Cell Line, Tumor ; Enzyme Inhibitors ; pharmacology ; Heterocyclic Compounds, 1-Ring ; pharmacology ; Humans ; Proteasome Endopeptidase Complex ; drug effects

OBJECTIVETo explore the changes of peripheral blood lymphocyte subsets in patients with acute hydrogen chloride gas poisoning.

METHODSWhen the patients were admitted or on the secondary day, the percentages of total T-cell lymphocyte subsets (CD(3)(+)CD(19)(-)), CD(4)(+)T cells (CD(3)(+)CD(4)(+)), CD(8)(+)T cells (CD(3)(+)CD(8)(+)), B cells (CD(3)(-)CD(19)(+)) and NK cells (CD(3)(-)CD(16)(+)CD(56)(+)), and the ration of CD(4)(+)/CD(8)(+) in 37 cases with acute hydrogen chloride gas poisoning and 49 healthy controls were detected with flow cytometer.

RESULTSThe total T-cell percentage and total CD(4)(+)T cell percentage in 37 cases were significantly lower than those in 47 controls (P < 0.05). The percentages of NK cells and B lymphocytes in 37 cases significantly increased, as compared with controls (P < 0.05). The ration of CD(4)(+)/CD(8)(+) in 37 cases significantly decreased, as compared with controls (P < 0.05).

CONCLUSIONThe lymphocyte subsets in the patients with acute hydrogen chloride gas poisoning changed, which could influence the immune function of patients.

Adolescent ; Adult ; Case-Control Studies ; Female ; Gas Poisoning ; blood ; Humans ; Hydrochloric Acid ; poisoning ; Lymphocyte Count ; Lymphocyte Subsets ; cytology ; Male ; Middle Aged ; Young Adult

OBJECTIVETo evaluate the prognostic significance of various clinicopathologic parameters in gastrointestinal stromal tumor (GIST), and to study the frequency of c-kit exon 11 mutations in this tumor.

METHODSOne hundred and fifty-six cases of gastric or small intestinal GIST were retrieved from the archival files of the Department of Pathology, Chinese PLA General Hospital. The clinical features, site of occurrence, tumor diameter, mitotic index, coagulative tumor necrosis, and risk grade were studied and analyzed statistically. Tumor DNA was extracted and c-kit exon 11 was amplified. Upon detection by denaturing high-performance liquid chromatography, the amplified exon 11 was sequenced.

RESULTSFor the 83 cases of gastric GIST studied, the mean age of patients was 55.4 years. Follow-up information was available in 62 cases, with 17 cases having local recurrence or distant metastasis. The 5-year survival rate was 66.5% +/- 17.1%. For the 73 cases of small intestinal GIST studied, the mean age of patients was 50.6 years. Follow-up information was available in 43 cases, with 22 cases having local recurrence or distant metastasis. The 5-year survival rate was 61.8% +/- 18.3%. In general, for gastric GIST, age younger than 50 years (P = 0.046), advanced clinical stage (P = 0.0001), large tumor size (P = 0.0001), high mitotic index (P = 0.0001), presence of coagulative tumor necrosis (P = 0.0001), and high risk grade (P = 0.004) were associated with lower survival rate. COX hazard proportional model revealed that advanced clinical stage (P = 0.001), large tumor size (P = 0.001), high mitotic index (P = 0.002) and high risk grade (P = 0.018) indicated worse prognosi. For small intestinal GIST, advanced clinical stage (P = 0.010) and presence of coagulative tumor necrosis (P = 0.036) were associated with lower survival rate. Advanced clinical stage was an independent prognostic factor. A total of 25 cases harbored c-kit mutations. The frequency of c-kit mutations was 32% and 22.5% for gastric and small intestinal GIST respectively. For gastric GIST, c-kit mutations occurred mainly in patients older than 50 years. In contrast, c-kit mutations in small intestinal GIST occurred in the age group of 40 to 49 years.

CONCLUSIONSFor gastric GIST, advanced clinical stage, tumor diameter, mitotic index and risk grade are the main prognostic indicators. For small intestinal GIST, advanced clinical stage and presence of coagulative tumor necrosis indicate poor prognosis. In general, small intestinal GIST is more frequently associated with metastasis and tumor relapse than gastric GIST. The occurrence of c-kit mutations also correlates with age of patients.

Adolescent ; Adult ; Age Factors ; Aged ; Aged, 80 and over ; Bone Neoplasms ; secondary ; DNA, Neoplasm ; genetics ; Disease-Free Survival ; Exons ; Female ; Follow-Up Studies ; Gastrointestinal Stromal Tumors ; genetics ; pathology ; Humans ; Liver Neoplasms ; secondary ; Male ; Middle Aged ; Mutation ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Proportional Hazards Models ; Proto-Oncogene Proteins c-kit ; genetics ; Survival Rate ; Tumor Burden ; Young Adult

OBJECTIVETo determine the predictive value of excision repair cross complementation group 1 (ERCC1),ribonucleotide reductase subunit M1 (RRM1), and β-tubulin 3 expressions in postoperative patients with stage 1- 3 non-small cell lung cancer (NSCLC) receiving adjuvant chemotherapy.

METHODSAll NSCLC patients received surgery therapy followed by at least one cycle of adjuvant chemotherapy in our hospital from January 2004 to December 2007. The expressions of ERCC1, RRM1, and β-tubulin 3 were detected by immunohistochemical methods. The relationships among clinicopathologic characteristics, chemotherapy regimens,biomarkers' expressions and disease-free survival (DFS) were analyzed.

RESULTSThe high-expression rates of ERCC1, RRM1, and β-tubulin 3 were 36.4%,43.7%,and 38.4%,respectively. The expressions of these three biomarkers were not correlated. After a median follow-up of 35.8 months, 80 patients experienced metastatic or recurrent tumors and 40 patients died. The median overall survival was not reached and the median DFS was 24.1 months. Univariate survival analysis showed that sex, clinical stage,and adenocarcinoma or not were related to DFS, while age, smoke history, chemotherapy regimens, and expression levels of ERCC1, RRM1, and β-tubulin 3 has no prognostic significance in these surgically resected NSCLC patients who were receiving adjuvant chemotherapy. Male (P=0.036), earlier clinical stage (P=0.001), and non-adenocarcinoma (P=0.004) predicted better DFS. Stratified analysis indicated that in RRM1 high-expression strata,the regimens with gemcitabine had curtailed DFS compared with other regimens (P=0.054); in β-tubulin 3 high-expression strata,the regimens containing taxane (including paclitaxel and docetaxel subgroups) had curtailed DFS compared with other regimens (P=0.076), although there was no statistical significance. However,there were no similar predictive significance in RRM1 and β-tubulin 3 low-expression strata or in ERCC1 strata with different expression levels. COX proportional regression analysis showed that adenocarcinoma or not and clinical stage were independent risk factors of DFS in this population.

CONCLUSIONSIn postoperative NSCLC patients who are receiving adjuvant chemotherapy, patients with high expression of RRM1 tends to be resistant to gemcitabine and patients with high expression of β-tubulin 3 tends to be resistant to taxane drugs. ERCC1, RRM1, and β-tubulin 3 detected by immunohistochemistry can be biomarkers to help to choose better chemotherapy regimen and predict the effectiveness of adjuvant chemotherapy.

Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; metabolism ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; metabolism ; Chemotherapy, Adjuvant ; DNA-Binding Proteins ; metabolism ; Endonucleases ; metabolism ; Female ; Follow-Up Studies ; Humans ; Lung Neoplasms ; drug therapy ; metabolism ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Treatment Outcome ; Tubulin ; metabolism ; Tumor Suppressor Proteins ; metabolism

OBJECTIVETo investigate the relationship between KRAS gene mutations and clinicopathological parameters in patients with colorectal carcinoma (CRC).

METHODSPCR-based direct sequencing was used to detect the mutations of KRAS gene and to correlate between clinicopathological characteristics and the presence of various KRAS mutations in 244 cases of CRC.

RESULTSKRAS mutations were identified in 92 cases (37.7%) of CRC. Five types of mutation were detected at codon 12, including G12D (40 cases, 16.4%), G12V (16 cases, 6.6%), G12A (7 cases, 2.9%), G12S (5 cases, 2.0%) and G12C (4 cases, 1.6%). Two types of mutation were detected at codon 13, including G13D (17 cases, 7.0%) and G13C (2 cases, 0.8%). One type of mutation was detected in codon 61, i.e. Q61K (1 case, 0.4%). KRAS mutation rate was higher in females (45.6%, 36/79) than in males (32.1%, 53/165; P < 0.05), but not related to another clinicopathological characteristics.

CONCLUSIONSFemale CRC patients have a higher KRAS mutation rate than the male patients. KRAS mutation has no significant correlation with patient's age, tumor site, tumor gross appearance, degree of differentiation, depth of invasion, TNM stages, lymphatic invasion, abdominal or distant metastases and prognosis in this study.

Adult ; Aged ; Aged, 80 and over ; Codon ; Colorectal Neoplasms ; genetics ; pathology ; surgery ; Female ; Genotype ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Mutation ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Polymerase Chain Reaction ; methods ; Proto-Oncogene Proteins ; genetics ; Proto-Oncogene Proteins p21(ras) ; Sequence Analysis, DNA ; Sex Factors ; Survival Rate ; Young Adult ; ras Proteins ; genetics

OBJECTIVETo evaluate the effect of cluster of differentiation 14 (CD-14) and Toll like receptors (TLR) on the expression of interleukin-6 (IL-6) mRNA induced by Porphyromonas endodontalis (Pe) lipopolysaccharides (LPS).

METHODSMC3T3-E1 cells were treated with 10 mg/L Pe-LPS for different hours, and the cells uninvolved by anything as the blank group. The expression of IL-6 was detected by reverse transcription polymerse chain reaction (RT-PCR) and enzyme-liked immunosorbent assay (ELISA). The expression of CD-14, TLR-2 and TLR-4 mRNA was observed at different time point (0 - 24 h) by RT-PCR. The protein of CD-14, TLR-2 and TLR-4 was analyzed with a flow cytometer. MC3T3-E1 cells were pretreated with anti-CD-14, anti-TLR-2 and anti-TLR-4 antibody for 1 h, and then cells were stimulated with 10 mg/L Pe-LPS for 6 h. The expression of IL-6 mRNA was examined by RT-PCR. Statistical analysis was performed using one-way ANOVA Dunnett-t test with SPSS 11.0 software package.

RESULTSThe IL-6 mRNA and proteins increased significantly after treatment with Pe-LPS. When MC3T3-E1 cells treated by Pe-LPS for 6 h, the expression of proteins soared from (11.696 ± 0.672) ng/L to (36.534 ± 0.574) ng/L (P < 0.01); In the control group, the CD-14 and TLR-4 mRNA are ambly-expression, and the ratios of CD-14 and TLR-4 positive cells were (39.038 ± 3.131)% and (11.438 ± 0.385)% respectively in MC3T3-E1. After treatment by Pe-LPS, the expression of CD-14 and TLR-4 mRNA increased significantly, and the ratios of CD-14 and TLR-4 positive cells markedly increased to (62.407 ± 1.800)% and (21.367 ± 2.271)%. TLR-2 expression did not change apparently after Pe-LPS treatment. The expression of IL-6 mRNA was partly inhibited by anti-CD-14 or anti-TLR-4 antibody, but not by TLR-2.

CONCLUSIONSPe-LPS can induce the expression of IL-6 in osteoblast MC3T3-E1 through CD-14 and TLR-4, but not TLR-2.

3T3 Cells ; Animals ; Antibodies ; immunology ; Interleukin-6 ; genetics ; metabolism ; Lipopolysaccharide Receptors ; genetics ; metabolism ; Lipopolysaccharides ; isolation & purification ; pharmacology ; Mice ; Porphyromonas endodontalis ; RNA, Messenger ; metabolism ; Toll-Like Receptor 2 ; genetics ; metabolism ; Toll-Like Receptor 4 ; genetics ; metabolism

OBJECTIVETo investigate the time trends of cancer mortality among residents in Kaifeng county, Henan province.

METHODSData on cancer mortality from the vital registration system in Kaifeng county from 1988 to 2005 was analyzed. A total of 9543 death records (5974 males and 3567 females) due to malignant tumors were studied. A two-year-period age-specified standardized mortality rates were directly adjusted by the world standard population, and the annual percentage change (APC) of mortality were estimated by a linear logarithm regression.

RESULTSThe crude cancer death rate for male was 95.09/100,000 and its age-standardized death rate was 117.41/100,000. While, the crude cancer death rate for female was 59.13/100,000 and the age-standardized death rate was 57.15/100,000. There was a significant growth tread for lung cancer (APC: 6.54%), liver cancer (5.07%) in males and breast cancer (7.04%) in females in the groups aged over 18. On the contrary, the decreasing treads for esophageal cancer in both of sexes (-7.09%, -13.53%) were also observed in this study. Meanwhile, there was no other significant changes in the trend, either in the tumor sites or mortality, was observed.

CONCLUSIONIn the past two decades, there has been a significant increasing trend for cancer mortality in Kaifeng county, of Henan Province. Hence, it is necessary to enhance epidemiological survey to identify risk factors at the earlier stages.

China ; epidemiology ; Death Certificates ; Female ; Humans ; Male ; Mortality ; trends ; Neoplasms ; mortality ; Rural Population

OBJECTIVETo investigate the clinicopathological significance of chromosome 17 polysomy in breast cancer.

METHODSRetrospective study of 200 cases of breast cancer including 106 cases of invasive ductal carcinoma and 94 cases of in-situ carcinoma was performed by fluorescence in-situ hybridization (FISH) to explore the relationship between chromosome 17 polysomy and age, nuclear atypia, lymphatic metastasis, HER2 gene amplification and HER2 protein expression.

RESULTSTwenty-six percent (52/200) of chromosome 17 polysomy was detected in 200 cases of breast ductal carcinoma, all of which were invasive ductal carcinoma. Overall 52. 8% (52/180) of invasive ductal carcinoma cases showed chromosome 17 polysomy, which was correlated to HER2 gene amplification (P = 0.000) and HER-2 protein expression (P=0.000), and to HER2 expression combined with HER2 gene amplification (P=0.001). Chromosome 17 polysomy with or without HER2 gene amplification was also associated with high-grade nuclear atypia (P = 0.012 or P = 0.010) and lymphatic metastasis (P = 0.002 or P = 0.009 ). However, chromosome 17 polysomy with or without HER2 gene amplification was not correlative with the age of patients (P = 1. 000 or P = 0. 415).

CONCLUSIONChromosome 17 polysomy may be related to the nuclear atypia, metastasis, HER2 gene amplification of invasive ductal carcinoma and thus a worse prognosis of the patients.

Breast Neoplasms ; genetics ; pathology ; Carcinoma, Ductal ; genetics ; Chromosome Aberrations ; Chromosomes, Human, Pair 17 ; genetics ; Gene Amplification ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; genetics ; Genes, erbB-2 ; genetics ; Humans

OBJECTIVETo study the feasibility of diagnosing of human papillomavirus (HPV) infection in paraffin-embedded cervical tissues by high-throughput gene chip technology and its clinical significance.

METHODSForty cases of HPV-related cervical lesions, including 18 cases of invasive squamous cell carcinoma, 12 cases of cervical intraepithelial neoplasia (CIN) III, 6 cases of CIN II and 4 cases of CIN I, were enrolled. DNA was extracted from paraffin-embedded tissues and amplified by polymerase chain reaction (PCR) using HPV DNA primers. The PCR products were then reversely hybridized with gene chip technology. The results were compared with that of in-situ hybridization (ISH).

RESULTSAll of the 18 cases of cervical squamous cell carcinoma were positive for high-risk HPV genotypes (with 1 case showing a mixture with low-risk genotypes). In contrast, 11 cases (91.7%) of CIN III, 5 cases (83%) of CIN II and none of the CIN I cases were positive for high-risk HPV genotypes. On the other hand, low-risk HPV genotypes were detected only in 1 case (17%) of CIN II and 2 cases (50%) of CIN I. The difference between the two groups (CIN III/squamous cell carcinoma versus CIN I/CIN II) was statistically significant (U = 80.0, P < 0.01). Among the 10 squamous carcinoma cases positive for HPV types 16 and 18 by gene chip technology, high-risk HPV DNA was also detected in 6 of them when using in-situ hybridization.

CONCLUSIONSGene chip technology is able to detect multiple HPV genotypes in paraffin-embedded tissues with high sensitivity and specificity. The distinction between low and high-risk HPV genotypes is seemed useful in prevention and management of cervical cancer.

Alphapapillomavirus ; genetics ; Carcinoma, Squamous Cell ; virology ; Cervical Intraepithelial Neoplasia ; diagnosis ; virology ; Cervix Uteri ; pathology ; virology ; DNA, Viral ; analysis ; Female ; Genotype ; Human papillomavirus 16 ; genetics ; Human papillomavirus 18 ; genetics ; Humans ; Oligonucleotide Array Sequence Analysis ; methods ; Papillomavirus Infections ; diagnosis ; virology ; Paraffin Embedding ; Polymerase Chain Reaction ; methods ; Uterine Cervical Neoplasms ; diagnosis ; virology

OBJECTIVETo observe the prophylactic effect of curcumin on hepatic fibrosis and the number, location, apoptosis of activated hepatic stellate cells (HSCs) in the livers and to discuss the relationship between the prophylactic effects and activated HSC.

METHODSA rat model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride. Curcumin doses of 5 mg, 10 mg, 20 mg per 100 gram per 100g of body weight were given to three groups of the model rats. No curcumin was given to one group of the model rats and it served as the control. After eight weeks, all rats were sacrificed and their left liver lobes were examined histopathologically with H.E and Masson stainings. Grades of hepatic fibrosis were evaluated according to the SSS system. Activated HSC was detected by the alpha-SMA immunohistochemistry staining. HSC apoptosis was detected by double-stainings of terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and desmin immunohistochemistry staining.

RESULTSDegrees (SSS system scores) of hepatic fibrosis in the curcumin groups were all less severe in comparison with those of the control group. Activated HSCs in the livers of the rats of the control group increased significantly compared with that of the treatment groups, and also fewer apoptotic HSCs were detected in the control group. On the contrary, fewer activated HSCs and more apoptotic HSCs were detected in the curcumin groups compared with those of the control group. The degrees of the effects were curcumin dose-dependent.

CONCLUSIONSCurcumin can prevent hepatic fibrosis. It can inhibit activation and proliferation of HSCs and induce HSCs apoptosis, which may be the mechanism(s) contributing to the prophylactic effects of curcumin on hepatic fibrosis.

Animals ; Apoptosis ; drug effects ; Carbon Tetrachloride ; Carbon Tetrachloride Poisoning ; Curcumin ; therapeutic use ; Enzyme Inhibitors ; therapeutic use ; Hepatocytes ; pathology ; Liver Cirrhosis, Experimental ; pathology ; prevention & control ; Rats ; Rats, Sprague-Dawley