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依托泊苷和顺铂诱导化疗后ⅢA期非小细胞肺癌石蜡包埋制剂中p21和bcl-2蛋白的表达

Expression of p21 and bcl-2 proteins in paraffin-embedded preparations of non-small cell lung cancer in stage IIIA after Etoposide and Cisplatin induced chemotherapy.

作者信息

Mańdziuk Sławomir, Dudzisz-Sledź Monika, Korszeń-Pilecka Iwona, Milanowski Janusz, Wojcierowski Jacek, Korobowicz Elzbieta

机构信息

Pulmonary Department, Medical University of Lublin, Lublin, Poland.

出版信息

Ann Univ Mariae Curie Sklodowska Med. 2003;58(1):149-53.

Abstract

Apoptosis plays an important role in cancer pathogenesis. Several oncogenes and antioncogenes regulate this process. Loss of their normal function leading to cell resistance to apoptosis seems to be a key factor of neoplasm development. In tumour cells, programmed cell death is a spontaneous process and its intensity increases after chemo-, radio- and hormonotherapy. Amongst several genes and their products, bcl-2 and p21 genes play a significant role in the process. p21 gene product, cyclin-dependent kinase inhibitor, along with p53 gene take part in cell cycle regulation. Our study aimed at evaluating p21 and Bcl-2 protein expression in the cells of patients afflicted with stage IIIA of non-small cell lung cancer who underwent neoadjuvant chemotherapy (three courses of Vepesid and Cisplatin). Protein expression was evaluated in slides of tissue material obtained before pharmacological treatment (during bronchofiberoscopy) and after three courses of Vepesid and Cisplatin (during surgical tumour resection). Protein activity in tissue slides was conducted using histochemical method with labelled antibodies (immunoperoxidase staining procedure). The control material was obtained from patients who had not undergone inductive chemotherapy. The results were documented as photographs and presented as charts after extinction level measurement using cytophotometric technique. Decrease in Bcl-2 protein activity and increase in p21 protein level in tumour cells of patients after inductive chemotherapy were observed.

摘要

细胞凋亡在癌症发病机制中起重要作用。多种癌基因和抗癌基因调节这一过程。它们正常功能的丧失导致细胞对凋亡产生抗性,这似乎是肿瘤发生发展的关键因素。在肿瘤细胞中,程序性细胞死亡是一个自发过程,在化疗、放疗和激素治疗后其强度会增加。在多种基因及其产物中,bcl-2和p21基因在这一过程中起重要作用。p21基因产物,即细胞周期蛋白依赖性激酶抑制剂,与p53基因一起参与细胞周期调节。我们的研究旨在评估接受新辅助化疗(三疗程的威派德和顺铂)的IIIA期非小细胞肺癌患者细胞中p21和Bcl-2蛋白的表达。在药物治疗前(纤维支气管镜检查期间)以及三疗程的威派德和顺铂治疗后(手术切除肿瘤期间)获取的组织材料切片中评估蛋白表达。使用标记抗体的组织化学方法(免疫过氧化物酶染色程序)检测组织切片中的蛋白活性。对照材料取自未接受诱导化疗的患者。结果以照片记录,并在使用细胞光度技术测量消光水平后以图表形式呈现。观察到诱导化疗后患者肿瘤细胞中Bcl-2蛋白活性降低,p21蛋白水平升高。

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