A better experimental method to detect the sensitivity of cancer cells to anticancer drugs after adenovirus-mediated introduction of two kinds of p53 in vivo.

p53 plays an important role in drug responses by regulating cell cycle progression and inducing programmed cell death. The C-terminal of p53 self-regulates the protein negatively; however, whether it affects the sensitivity of cancer cells to anticancer drugs is unclear. In this study, two experimental methods were used to compare the sensitivity to anticancer drugs of human lung 801D cancer cells transfected with adenovirus bearing either full-length p53 or the deleted-C-terminal p53 in vivo.

Polymorphisms in GSTM1, CYP1A1, CYP2E1, and CYP2D6 are associated with susceptibility and chemotherapy response in non-small-cell lung cancer patients.

Background: Studies of polymorphisms in CYP1A1, CYP2E1, CYP2D6, and GSTM1 and their relationship to lung cancer susceptibility and chemotherapy response have been reported, but the results are not consistent. In this study we selected four polymorphisms in these genes, several of which have previously been researched, and investigated their association with lung cancer susceptibility and chemotherapy response.

Methods: We genotyped the four polymorphisms in a cohort composed of 217 non-small-cell lung cancer (NSCLC) patients and 198 controls.

Overexpression of cyclin Y in non-small cell lung cancer is associated with cancer cell proliferation.

Cyclin Y (CCNY) is a key cell cycle regulator that acts as a growth factor sensor to integrate extracellular signals with the cell cycle machinery. The expression status of CCNY in lung cancer and its clinical significance remain unknown. The data indicates that CCNY may be deregulated in non-small cell lung cancer, where it may act to promote cell proliferation.

The study of ginsenoside on PPARgamma expression of mononuclear macrophage in type 2 diabetes.

Peroxisome proliferator-activated receptors (PPARs) are transcriptional factors, which play a key role in modulating glucose and lipid metabolism and in the pathogenesis of atherosclerosis. Ginsenosides are the active components of ginseng, which is a perennial aromatic herb that is widely used in China for medicinal purposes. Some studies have reported that ginsenosides have anti-hyperglycemia and anti-obesity effects that involve the PPAR-mediated pathway.

[Effects of RNA interference of COX-2 gene expression on malignant proliferation of A549 cells in vitro].

Objective: To investigate the inhibition of COX-2 gene expression and its effects on malignant proliferation of human lung adenocarcinoma A549 cells after interfering at different target sites in vitro.

Methods: The 3rd, 7th and 10th exon of COX-2 were selected as the targets and three COX-2 siRNA expression vectors with human U6 promoter were constructed. Three siRNA expression vectors and two vacant vectors were transfected into A549 cells expressing COX-2 with lipofectamine, respectively.

Efficacy of low-dose tamsulosin in chinese patients with symptomatic benign prostatic hyperplasia.

Objective: To determine the efficacy and tolerability of low-dose tamsulosin 0.2 mg/day in Chinese patients with symptomatic benign prostatic hyperplasia (BPH).

Methods: A total of 505 patients were enrolled in a 6-week nonblind, multicentre study, and 499 patients were followed for the entire 6-week treatment period.

[Ectogenous fragile histidine triad gene inhibits the malignant phenotype of human lung cancer cell line A549 in vitro and in vivo].

Objective: To investigate the inhibition effects of fragile histidine triad (FHIT) gene on the malignant growth of A549 cell line.

Methods: A mammalian expression vector PEGFP-FHIT was constructed and transfected into the A549 cell line by lipofectamine. Then the transfected cell line was screened by G418.

[Inhibitory effect of p53 with deletion of c-terminal 356 - 393 amino acids on malignant phenotype of human lung cancer cell line].

Objective: To study the effect of extraneous p53 gene with deletion of c-terminal 356 - 393 amino acids on inhibition of malignant phenotype of human lung cancer cell line.

Methods: Recombinant plasmid pEGFP-p53 (del) with codon deletion of c-terminal 37 amino acids from 393 to 356 region and pEGFP-p53 (wild type) were constructed. The human lung cancer cell line 801D served as a receipt cell had p53 deletion and mutation at 248 codon.