Objective To investigate the relationship of p53 codon 72 polymorphism and susceptibility to gastric cancer in high incidence area of Hexi area of Gansu province. Methods The Arg/Pro polymorphism of p53 gene was detected by real-time PCR in 140 patients with gastric cancer, 110 patients with gastric precancerous lesion and 125 healthy controls; Helicobacter pylori (Hp) infection was detected by Warthin-Starry silver method． Results The Pro allele frequencies of p53 gene in gastric cancer cases (0.543) were higher than those in gastric precancerous lesion (0.482) and controls (0.472). The Pro genotype had a more than 1.846 fold increased risk of gastric cancer 〔OR=1.846; 95% 〗CI (1.006-3.387); P =0.046〕． With statistical analysis， the genotype of p53 gene was correlated with location and Laurens histological type （ P ＜ 0.05）. A significantly higher risk of gastric cancer was also seen in cases with p53 Pro genotype, food, Hp infection, positive mind factor and positive family history． Conclusion There is a b correlation between the p53 gene codon 72 Arg/Pro polymophism and susceptibility to gastric cancer in Hexi area of Gansu province and the Pro/Pro genotype may be one of the major risk factors in patients with gastric cancer.
ObjectiveTo study the relationship between mutation of the p53 gene, p21 gene and bacteria Lform in gallbladder carcinoma. MethodsForty cases of gallbladder carcinoma and 40 cases of chronic cholecystitis were studied by using Gram staining and immunohistochemistry (SP method) to detect the positive rate of Lforms antigen, p21 and p53 protein overpression. And the relationship between the expression of p21 and p53 in Lform infection positive group and that in Lform infection negative group was discussed. ResultsThere was no statistical difference between the Lform positive rate in patients with gallbladder carcinoma with Gram staining and immunohistochemistry (Pgt;0.05). The positive expression rate of p21 and p53 in gallbladder carcinoma was 62.5%(25/40) and 65.0%(26/40) respectively. The expression values of p21 and p53 in chronic cholecystitis was 2.5%(1/40) and 5.0%(2/40) respectively, which was significantly different from that of gallbladder carcinoma (P＜0.05). The expression of p21 and p53 was significantly higher in Lform infection positive group than in that with Lform infection negative group (P＜0.05). ConclusionBacteria Lform may be one of the direct factor leading to mutation of p53 and p21 during gallbladder oncogenesis.
Objective To study the effect of 5-fluorouracil (5-FU) induced apoptosis of the rectal carcinoma cell line HR8348 in vitro and the relationship between apoptosis induced by 5-FU and the expression of bcl-2，bcl-xl，bax and p53,and to investigate the possible mechanism of apoptosis of rectal carcinoma cell line HR8348 induced by 5-FU.Methods After treatment with 5-FU for 24 h,the apoptotic index was detected by methyl green and pyronine Y staining and by terminal deoxynucleotidyl transferase (TdT)mediated dUTP nick end labeling (TUNEL).The bcl-2,bcl-xl,bax and p53 gene expression of HR8348 cells were examined by immunohistochemical method.Results After treatment with 5-FU,the apoptotic index of experiment group was significantly increased,there was significant difference as compared with the control.Exposed to 5-FU for 12 h,24 h and 36 h,the expression of bcl-2 of HR8348 cell line remained unchanged,but the expression of bcl-xl slightly diminished,while the expression of bax was remarkly increased,the expression of p53 was not detected in both experiment and control groups.Conclusion This results indicate that 5-FU may induce apoptosis of rectal carcinoma cell line HR8348 and the possible mechanism of apoptosis induction is through upregulation of bax expression and the change of bax to bcl-xl ratio.
Objective To investigate the relationship between p53 codon 72 polymorphism and susceptibility to keloid. Methods The p53 genotypes were detected by polymerase chain reactionreverse dot blot(PCRRDB) and DNA direct sequencing among 15 healthy controls and 15 patients with keloid. Results The frequency of the Proallele(P=0.035) and Pro/Pro genotype(P=0.030) in patients was significantly higher than that in the controlls. There was no significant difference in the frequency of Pro/Arg and Arg/Arg genotypes between patients and controls. Conclusion The p53 gene codon 72 polymorphism may play a role in susceptibility to keloid.
Objective To explore the effect of exogenous estrogen receptor β1 (ERβ1) gene on the expression of p53 as well as the changes of apoptosis in MDA-MB-231 cell line and to investigate the biological role of ERβ1 in breast cancer. Methods Recombinant eukaryotic expressing vector containing ERβ1 cDNA was transfected into human breast cancer cell MDA-MB-231 by using cationic liposome LipofectamineTM 2000. The expression levels of p53 and ERβ1 in mRNA and protein were evaluated by real-time PCR and Western blot, respectively. Cell growth curve was used to detect the changes of cell proliferation ability. Cell apoptosis was detected by flow cytometry. Results After transfected with vector containing ERβ1 cDNA, proliferation ability of MDA-MB-231 cell decreased and the expression levels of both ERβ1 and p53 in both mRNA and protein increased (Plt;0.01). Rate of cell apoptosis increased in ERβ1 upregulation groups （Plt;0.01）. Conclusion ERβ1 can induce apoptosis and inhibit the growth of MDA-MB-231 cells by upregulating p53 expression.
Objective To explore the progress of the relationship between the tumor suppressor gene p53 and oncogene c-erbB-2 and gastric cancer in recent years. Methods Relevant literatures about p53 and c-erbB-2 in gastric cancer were collected and analyzed. Results The mutation of p53 gene and the over-expression of c-erbB-2 gene were a common event in gastric cancer. The mutation of p53 gene was correlated with the location of gastric cancer and its aggressive biological behavior. The over-expression of c-erbB-2 gene could be used as an independent prognostic parameter in gastric cancer. The drugs targeted on p53 and c-erbB-2 gene were being developed. Conclusion Further research on the role of p53 and c-erbB-2 gene in the development of gastric cancer is helpful to understand the biological behavior and provide theoretical basis for gene therapy.
Objective To explore whether mutations of p53 gene and hMLH1 gene may be an early event of carcinogenesis in rectal cancer. Methods The expressions of p53 and hMLH1 protein in 32 patients with early rectal cancer, 32 patients with rectal adenoma， and 30 patients with normal rectal mucosa were detected by PV-9000 immunohistochemical method between February 2003 and July 2009 in this hospital. Results ① The positive expression rates of p53 protein were 0 (0/30), 59.38% (19/32), and 68.75% (22/32) in the normal rectal mucosa, rectal adenoma, and early rectal cancer, respectively. There was no difference between the rectal adenoma and early rectal cancer (Pgt;0.05), but which were higer than that of the normal rectal mucosa (Plt;0.01). The negative expression rates of hMLH1 protein were 0 (0/30), 12.50% (4/32), and 50.00% (16/32) in the normal rectal mucosa, rectal adenoma, and early rectal cancer, respectively. The negative expression rate of hMLH1 protein in the early rectal cancer was significantly higher than that in the rectal adenoma or the normal rectal mucosa (Plt;0.01). ② The positive expression of p53 concomitant negative expression of hMLH1 in the rectal adenoma and early rectal cancer were 9.38% (3/32) and 37.50% (12/32), respectively, the difference was statistically significant (P=0.008). ③ In the early rectal cancer, the positive expression of p53 and the negative expression of hMLH1 were closely related to the degree of differentiation (Plt;0.05), but which weren’t related to the patient’s gender, age, tumor maximum diameter, depth of invasion or fecal occult blood (Pgt;0.05). ④ The positive expression of p53 was closely related to higher adenoma hyperplasia (P=0.009), while not of negative expression of hMLH1 (Pgt;0.05). Conclusion Simultaneous mutations of p53 gene and hMLH1 gene may be an early event of carcinogenesis in rectal cancer.
【Abstract】Objective To investigate whether SUMO-1 enhances the apoptosis induced by wild-type p53 plasmid transfection in HepG2 cells. Methods The HepG2 cells were transfected respectively or simultaneouly with the following expressional plasmids as pcDNA3-wtp53（pwtp53，including human wild-type p53 gene），pCMV-HDM1B（pMDM2，including HDM2 gene， homologous gene as murine double minute gene 2），pcDNA3-His6-SUMO-1（pSUMO-1 ，including small ubiquitin-like modifier1 gene）and plasmid pcDNA3.The proteins expressed in cells were detected by means of Western blotting and the apoptosis rates of cells were measured by flow cytometry. Results The protein bands of p53 and MDM2 could be seen in cells transfected with pwtp53 and pMDM2. Meanwhile，the relative larger molecular weight bands were also seen in cells transfected with pSUMO-1 which represented the p53 and MDM2 protein modification by SUMO-1. Merely the trace of p53 protein was detected in cells not transfected with any plasmid or only transfected with empty plasmid and pSUMO-1. In cells transfected with pwtp53 and pwtp53+pSUMO-1，the apoptosis rates were (16.79±1.62)%and (18.15±1.36)%. When transfected with pwtp53+pMDM2，the rate decreased to (5.17±1.23)%. The apoptosis rate would come up again to (14.06±1.84)% after transfected with pwtp53+pMDM2+pSUMO-1 and the difference of rates were significant compared to the cells transfected with pwtp53+pMDM2 (PH＜0.01）. The apoptosis rates in other cells were less than 2% and had no significant difference. Conclusion SUMO-1 could increase the apoptosis induced by wild-type p53 plasmid transfection in HepG2 cells through combining to p53 protein or its post-translational modification and inhibiting p53 degradation by MDM2.
【Abstract】ObjectiveTo study the expressions of P-gp, nm23 and p53 in primary breast cancer tissues and to evaluate the prediction significance in recurrence of the primary breast cancer. MethodsExpressions of P-gp, nm23 and p53 in 57 benign and malignant breast paraffin-embedded specimens, the difference of the rate and intensity of positive reaction of P-gp,nm23 and p53 were checked by immunohistochemical staining.ResultsThe positive rate of nm23 significantly increased in benign breast tissues compared with the tissues of recurrence of breast cancer. The positive intensity of nm23 was significantly decreased in the tissues of recurrence of breast cancer compared with the tissues of primary breast cancer. The positive rate of p53 was significantly increased in malignant breast tissues compared with benign breast tissues. The positive intensity of p53 was significantly increased in the tissues of recurrence of breast cancer compared with the tissues of primary breast cancer. There was no difference in the positive rate of P-gp in the tissue of recurrence and primary of breast cancer compared with benign breast tumor. But the positive intensity of P-gp was significantly decreased in the tissues of recurrence and primary of breast cancer compared with benign breast tumor. ConclusionThe expression of p53 may indicate the proliferating activity of carcinoma cell. The positive intensity of expression of p53 and nm23 is valuable in prediction of the recurrence of primary breast cancer.
Objective To investigate the possible interaction between the ras and p53 genes overexpression in thyroid carcinoma, and whether there is correlation between the ras and p53 overexpression and clinico-pathological criteria. Methods Thyroid lesions from eighty patients were examined for expression of ras and p53 genes by the LSAB immunohistochemistic method. Of these patients, 54 were diagnosed as malignant lesions and 26 benign nodular thyroid disorders. Results The positive immunostain rate for ras and p53 genes was 90.7%, 23.0% and 55.5%, 30.7% in carcinoma and benign lesions respectively with statistically significance between thyroid carcinomas and benign disorders (Ｐ＜0.05). Both ras and p53 overexpressions coexisted in 30 thyroid carcinomas and follow-up showed that 3 of them died and 5 of them had recurrence within 4 years.Conclusion Activation of ras gene and inactivation of p53 gene are cooperatively associated in thyroid tumorigenesis. The concurrent overexpression of ras and p53 could result in a poor prognosis.