrane of the breast cancer cell, activating several elements of breast tumor progression including proliferation and survival.

Voltammetric behavior of the MCF-7 cell cytoplasm and the effect of taxol on voltammetric response.

The aims of this study were to find the electroactive species in the human breast cancer (MCF-7) cell cytoplasm causing a voltammetric response of the cells and to establish a simple and rapid measurement method to obtain strong and direct electrochemical responses objectively reflecting the cell viability. Ultrasonication was carried out for the electrochemical detection. The presence of guanine and xanthine in the MCF-7 cell eluent secreted by the living cells and in the MCF-7 cell cytoplasm was verified by HPLC assay with a DAD system and chemometric method.

Determination of a hydrophilic paclitaxel derivative, 7-xylosyl-10-deacetylpaclitaxel in rat plasma by LC-MS/MS.

A LC-MS/MS method for the determination of a hydrophilic paclitaxel derivative 7-xylosyl-10-deacetylpaclitaxel in rat plasma was developed to evaluate the pharmacokinetics of 7-xylosyl-10-deacetylpaclitaxel in the rats. 7-Xylosyl-10-deacetylpaclitaxel and docetaxel (IS for 7-xylosyl-10-deacetylpaclitaxel) were extracted from rat plasma with acetic ether and analyzed on a Hypersil C(18 )column (4.6 x 150 mm i.

Development of resistance to targeted therapies transforms the clinically associated molecular profile subtype of breast tumor xenografts.

The effectiveness of therapies targeting specific pathways in breast cancer, such as the estrogen receptor or HER2, is limited because many tumors manifest resistance, either de novo or acquired, during the course of treatment. To investigate molecular mechanisms of resistance, we used two xenograft models of estrogen receptor-positive (ER+) breast cancer, one with and one without HER2 overexpression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the epidermal growth factor receptor tyrosine kinase inhibitor gefitinib (G).

Mechanisms of tumor regression and resistance to estrogen deprivation and fulvestrant in a model of estrogen receptor-positive, HER-2/neu-positive breast cancer.

HER-2/neu in breast cancer is associated with tamoxifen resistance, but little data exist on its interaction with estrogen deprivation or fulvestrant. Here, we used an in vivo xenograft model of estrogen receptor (ER)-positive breast cancer with HER-2/neu overexpression (MCF7/HER-2/neu-18) to investigate mechanisms of growth inhibition and treatment resistance. MCF7/HER-2/neu-18 tumors were growth inhibited by estrogen deprivation and with fulvestrant, but resistance developed in 2 to 3 months.

Advanced concepts in estrogen receptor biology and breast cancer endocrine resistance: implicated role of growth factor signaling and estrogen receptor coregulators.

Estrogen receptor (ER), mediating estrogen-signaling stimuli, is a dominant regulator and a key therapeutic target in breast cancer etiology and progression. Endocrine therapy, blocking the ER pathway, is one of the most important systemic therapies in breast cancer management, but de novo and acquired resistance is still a major clinical problem. New research highlights the role of both genomic and nongenomic ER activities and their intimate molecular crosstalk with growth factor receptor and other signaling kinase pathways in endocrine resistance.

Molecular changes in tamoxifen-resistant breast cancer: relationship between estrogen receptor, HER-2, and p38 mitogen-activated protein kinase.

Purpose: To evaluate growth factor receptor cross talk with the estrogen receptor (ER) in paired clinical breast cancer specimens and in a xenograft model before tamoxifen and at tumor progression as a possible mechanism for tamoxifen resistance.

Methods: Specimen pairs from 39 patients were tissue arrayed and stained for ER, progesterone receptor (PgR), Bcl-2, c-ErbB2 (HER-2), and phosphorylated (p) p38 mitogen-activated protein kinase (MAPK), p-ERK1/2 MAPK, and p-Akt. Xenograft MCF-7 tumors before and after tamoxifen resistance were assessed for levels of p-p38.

Crosstalk between estrogen receptor and growth factor receptor pathways as a cause for endocrine therapy resistance in breast cancer.

Data suggest that breast cancer growth is regulated by coordinated actions of the estrogen receptor (ER) and various growth factor receptor signaling pathways. In tumors with active growth factor receptor signaling (e.g.

Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer.

Background: Patients receiving adjuvant tamoxifen whose tumors express high levels of both HER2/neu (HER2) and the estrogen receptor (ER) coactivator AIB1 often develop tamoxifen resistance. We used a breast cancer model system with high expression of AIB1 and HER2 to investigate the possible mechanisms underlying this resistance.

Methods: MCF-7 breast cancer cells, which express high levels of AIB1, and a tamoxifen-resistant derivative cell line engineered to overexpress HER2 (MCF-7/HER2-18) were treated with estrogen, tamoxifen, epidermal growth factor (EGF), or heregulin in the absence or presence of the EGF receptor (EGFR) tyrosine kinase inhibitor gefitinib.

Cross-talk between estrogen receptor and growth factor pathways as a molecular target for overcoming endocrine resistance.

Introduced more than 100 years ago, endocrine therapy is still the most important systemic therapy for all stages of estrogen receptor (ER) -positive breast tumors. A major clinical problem limiting the usefulness of this therapy is tumor resistance, either de novo or acquired during the course of the treatment. Relatively new discoveries emphasize the complexity of ER signaling and its multiple regulatory interactions with growth factor and other kinase signaling pathways.

Breast cancer endocrine resistance: how growth factor signaling and estrogen receptor coregulators modulate response.

Endocrine therapy, and especially tamoxifen, is the most important systemic treatment of estrogen receptor (ER)-positive breast cancer at all stages. A serious obstacle, however, is intrinsic or acquired resistance to these therapies, which in the case of selective ER modulators, such as tamoxifen, involves some imbalance of their agonist versus antagonist actions. Recent data suggest that levels of both ER coregulatory proteins and extra and intracellular signaling from growth factor-related pathways may be important in adjusting this mixed agonist/antagonist activity of selective ER modulators in resistant breast tumors.

Human Dkk-1, a gene encoding a Wnt antagonist, responds to DNA damage and its overexpression sensitizes brain tumor cells to apoptosis following alkylation damage of DNA.

The human Dkk-1 (hDkk-1) gene, a transcriptional target of the p53 tumor suppressor, encodes a powerful inhibitor of the Wnt signaling pathway and regulates the spatial patterning/morphogenesis of the mammalian central nervous system. We investigated the p53-related functions of the hDkk-1 gene by studying its response to DNA damage and its modulation of apoptosis in human glioma cells. Various chemotherapeutic and other agents that induce DNA adducts and compromise its integrity (1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, H(2)O(2) and UV rays) enhanced the expression of hDkk-1 significantly.