Transcription of TIMP3, DAPK1, and AKR1B10 in squamous-cell lung cancer

التفاصيل البيبلوغرافية
العنوان: Transcription of TIMP3, DAPK1, and AKR1B10 in squamous-cell lung cancer
المؤلفون: Lev L. Kisselev, E. P. Kopantsev, N. Yu. Oparina, A. B. Poltaraus, T. D. Mashkova, M. V. Zinov’eva, I. B. Zborovskaya, E.D. Sverdlov, O. T. Kasymova, Tatyana V. Vinogradova, V. I. Dubovaya, K. K. Laktionov, Zinov'eva Ol, M. V. Fridman, Kropotova Es
المصدر: Molecular Biology. 40:945-951
بيانات النشر: Pleiades Publishing Ltd, 2006.
سنة النشر: 2006
مصطلحات موضوعية: Lung, Oncogene, Biophysics, Biology, medicine.disease, medicine.disease_cause, law.invention, stomatognathic diseases, Real-time polymerase chain reaction, medicine.anatomical_structure, Structural Biology, Transcription (biology), law, Immunology, Cancer research, medicine, Suppressor, Lung cancer, Carcinogenesis, Gene
الوصف: Lung cancer is among the most common neoplasms in Russia, the United States, and in Western Europe and is accompanied by changes in the functional activity of many genes. The transcription levels of TIMP3, DAPK1, and AKR1B10 were compared for normal and tumor lung tissues of patients with squamous-cell cancer (SCC) by RT-PCR. A substantial increase in AKR1B10 transcription level was observed in 80% of the tumors. The transcription levels of TIMP3 and DAPK1 were significantly decreased in 76 and 72% of the tumors, respectively. The results implicated the genes in carcinogenesis in SCC, AKR1B10 acting as a potential oncogene, and TIMP3 and DAPK1 acting as potential tumor suppressor genes. It was assumed that dramatic changes in their transcription levels could be used for early diagnosis of SCC.
تدمد: 1608-3245
0026-8933
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::f05c14b6e078140d442d70a9132766ed
https://doi.org/10.1134/s0026893306060148
حقوق: CLOSED
رقم الأكسشن: edsair.doi...........f05c14b6e078140d442d70a9132766ed
قاعدة البيانات: OpenAIRE