Fascin and CK4 as biomarkers for esophageal squamous cell carcinoma.

Background: Several studies have suggested that fascin, cytokeratin 14 and cytokeratin 4 may have significant roles as biomarkers for the progression and survival of esophageal squamous cell carcinoma (ESCC).

Materials And Methods: This study performed immunohistochemistry in tissue microarrays, profiling premalignant lesions and invasive tumors.

Results: Fascin increased across the following states as follows: normal-appearing epithelium (26%) to dysplasia (46%) to ESCC (68%), while CK4 was undetectable in ESCC (0%) compared to normal-appearing epithelium (45%) or dysplasia (41%).

Global gene expression profiling and validation in esophageal squamous cell carcinoma and its association with clinical phenotypes.

Purpose: Esophageal squamous cell carcinoma (ESCC) is an aggressive tumor with poor prognosis. Understanding molecular changes in ESCC will enable identification of molecular subtypes and provide potential targets for early detection and therapy.

Experimental Design: We followed up a previous array study with additional discovery and confirmatory studies in new ESCC cases by using alternative methods.

[A comparative study on the risks of esophagus-cancer patients among factors as blood relatives, paternal line, matriarchal and different sex].

Objective: In order to provide new clues on the cause of esophagus-cancer through seeking for information among the relatives of esophagus-cancer-patients at high-risk, contrast analysis was carried out to compare the ORs between esophagus-cancer cases and the relatives of the patients.

Methods: Case-control study was adopted on 720 cases and 720 controls who were kin relatives of the patients.

Results: (1) Risk of the relatives to the esophagus-cancer-patient group (1.

[Studies on hereditary epidemiology of cardia cancer in Shanxi province.].

Objective: Studies on cardia-cancer caused by hereditary factors.

Methods: Case-control method was adopted, with information including name, sex, date of birth, date of death of all the I, II, III relatives of the patients, diagnosis and the treatment collected. The hereditary probability of cardia cancer and the separation degree were calculated by Falconer and Li-Mentel-Gart.

Biomarkers of apoptosis and survival in esophageal squamous cell carcinoma.

Background: Cancer of the esophagus is a deadly malignancy, and development of biomarkers that predict survival is an urgent need. The apoptotic pathways have been hypothesized as important in progression of esophageal squamous cell carcinoma (ESCC). We investigated a panel of proteins that regulate apoptosis as candidate of biomarkers of prognosis in ESCC.

Genomic characterization of esophageal squamous cell carcinoma from a high-risk population in China.

Genomic instability plays an important role in most human cancers. To characterize genomic instability in esophageal squamous cell carcinoma (ESCC), we examined loss of heterozygosity (LOH), copy number (CN) loss, CN gain, and gene expression using the Affymetrix GeneChip Human Mapping 500K (n = 30 cases) and Human U133A (n = 17 cases) arrays in ESCC cases from a high-risk region of China. We found that genomic instability measures varied widely among cases and separated them into two groups: a high-frequency instability group (two-thirds of all cases with one or more instability category of > or =10%) and a low-frequency instability group (one-third of cases with instability of <10%).

[Testosterone induces different-featured prostate hyperplasia in castrated and uncastrated mice].

Objective: To study the different features of hyperplasia in castrated and uncastrated mice after testosterone (T) treatment.

Methods: Forty-eight BALB/c mice were randomly divided into 6 groups of 8 in each: castrated (A), uncastrated (B) , castrated + low T (C), uncastrated + low T (D), castrated + high T (E), uncastrated + high T (F). Groups C and D were treated with testosterone solution at the dose of 12.

COX-2 (PTGS2) gene methylation in epithelial, subepithelial lymphocyte and stromal tissue compartments in a spectrum of esophageal squamous neoplasia.

Background: Previous studies have shown important effects of stromal elements in carcinogenesis. To explore the tumor-stromal relationship in esophageal neoplasia, we examined methylation of COX-2 (PTGS2), a gene etiologically associated with the development of gastrointestinal cancers, in adjacent foci of epithelium, subepithelial lymphocytes and non-lymphocytic stromal cells found in sections of normal squamous epithelium, squamous dysplasia and invasive esophageal squamous cell carcinoma.

Methods: Adjacent foci of epithelium, subepithelial lymphocytic aggregates and non-lymphocytic stromal tissues were laser microdissected from six fully embedded, ethanol fixed, esophagectomy samples from Shanxi, China, a high-risk region for esophageal cancer.

Overexpression of CDC25B and LAMC2 mRNA and protein in esophageal squamous cell carcinomas and premalignant lesions in subjects from a high-risk population in China.

Molecular events associated with the initiation and progression of esophageal squamous cell carcinoma (ESCC) remain poorly understood but likely hold the key to effective early detection approaches for this almost invariably fatal cancer. CDC25B and LAMC2 are two promising early detection candidates emerging from new molecular studies of ESCC. To further elucidate the role of these two genes in esophageal carcinogenesis, we did a series of studies to (a) confirm RNA overexpression, (b) establish the prevalence of protein overexpression, (c) relate protein overexpression to survival, and (d) explore their potential as early detection biomarkers.

[Expression of GLUT-1, p63 and DNA-Pkcs in serous ovarian tumors and their significance].

Objective: To investigate the expression of GLUT1, p63 and DNA-Pkcs in serous ovarian tumors and their significance.

Methods: GTUL1, p63 and DNA-Pkcs expression at protein level was detected by immunohistochemistry in patients with serous ovarian tumors. Chi-square analysis was used to assess if their expression is associated with clinicopathologic characteristics of the tumors.

[Expression and significance of GLUT-1 and DNA-PKcs in serous ovarian tumors].

Background & Objective: Cancer cell growth is supported by glucose metabolism of glucose transporter protein 1 (GLUT-1). In addition, the participation of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) in genome damage-repairing is important for oncogenesis prevention. This study was to evaluate the expression and biologic significance of GLUT-1 and DNA-PKcs in serous ovarian tumors.

Genome-wide loss of heterozygosity and copy number alteration in esophageal squamous cell carcinoma using the Affymetrix GeneChip Mapping 10 K array.

Background: Esophageal squamous cell carcinoma (ESCC) is a common malignancy worldwide. Comprehensive genomic characterization of ESCC will further our understanding of the carcinogenesis process in this disease.

Results: Genome-wide detection of chromosomal changes was performed using the Affymetrix GeneChip 10 K single nucleotide polymorphism (SNP) array, including loss of heterozygosity (LOH) and copy number alterations (CNA), for 26 pairs of matched germ-line and micro-dissected tumor DNA samples.

A multiplex tissue immunoblotting assay for proteomic profiling: a pilot study of the normal to tumor transition of esophageal squamous cell carcinoma.

Esophageal cancer remains a highly lethal malignancy for which the genetic and proteomic events are poorly understood. Studies have reported dysregulated proteins in esophageal carcinoma; however, the magnitude of these changes remains largely uncharacterized. Little is known about alterations early in the neoplastic pathway.

p16, MGMT, RARbeta2, CLDN3, CRBP and MT1G gene methylation in esophageal squamous cell carcinoma and its precursor lesions.

Esophageal squamous cell carcinoma (ESCC) is a common cancer with a very poor prognosis. New methods are needed to screen high-risk populations and identify curable tumors and precursor lesions early. Molecular markers may be useful in such screening efforts.

[Loss of heterozygosity in esophageal squamous cell carcinoma and its precursor lesion].

Objective: To detect the loss of heterozygosity (LOH) in esophageal squamous cell carcinoma and adjacent high-grade squamous dysplasia, and to evaluate possible tumor suppressor genes in the development and progression of invasive malignancy.

Methods: LOH was detected in normal esophageal mucosa, high grade squamous dysplasia and esophageal squamous cell carcinoma using microdissection and polymerase chain reaction technology. The changes of LOH at seven microsatellite markers and the relationship between LOH rate and clinicopathologic parameters were analyzed.

Gene expression analysis of esophageal squamous cell carcinoma reveals consistent molecular profiles related to a family history of upper gastrointestinal cancer.

Tumor and matched normal tissue from 19 esophageal squamous cell carcinoma patients from a high-risk area of China were analyzed with 7680 gene cDNA microarrays. Forty-one genes were differentially expressed (P < 0.001; >/==" BORDER="0">2-fold change) between tumor and matched normal samples (13 overexpressed and 28 underexpressed).

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.

[Serum level and expression of vascular epithelial growth factor in ovarian epithelial carcinoma].

Background & Objective: This study was designed to examine the level of serum vascular epithelial growth factor (VEGF) and VEGF expression in the patients with ovarian epithelial carcinoma (EOC) and to evaluate the relationship between VEGF and the clinicopathological factors.

Methods: Seventy-three patients with ovarian epithelial tumor were selected as study group, including 24 benign epithelial ovarian tumor (BET), 7 borderline epithelial ovarian tumor (BOT), 42 EOC. Twenty women without obvious gynecologic diseases were selected as serum control group (CON).

Microsatellite alterations in esophageal dysplasia and squamous cell carcinoma from laser capture microdissected endoscopic biopsies.

Esophageal squamous cell carcinoma (ESCC), with a 5 year survival below 15%, is one of the most common fatal cancers worldwide. Significant reduction in mortality may be achieved by detecting and treating asymptomatic precursor lesions and curable early cancers. To explore this possibility and look for potential early detection markers, we examined alterations in 16 microsatellite markers in laser capture microdissected (LCM) endoscopic biopsies from the esophagus, including 15 dysplasias and 22 ESCCs, in patients from Shanxi Province, a region in north-central China.

[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.

Infrequent mutation in the BRCA2 gene in esophageal squamous cell carcinoma.

Purpose: Previous studies have shown a high rate of allelic loss in esophageal squamous cell carcinoma (ESCC) in the vicinity of the BRCA2 gene. We aimed to assess whether the tumor suppressor gene BRCA2 was the inactivation target for allelic loss observed on chromosome 13q in ESCC.

Experimental Design: We examined the entire coding sequence of the BRCA2 gene for mutations using single-strand conformation polymorphism analysis and DNA sequencing in 56 ESCC patients from Shanxi, China.