ABSTRACT
Objective To investigate ERCC1 expression in advanced breast cancer and its relationship with cisplatin resistance. Methods ERCC1 expression in 50 cases of advanced breast cancer was measured by RT-QPCR. The chemotherapy (CAF) was given. Gemcitabine and cisplatin were given because of metastasis. Results The expression of ERCC1 has no relationship with age, lymph node metastasis, clinicl stage, histologi-cal grade or human epidermal growth factor receptor-2 (HER2) expression. The effective rate was 18.8% (3/16) for ERCC1 high-expressed patients and 79.4%(27/34)for ERCC1 low-expressed patients in terms of cisplatin chemotherapy. The sensitity for cisplatin chemotherapy was high for patients with low ERCC1 expression and it was low for patients with high ERCC1 expression. The effective rate (complete remission+partial remission), and ineffective rate (stable disease+progressive disease) between the two had statastical significance (P<0.001). Con-clusions ERCC1 low-expressed patients can benefit from cisplatin. ERCC1 can be used as a moleculer marker for predicting chemotherapy efficacy in breast cancer.
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Objective To study the efficacy and toxicity related gene polymorphism in non-small cell lung cancer patients with gemcitabine chemotherapy.Methods 40 patients with non-smallcell lung cancer were chosen in the present study.The leukocyte DNA was extracted from blood samples.ERCC1 118 genotypes were detected by PCR-RFLP.The relationship between ERCC1 118 genotype and the chemotherapy efficacy and toxicity of patients received gemcitabine was analyzed.Results The age,gender,pathological type,clinical stage,and other factors had no relation with the treatment effects (P ＞ 0.05).The frequency of C/C genotype was 55.0％ (22/40),the frequency of C/T +T/T genotype was 45.0％ (18/40).The effective rate was 45.5％ in patients carrying the C/C gene,The effective rate was 22.2％ in patients carrying the C/T + T/T gene,the difference between the two groups was not statistically significant (x2 =2.3488,P ＞ 0.05).Conclusion The ERCC1 gene polymorphism is not significantly correlated with the efficacy and toxicity of gemcitabine chemotherapy.
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Objective:This study aims to detect the CpG island methylation status of the ERCC1 gene promoter and the expres-sion of the ERCC1 protein in gastric cancer tissues, as well as to investigate the correlation and significance between ERCC1 gene pro-moter CpG island methylation and protein expression. Methods:Methylation-specific PCR was performed to detect the methylation sta-tus of the ERCC1 gene in tumor tissues and adjacent cancerous tissues from 30 gastric cancer patients. Ten cases of normal gastric tis-sues were used as control. Expression of the ERCC1 protein in gastric cancer tissues, adjacent cancerous tissues, and normal gastric tis-sues was examined by immunohistochemistry S-P method. Results:The methylation rate of the ERCC1 gene promoter CpG island in gastric cancer tissues was significantly higher than that in adjacent cancerous tissues (76.7%vs. 13.3%, P<0.05), and the difference was statistically significant. The incidence of promoter methylation was not found in 10 normal gastric tissues. The negative rate of ERCC1 protein expression in 30 cases of gastric carcinoma tissues was significantly higher than that in adjacent cancerous tissues (70.0% vs. 33.3%, P<0.05), whereas 10 normal gastric tissues all exhibited positive expression for the ERCC1 protein. The tumor tissues with ER-CC1 gene promoter CpG island methylation showed a lower expression of ERCC1 protein than the unmethylated tumor tissues in gas-tric cancer patients. Conclusion:Methylation of the ERCC1 gene promoter CpG island and protein expression are negatively correlat-ed, and methylation of the CpG island of the ERCC1 gene may be one of the main reasons for the down-regulation of protein expres-sion.
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Background and purpose: At present, gastric cancer is considered to be both genetic and epigenetic disease, and epigenetic alterations play a significant role in the development of gastric cancer. DNA methylation is the most well studied and most in-depth epigenetic modiifcations in human-beings. The silencing of tumor-related genes by DNA methylation is reversible. ERCC1 is a kind of DNA repair gene. The present study was aimed to detect the CpG island methylation status of ERCC1 gene promoter in gastric cancer tissues and corresponding peripheral blood, and to explore the relationship between methylation of ERCC1 gene in peripheral blood and in gastric cancer tissues. Methods:Methylation speciifc PCR was performed to detect the methylation status of ERCC1 gene in the tumor tissues and the paired peripheral blood from 30 gastric cancer patients. Results:The positive rate of methylation of ERCC1 gene promoter CpG island was 76.7%(23/30) in the tumor tissues and 63.3%(19/30) in serum of gastric cancer patients, and the difference had no statistical signiifcance. Conclusion:Our studies suggest that ERCC1 gene promoter CpG island methylation can be detected in a high proportion of the serum consisting with that in tumor tissues of gastric cancer patients, and the detection of methylation status of ERCC1 gene in peripheral blood provides a more simple, fast and reliable way for the medical treatment of gastric cancer and also provides the possible theoretical basis for the CpG island methylation of ERCC1 gene promoter as a target for the treatment of gastric cancer.
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Objective To study changes of cisplatin sensitivity by RNA interfering the excision repair cross-complementing (ERCC) 1 gene in ovarian cancer cell lines. Methods The small interference RNA (siRNA) targeting ERCC1 gene was designed and synthesized by transcription in vitro, and transfected to ovarian cancer cell line ES-2. The mRNA and protein of ERCC1 were evaluated by means of RT-PCR, western blot and immunocytochemistry. The changes of cisplatin sensitivity after interference were examined by methyl thiazolyl tetrazolium (MTT) assay. Results In ES-2 cell, the mRNA and protein levels of ERCC1 were dramatically decreased 24, 48 and 72 hours after transfection. The sensitivity to cisplatin of ES-2 cell line was increased by 53.88 times after disturbing the ERCC1 gene. Conclusion The sensitivity to cisplatin of ovarian cancer cell lines ES-2 could be enhanced by RNA interfering ERCC1 gene.