Copy number variations of neurotrophic tyrosine receptor kinase 3 (NTRK3) may predict prognosis of ovarian cancer.

Platinum resistance is a critical barrier for clinicians to improve the survival of ovarian cancer. Our study evaluated the correlation between copy number variations (CNVs) of neurotrophic tyrosine receptor kinase 3 (NTRK3) and the prognosis of ovarian cancer, which might predict platinum resistance in ovarian cancer patients.Array comparative genomic hybridization (CGH) was used to test gene backgrounds between platinum-sensitive and platinum-resistant relapsed populations and CNVs of NTRK3 were indicated by cluster analysis.

MicroRNA-mRNA functional pairs for cisplatin resistance in ovarian cancer cells.

Ovarian cancer is the leading cause of death in women worldwide. Cisplatin is the core of first-line chemotherapy for patients with advanced ovarian cancer. Many patients eventually become resistant to cisplatin, diminishing its therapeutic effect.

[MiR-17-92 in cancer].

MicroRNAs (miRNAs) are a class of short regulatory non-coding RNAs (22-24 nt) widely expressed in living organisms. Shortly after their discovery, microRNAs are found to participate in the development of a variety of diseases. miR-17-92 and its paralog are one of them, recent studies have revealed their critical roles not only in the development of lung, heart, immune system but also in carcinogenesis.

[Effects of survivin siRNA on growth, apoptosis and chemosensitivity of ovarian cancer cells SKOV3/DDP].

Objective: To explore a new approach in gene therapy of ovarian cancer, we used RNAi to inhibit survivin gene expression, and explore the effect of survivin and neu RNAi on growth, apoptosis and chemosensitivity of ovarian cancer cell line SKOV3/DDP cells.

Methods: Expression vector of survivin gene-targeting siRNA was constructed using pSilencer 1.0-U6 vector containing U6 promotor (pSilencer-survivin) and transfected into SKOV3/DDP cells by lipofectamine.

[Establishment of a model to assess the clinical efficacy of Gefitinib in treatment of non-small cell lung cancer].

Objective: To establish a model to predict the clinical response of Gefitinib in non-small cell lung cancer (NSCLC).

Methods: The clinical outcomes of 262 consecutive advanced NSCLC patients to oral treatment of gefitinib 250 mg daily in the past 4 years were reviewed. DNA sequencing was used to detect the mutations in the exons 18, 19, 20, and 21 of the epidermal growth factor receptor (EGFR) tyrosine kinase domain in 55 patients who had enough tumor tissues.

[Current advances in the mechanic studies of human papillomavirus-induced oncogenesis].

Human papillomavirus (HPV) is a common small DNA tumor virus that specifically infects squamous epithelial cells and causes benign or malignant epithelial lesions such as genital warts and cervical cancer. High-risk HPV is detected in specimens of more than 90% of cervical cancer. In the 7.

Amplification and overexpression of Aurora-A in esophageal squamous cell carcinoma.

Aurora-A/BTAK/STK15 gene which encodes a centrosome-associated kinase is located on chromosome 20q13.2, a highly amplified region in various human tumors. Recent studies have demonstrated the overexpression and amplification of Aurora-A in many malignant human cancers.

[Expression of survivin and its significance in esophageal cancer].

Objective: To detect the expression of survivin in esophageal cancer and elucidate its function in esophageal cancer.

Methods: Expression of surviv in was detected in paired normal and tumor tissues from patients with esophageal cancer by semi-quantitative RT-PCR. A dominant-negative survivin (surT34A) was transfected into esophageal cancer EC9706 cells (EC9706surT34A).

Knockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo.

Introduction: Breast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy. For a better understanding of its role in maintaining the malignant phenotype, we used RNA interference (RNAi) directed against c-Myc in our study.

[Suppression of c-myc expression by interference RNA in HepG2 hepatocellular carcinoma cells].

Objective: To study the inhibitory effect of RNA interference (RNAi) on c-myc expression in hepatocellular carcinoma cell line, HepG2.

Methods: Expression vector of c-myc gene-targeting small interference RNA (siRNA) was constructed (psilencer-c-myc) and transfected into HepG2 cells by lipofectamine, and the unloaded vector was used as control (mock). The expression of c-myc mRNA and protein was identified by quantitive PCR and Western blot.

[Indomethacin induces apoptosis through inhibition of survivin regulated by beta-catenin/TCF4 in human colorectal cancer cells].

Background & Objective: Although Wnt pathway plays important role in colorectal carcinogenesis, but the mechanism of this pathway in anti-apoptosis is not clear. This study is to investigate the molecular mechanism of Wnt pathway in anti-apoptosis.

Methods: Survivin promoter region was constructed into luciferase reporter system (pGL3-sur1.

Down-regulation of gamma-synuclein in human esophageal squamous cell carcinoma.

Aim: To investigate gene expression pattern of human gamma-synuclein gene in human esophageal squamous cell carcinoma (ESCC) by using semi-quantitive reverse transcription polymerase chain reaction (RT-PCR), and to study the role of gamma-synuclein in the development of human ESCC.

Methods: Semi-quantitive RT-PCR of 27 pairs of specimens of human ESCC tissues and corresponding normal tissues was used to investigate the expression pattern of gamma-synuclein in ESCC. 9706/gamma-syn cells in which gamma-synuclein was overexpressed were obtained through cloning gamma-synuclein gene by PCR and transfecting it into ESCC 9706 cells, then selecting with G-418 for 14 days.

Detection of human papillomavirus in Chinese esophageal squamous cell carcinoma and its adjacent normal epithelium.

Aim: To investigate the putative role of human papillomavirus (HPV) infection in the carcinogenesis of esophageal squamous cell carcinoma in China.

Methods: Twenty-three esophageal squamous cell carcinoma samples and the distal normal epithelium from Shanxi Province, and 25 more esophageal squamous cell carcinoma samples from Anyang city, two areas with a high incidence of esophageal cancer in China, were detected for the existence of HPV-16 DNA by PCR, mRNA in situ hybridization (ISH) and immunohistochemistry (IHC) targeting HPV-16 E6 gene.

Results: There were approximately 64 % (31/48) patients having HPV-16 DNA in tumor samples, among them nearly two-thirds (19/31) samples were detected with mRNA expression of HPV-16 E6.

[Survivin mutants reverse the malignancy of HeLa cells].

Background & Objective: Survivin was aberrantly expressed in most cancer tissues, suggesting that survivin plays an important role in carcinogenesis. This study was designed to investigate the function and mechanism of survivin mutants in tumor cells.

Methods: The site-mutant and truncated survivin mutants were transfected into HeLa cells and selected using G418.

[Expression and significance of beta-catenin in esophageal carcinoma].

Background & Objective: Many reports have characterized the aberrant expression of beta-catenin in diverse types of human cancer. To determine whether beta-catenin has possible roles in esophageal carcinogensis, we designed this study to detect the expression pattern of beta-catenin in normal esophageal epithelium and esophageal cancer tissue, then to study the relevance of its expression and localization to tumor differetiation degree and lymph node metastasis.

Methods: By using immunohistochemical staining(SP method), the expression of beta-catenin was detected in 22 normal esophageal tissue slides and 52 esophageal carcinomas.