title: Expression of p21 and bcl-2 proteins and p53 mRNA in surgically resected preparations of non-small cell lung cancer (stage IIIA) after etoposide and cisplatin chemotherapy.
abstract: Apoptosis which is also a called programmed cell death plays an important role during development, homeostasis and in many diseases such as cancer. Apoptosis is a genetically encoded cell death program defined by characteristic morphological and biochemical features. It is well recognized as a distinct pathologic mechanism in tumours responding to anticancer therapies. Many genes play an important role in this process. We evaluated an expression of the tumour supressor gene p53 and proteins p21 and bcl-2 in non-small cell lung cancer. We examined resected tumour tissues from 30 patients who received neoadjuvant chemotherapy. As a control we assessed tissues from patients treated without chemotherapy. Histological slides of the resected tumours were evaluated by TUNEL, in situ hybridisation and with immunoperoxidase staining procedure. The results were documented by photography. We examined the level of extinction using cytophotometry. In conclusion, preoperative chemotherapy induces apoptosis in cancer cells. The level of p53 correlates with the acceleration of TUNEL reaction. The loss of bcl-2 expression correlated with an increased apoptotic cell death. There was an increased p21 protein expression in the examined cancer tissues after chemotherapy.
authors.affiliation: Department of Lung Diseases and Tuberculosis, Medical Academy, Lublin, Poland. slawman@yahoo.com.pl
authors.forename: S
authors.initials: S
authors.lastname: Mańdziuk
authors.forename: M
authors.initials: M
authors.lastname: Dudzisz-Sledź
authors.forename: B
authors.initials: B
authors.lastname: Rybacka-Chabros
authors.forename: M
authors.initials: M
authors.lastname: Zdunek
authors.forename: A
authors.initials: A
authors.lastname: Jakubowicz-Klecha
authors.forename: E
authors.initials: E
authors.lastname: Korobowicz
authors.forename: J
authors.initials: J
authors.lastname: Milanowski
authors.forename: J
authors.initials: J
authors.lastname: Wojcierowski
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use; D000972:Antineoplastic Agents, Phytogenic / Q000627:therapeutic use; D017209:Apoptosis; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D002945:Cisplatin / Q000627:therapeutic use; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000235:genetics*; D005047:Etoposide / Q000627:therapeutic use; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D020287:In Situ Nick-End Labeling; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D000970:Antineoplastic Agents; D000972:Antineoplastic Agents, Phytogenic; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D005047:Etoposide; D002945:Cisplatin