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ABSTRACT: Sterigmatocystin (ST), a mycotoxin commonly found in foodstuff and feedstuff, has been shown to be a carcinogenic mycotoxin in animal models. Many studies showed that the high level of ST contamination in grains might be related to the high incidence of gastric carcinoma in rural areas of China. However, up to now, the potential effects of ST on human gastric epithelium cells remain largely unknown. In this study, we explored the effects of ST on cell-cycle distribution and the regulatory mechanism in immortalized human gastric epithelium cells (GES-1).
The effects of ST on the cell cycle distribution of GES-1 cells were determined with flow cytometric (FCM) analysis, Giemsa staining and immunofluorescence staining, while that on the expression of related gene-Cdc25C, Cdc2, CyclinB1 and the complex of CyclinB1-Cdc2 were studied with Western blot, reverse transcription polymerase chain reaction (RT-PCR) and immunoprecipitation assay respectively. We found that ST induced GES-1 cells arrested at G2 phase by regulating the expression of Cdc25C, Cdc2, CyclinB1 and the formation of CyclinB1-Cdc2 complex. Further study suggested JNK, ERK and PI3K/AKT/mTOR pathways to be involved in the process of G2 arrest induced by ST. The specific inhibitors of JNK and ERK reversed the role of ST, whereas that of PI3K/AKT/mTOR reinforced the effect of ST on cell-cycle distribution.
This study demonstrates that JNK, ERK and PI3K/AKT/mTOR pathways participated in the G2 arrest induced by ST through the deregulation of CyclinB1, Cdc2 and Cdc25C. It may play some roles in the gastric carcinogenesis in ST exposure populations.
Molecular Nutrition & Food Research 02/2011; 55(5):749-60. · 4.30 Impact Factor
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ABSTRACT: To evaluate the expression of vascular endothelial growth factor C (VEGF-C) and peroxisome proliferators-activated receptors (PPARgamma) in extrahepatic cholangioadenocarcinoma (EHCAC) and to elucidate its correlation with clinicopathological factors and their significance in prognosis.
The expressions of PPARgamma and VEGF-C were detected by immunohistochemistry in 69 cases of EHCAC, 12 cases of non-tumor bile duct epithelium, and their relationship to clinicopathological parameters and follow-up were analyzed.
The positive rate of PPARgamma expression in 69 cases of EHCAC was 59.4%, significantly higher than that in 12 cases of non-tumor bile duct epithelium (0%), (P < 0.01). The positive rate of VEGF-C in 69 cases of EHCAC was 84.1%, also significantly higher than 16.7% in 12 cases of benign bile duct epithelium (P < 0.05). PPARgamma expression was associated with clinical TNM stage and lymph node metastasis. VEGF-C expression was associated with lymph node metastasis. Cox analysis results showed that portal vein and/or hepatic artery invasion, lymph node metastasis and VEGF-C expression were independent prognostic factors of EHCAC (P < 0.05).
PPARgamma expression may play an important role during tumorigenesis of extrahepatic cholangioadenocarcinoma. The expressions of PPARgamma and VEGF-C are significantly correlated with the clinicopathological characteristics and biological behavior of EHCAC. Expression of VEGF-C is an independent prognosis factors in EHCAC. The detection of PPARgamma and VEGF-C is valuable for evaluation of prognosis of EHCAC.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 10/2009; 31(10):773-7.
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ABSTRACT: To investigate the variation in expression of ARHI, STAT3 and E2F1 and the correlation among them during carcinogenesis of ovarian serous carcinoma.
Immunohistochemical staining was used to detect the expression of ARHI, STAT3 and E2F1 in samples of 25 normal ovaries, 35 ovarian serous cystadenomas, 18 borderline serous cystadenomas and 56 ovarian serous carcinomas. The variation in expression of the three genes and relationship among them were analyzed.
ARHI expression was detected in 22 of 25 (88.0%) normal ovaries and 30 of 35 (85.7%) cystadenomas, but only in 10 of 18 (55.6%) borderline serous cystadenomas and 22 of 56 (39.3%) ovarian serous carcinomas, significantly lower than that in the normal ovaries and ovarian serous cystadenomas (P < 0.05). STAT3 expression was found in 14 of 18 (77.8%) borderline serous cystadenomas and 49 of 56 (87.5%) ovarian serous carcinomas, significantly higher than that in the normal ovaries and ovarian serous cystadenomas (P < 0.05). To compare with E2F1 expression in the normal ovaries, serous cystadenomas and borderline serous cystadenomas, E2F1 expression in 46 of 56 (82.1%) ovarian serous carcinomas was significantly higher (P < 0.05). It was found that the expression of ARHI was inversely correlated with that of STAT3 and E2F1.
Our findings indicate that ARHI expression is down-regulated, but STAT3 and E2F1 expressions are up-regulated, with an inverse correlation between ARHI and STAT3 in the carcinogenesis of ovarian serous carcinoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 01/2009; 30(12):905-9.
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ABSTRACT: To investigate the relationship of ezrin protein expression to the carcinogenesis and prognosis of infiltrating breast ductal carcinoma.
S-P immunohistochemical staining was used to detect the ezrin protein expression in 88 patients with infiltrating ductal carcinoma, and in 54 patients with intraductal hyperplastic lesions of the breast. The clinicopathological data and follow-up information of these patients were all obtained. The relationship of ezrin protein expression to the clinicopathological parameters and the prognostic significance in the infiltrating breast ductal carcinoma was analyzed using Chi-square test (chi2), Kaplan-Meier and Cox models.
The immunohistochemical staining results showed that the strong positive expression rate of ezrin protein in the normal ductal epithelium, simple ductal hyperplasia, atypical hyperplasia and infiltrating ductal carcinoma of the breast was 9.1%, 16.7%, 43.3% and 64.8%, respectively, which was significantly higher in atypical hyperplasia and infiltrating ductal carcinoma than that in the normal ductal epithelium and simple ductal hyperplasia (P < 0.05). The strong ezrin protein expression in the infiltrating ductal carcinoma was positively correlated with axillary lymph node metastasis, histological differentiation grade, TNM stage and CD44v6 expression, but negatively correlated with the expression of E-cadherin (P < 0.05). It was also found that the survival of the patient with strong positive expression of ezrin protein was significantly shorter than that of the control (P < 0.05).
Ezrin protein may play an important role in the carcinogenesis of infiltrating breast ductal carcinoma. The strong expression of ezrin protein may be used as a biomarker for predicting poor prognosis in the patients with infiltrating breast ductal carcinoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 05/2008; 30(4):279-83.
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ABSTRACT: To study the effects of Fumonisin B1(FB1) on HLA-I on human peripheral blood mononuclear cells (PBMC) in vitro.
The expression of HLA-I on PBMC by FB1 pretreatment at different dosage(10, 50 micromol/L) was detected with flow cytometry (FCM), Western blot, and semi-RT-PCR, respectively.
The expression of HLA-I on PBMC in vitro at the two experimental concentration was both lower than that of the control after FB1 treatment for 24 h as represented by fluorescence intensity by FCM analysis. Western blot results further confirmed the above results. At mRNA level, HLA-A, B and C mRNA were detected by RT-PCR, and the results showed that no changes were found on the expression of HLA-A, B mRNA between FB1 treated group and the control group, but HLA-C mRNA was inhibited in FB1 treated groups.
10 and 50 micromol/L FB1 could inhibit the expression of HLA-I on human PBMC in vitro at 24 h treatment.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 10/2007; 23(9):794-6.
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Zhonghua bing li xue za zhi Chinese journal of pathology 05/2007; 36(4):265-6.
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ABSTRACT: Matrix metalloproteinases (MMPs) are key enzymes involved in tumor development, invasion and metastasis. The single nucleotide polymorphisms (SNPs) in the promoter regions of MMP genes may influence tumor development and progression via modulating mRNA transcription and protein expression. This study was to explore the correlations of the promoter SNPs in MMP-3 and MMP-7 genes to susceptibility to brain astrocytoma.
The genotype of MMP-3 -1171 5A/6A and MMP-7 -181A/G polymorphisms in 236 patients with brain astrocytoma and 366 healthy controls was detected by polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP).
The allelotype and overall genotype distribution of MMP-3 SNP among the astrocytoma patients and healthy controls were similar (P>0.05). Stratified by sex, age, and histological grade, the susceptibility to brain astrocytoma among the subjects with 5A/5A and 5A/6A genotypes and the subjects with 6A/6A genotype were similar(P>0.05). The overall genotype distribution of MMP-7 SNP among the astrocytoma patients and healthy controls were significantly different (P = 0.001). Compared with the A/A genotype, both the G/G and the A/G genotypes significantly increased the susceptibility to astrocytoma [sex-and age-adjusted odds ratio (OR) = 2.77 and 1.69, 95% confidence interval (CI)=1.27-6.02 and 1.01-2.84, respectively]. Stratification analysis showed that the G/G genotype significantly increased the susceptibility to astrocytoma in men (adjusted OR = 3.24, 95% CI = 1.12-9.41) and in the individuals younger than 45 years (adjusted OR = 3.16, 95% CI = 1.09-9.16). When stratified by histological grade, the A/G genotype increased the susceptibility to grade II astrocytoma by about 2 folds (adjusted OR = 2.06, 95% CI = 1.05 - 4.05), while the G/G genotype increased the susceptibility to grade II-IV astrocytoma by about 3 folds.
MMP-7 -181A/G polymorphism may influence the susceptibility to astrocytoma, while MMP-3-1171 5A/6A polymorphism has no correlation to the susceptibility.
Ai zheng = Aizheng = Chinese journal of cancer 05/2007; 26(5):463-8.
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ABSTRACT: To evaluate the fast serum pepsinogen level of the healthy adults among local population in areas with high incidence of gastric cancer and to study the suitable cut-off values of serum pepsinogen abnormality for the screen of chronic atrophic gastritis (CAG) and gastric carcinoma (GC) in China.
Serum PG I and PG II levels were detected with time resolved fluorescence immunoassay (TRFIA). The fast serum PG I and PG I level as well as PG I/PG II ratio of 606 healthy adult residents among local population in Zanhuang county, Hebei province were detected and the normal distribution ranges determined. The relationship between different cut-off values of serum PG I level, PG I/PG II ratio and corresponding pathological changes in gastric mucosae were comparatively analyzed with serum PG detection, endoscopic biopsy and pathological observation in 720 cases of local residents receiving endoscopic examination in the high incidence area of gastric cancer. The efficacy, sensitivity and specificity of different PG I, PG II abnormality cut-off values in the screen p rogram of CAG and GC were statistically analyzed.
The serum PG I, PG II and PG I/PG II ratio levels of healthy adults from a local natural population in the high incidence area of gastric cancer were all skewed from normal distribution. The median level of PG I, PG II and PG I/PG II were 161 microg/L, 14.8 microg/L and 10.5 respectively. Data from comparative studies on serum PG level and pathological changes of gastric mucosae showed that within the serum PG I range from 40 microg/L to 80 microg/L and PG I/PG II ratio range from 3 to 8, sensitivity of the screening program for CAG and GC increased while the specificity decreased along with the increase of cutoff values of serum PG I and PG I/PG II ratio. Results from statistical receiver operator characteristic curve (ROC) analysis suggested that the best cut-off value of PG I and PG I/PG II abnormality for the screening of CAG and GC being PG I < or =60 microg/L,PG I/PG II < or =6 respectively.
The serum PC I, PG II and PG I/PG II ratio levels of healthy adults from a local natural population in the high incidence area of gastric cancer were all skewed from normal distribution. Serum PG I < or =60 microg/L and PG I/PG II ratio < or =6 as abnormal cut-off value for the screen of CAG and GC could result relatively good sensitivity and specificity.
Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 10/2006; 27(10):840-4.
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ABSTRACT: To explore the effects of Vitamin C (Vit C) on the apoptosis and proliferation inhibition of human peripheral blood mononuclear cells (HPBMCs) induced by deoxynivalenol (DON) in vitro.
The effects of Vit C pretreatment at different dosages (25 micromol/L and 100 micromol/L) on apoptosis, apoptosis related genes expression and proliferation inhibition of HPBMCs induced by DON were evaluated with cell culture, flow cytometric DNA analysis and Western blotting.
Flow cytometry (FCM) analysis showed that the apoptosis rate of HPBMCs in 2000 microg/L DON group was (28.82 +/- 1.67)%, which was significantly higher than that in control group (14.07 +/- 0.70, P < 0.05). Compared with DON group, the apoptosis rate of HPBMCs in 25 micromol/L Vit C pretreatment group was significantly decreased (28.82 +/- 1.67)% vs (22.39 +/- 1.05)%, P < 0.05, while that in 100 micromol/L Vit C pretreatment group was obviously increased (36.07 +/- 2.92)%, P < 0.05. Western blotting analysis showed that the expression of Bax and Caspase-3 up-regulated by DON was markedly decreased, while the expression of Bcl-2 down-regulated by DON was increased by 25 micromol/L Vit C pretreatment (P < 0.05). 100 micromol/L Vit C pretreatment could further increase the expression of Bax and Caspase-3 of HPBMCs induced by DON, while no significant effects on the Bcl-2 expression induced by DON were seen. FCM analysis showed that the proliferation index of HPBMCs in Vit C pretreatment groups at different dosages was all dramatically increased as compared with that in DON groups (P < 0.05).
25 micromol/L Vit C pretreatment could at certain extent inhibit the apoptosis and reverse the abnormal expression of apoptosis related genes of HPBMCs induced by DON in vitro, while 100 micromol/L Vit C pretreatment could further increase the apoptosis rate of HPBMCs induced by DON. Vit C pretreatment could reverse the proliferation inhibition of HPBMCs induced by DON in vitro.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 10/2006; 40(5):309-13.
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ABSTRACT: To explore the putative effects of Vitamin C (Vit C) on inhibition of human leucocyte antigen class I (HLA-I) expression of human peripheral blood mononuclear cells (HPBMCs) induced by deoxynivalenol (DON) in vitro.
The effects of Vit C on the changes of HLA-I expression of HPBMCs induced by DON in vitro were evaluated with cell culture, flow cytometry (FCM), Western blotting and immunocytochemical methods.
FCM analysis showed that HLA-I expression of HPBMCs in DON treated cells was significantly lower than that in controls (FI 0.88 +/- 0.02 vs 1.00 +/- 0.03, P < 0.05). As compared with DON group, the HLA-I expressions of HPBMCs in the two Vit C (25 micromol/L and 100 micromol/L) pretreatment groups were all significantly increased (1.15 +/- 0.06 and 1.10 +/- 0.02 vs 0.88 +/- 0.02, P < 0.05). Exposure to different dosage of Vit C alone could dramatically increase the expression of HLA-I of HPBMCs in vitro as compared with that in the normal control (FI for 25 micromol/L and 100 micromol/L Vit C treatment group was 1.28 +/- 0.03 and 1.25 +/- 0.05 respectively, P < 0.05). Immunocytochemical results showed that the percentages of HLA-I positive expression of HPBMCs in Vit C pretreatment groups at different dosages were significantly higher than those in DON group (70.10 +/- 6.90)%, (64.50 +/- 5.50)% vs (42.20 +/- 4.30)%, P < 0.05. Western blotting confirmed the results of FCM and immunocytochemistry.
Vitamin C pretreatment at different dosages could reverse at some extent the inhibitive effects of DON on HLA-I expression of HPBMCs.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 10/2006; 40(5):314-8.
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ABSTRACT: To study the correlation between serum pepsinogen (PG) level and gastric mucosal changes of the residents who live in the high incidence area of gastric cancer, and investigate the value of serum PG level in screening for chronic atrophic gastritis (CAG) and gastric cancer (GC).
Serum PG level was detected with time resolved fluorescence immunoassay (TRFIA). The correlation between serum PG level and gastric mucosal changes was analyzed through endoscopic biopsy and pathological examination in 720 adult residents.
The median serum PG I, PG II level and PG I / PG II ratio in 30 healthy residents with normal gastric mucosa was 172.0 microg/L, 9.6 microg/L and 17.5, respectively. The median serum PG I level of GC patients was significantly lower than that of chronic gastritis patients, gastric ulcer (GU) patients and local healthy residents (P < 0.05). The median PG I level of GU patients was significantly higher than that of the healthy resident group and the other groups (P <0.05). Serum PG II level in CAG, GC and GU groups were all significantly higher than that in CSG and healthy resident group (P <0.05). The PG I/PG II ratio in CAG or GC patients was significantly lower than that in the other groups (P < 0.05). The sensitivity and specificity of serum PG I < or = 60 microg/L for screening CAG or GC was 19.7% and 95.5% respectively, which were 34.7%, 89.3% for PG I/PG II < or =6, and 14.1%, 97.3% for PG I < or =60 microg/L + PG I /PG II < or =6. None in GU group was found to have serum PG I < or =60 microg/L. The median serum PG I level and PG I /PG II ratio in chronic gastritis (including CSG and CAG) with intestinal metaplasia were significantly lower than that of healthy resident group (P < 0.05). The sensitivity and specificity for screening of intestinal metaplasia were 16.6% and 92.9% by PG I < or =60 microg/L; 25.6% and 80.4% by PG I/PG II < or =6; 11.9% and 93.9% by PG I < or =60 microg/L + PG I/ PG II < or = 6.
Serum pepsinogen level of the residents in the high incidence area of gastric cancer is closely correlated with the pathological changes of gastric mucosa. Though the sensitivity of serum pepsinogen level is relatively lower in the screening for chronic gastritis, gastric cancer and intestinal metaplasia, the specificity was quite high. PG I < or = 60 microg/L may be usful in differential diagnosis of gastric cancer from gastric ulcer.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 08/2006; 28(7):507-11.
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ABSTRACT: To study the effects of sterigmatocystin (ST) on HLA-I of human peripheral blood mononuclear cells (HPBMc) in vitro.
The expression of HLA- I of HPBMc by ST pretreatment at six different dosages (0, 0.125, 0.25, 0.5, 1, 2 mg/L) were detected with Flow cytometry (FCM) and Western blot respectively.
FCM quantitative analysis revealed that the expressions of HLA-I of HPBMc in vitro as represented by fluorescence intensity after ST treatment for 24 hrs at all the five experimental concentrations were all lower than that of the control group. The inhibiting effects at relatively higher concentration groups (0.5, 1 and 2 mg/L) were of significance (P < 0.05). A dose-effect relationship between ST concentration and the inhibiting effect on HLA-I expression was found at the concentration range from 0.125mg/L to 2 mg/L (r = 0.841, P < 0.01). Western Blotting results further confirmed the above results.
Within the dosage range from 0.125 mg/L to 2 mg/L, ST could inhibit the expression of HLA- I of HPBMc in vitro negative dose-dependently.
Wei sheng yan jiu = Journal of hygiene research 08/2005; 34(4):454-6.
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ABSTRACT: To study the histogenesis and the putative mechanisms of adenocarcinoma induced by AFG1 and ST in NIH mice.
Thirty-four cases of lung adenocarcinomas induced by AFG1 and ST in NIH mice were included in this study and 12 cases of normal lung tissues were used as control. The phenotype of the lung adenocarcinomas was determined by immunohistochemical expression of SP-C and CC-10 at protein level. The expression of P53, Ras P21 and PCNA was studied with immunohistochemical staining.
The positive expression of SP-C was found in all the lung adenocarcinomas, while no expression of CC-10 could be seen. The labelling index of PCNA in the adenocarcinomas were significantly higher than that of control (P < 0.01). No positive expression of mutant P53 and Ras at protein level could be found.
The lung adenocarcinomas induced by the two mycotoxins in NIH mice arise from alveolar type II cells and no expression of mutant P53 and Ras at protein level was found in the lung adenocarcinomas.
Wei sheng yan jiu = Journal of hygiene research 05/2005; 34(3):341-4.
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ABSTRACT: To explore the effects of deoxynivalenol (DON) on transporter associated with antigen processing-1 (TAP-1) expression in human peripheral blood mononuclear cells (PBMCs).
Effects of various concentrations of DON on TAP-1 expression of in vitro cultured human PBMCs and the dose-effect relationship were analyzed by flow cytometry (FCM) and semi-quantitative RT-PCR at the protein and mRNA levels.
FCM analysis indicated that treatment with various concentrations of DON could inhibit TAP-1 expressions in PBMCs, showing a negative correlation between DON concentration and TAP-1 expression. Semi-quantitative RT-PCR detection indicated that high concentrations of DON (1,000 and 2,000 microg/L) could distinctly inhibit TAP-1 mRNA expression.
DON can down-regulate TAP-1 expression in human PBMCs in a dose-dependent manner in vitro, which suggests DON may interfere with host immunosurveillance, and this may account for the correlation between DON-contaminated grain and esophagus cancer in high risk area.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 04/2005; 21(2):246-8.
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ABSTRACT: To further explore the carcinogenic activity of Sterigmatocystin (ST) and the possible synergistic carcinogenic effect of deoxynivalenol (DON) in NIH mice.
NIH mice were randomly divided into 6 groups, 30 in each. Five groups of mice were given by gastric intubation ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg respectively, 3 times a week for 24 weeks. The remaining group of mice was given normal saline accordingly, serving as control. All mice were fed with HPLC-confirmed mycotoxin-free food, analysis. The mice were killed and pathologically examined at 58th and 74th weeks.
No pathological changes were found in the control group of mice. Adenocarcinoma of lung was observed in 25.0%, 41.7%, 62.5%, 69.2% and 37.5% of mice given ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg, respectively. In addition, dysplasia of glandular stomach was detected in 50.0%, 58.3%, 37.5%, 53.8% and 25.0% of mice similarly treated.
Oral administration of ST or DON can induce adenocarcinoma in lung and dysplasia of glandular stomach in NIH mice. There is synergistic carcinogenic effect when both ST and DON are given.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 01/2005; 26(12):705-8.
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ABSTRACT: Aflatoxin G1 (AFG1) is a member of the carcinogenic aflatoxin family produced by aspergillus flavus. It is a major contaminating mycotoxin in food in areas of China with high cancer incidence. The purpose of this study is to explore the carcinogenic effects of AFG1 in NIH mice.
NIH mice were randomly divided into three groups. Two experimental groups were treated intragastrically by gavage with AFG1 3 microg/kg and AFG1 30 microg/kg respectively, 3 times a week for 24 weeks. The control group was treated with normal saline. All mice were fed with food that was free of AFGs as confirmed by HPLC analysis. The mice were weighed every week throughout the entire experiment, and then sacrificed and examined pathologically at the 58th and 74th weeks respectively.
Compared with control mice receiving no AFG1, bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were observed in mice receiving AFG1 treatment. The incidences of bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were 60.0%, 10.0% and 30.0% for mice receiving 3 microg/kg AFG1 and 28.6%, 35.7%, 42.9% for mice receiving 30 microg/kg of the toxin, respectively.
Oral administration of AFG1 can induce hyperplastic lesions and adenocarcinoma of lung in NIH mice.
Zhonghua bing li xue za zhi Chinese journal of pathology 07/2004; 33(3):260-3.
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ABSTRACT: Cixian County is one of the high incidence areas of esophageal carcinoma in China. Up to now, no work has been conducted on the possible etiological role of human papilloma virus (HPV) infection on esophageal carcinoma in this local area. The aim of this study was to explore the putative roles of HPV infection on the esophageal carcinogenesis of the patients in Cixian and to elucidate the possible relationship between HPV existence and fragile histidine triad gene (FHIT gene, a putative tumor suppressor gene), expression in squamous cell carcinoma of esophagus.
The existence of HPV DNA and the expression of FHIT gene at protein level in esophageal carcinoma tissues were determined with PCR and immunohistochemical staining, respectively, in 128 archival paraffin-embedded tissue blocks of esophageal squamous carcinoma from the high incidence area of Cixian and 24 tissue blocks from the non-high incidence area.
PCR results showed that the positive detection rate of HPV in esophageal carcinoma tissues from the high incidence area was 20.3%, which was slightly higher than that from the non-high incidence area (8.3%)(P >0.05). Immunohistochemically, aberrant expression of FHIT gene in esophageal carcinoma tissue was found in 75.6% cases from the high incidence area and only 54.2% from the non-high incidence area, which was significantly lower than that of the former (P< 0.05). No correlation was found between the abnormal expression of FHIT and existence of HPV DNA in esophageal squamous carcinoma tissues.
HPV DNA could be detected in partial esophageal carcinoma cases from the high incidence area of esophageal carcinoma in Cixian. The aberrant expression rate of FHIT protein in the cases from the high incidence area of esophageal carcinoma in Cixian is higher than that from the non-high incidence area.
Ai zheng = Aizheng = Chinese journal of cancer 06/2003; 22(5):492-5.
