Type of document : Magazine article Edition cipher : Author(s) : Matveeva A., Kovalevska L., Kholodnyuk I., Ivanivskaya T., Kashuba E. Title : The TGF-beta — SMAD pathway is inactivated in cronic lymphocytic leukemia cells Place of publication : Экспериментальная онкология. - 2017. - Т. 39, № 4. - С. 286-290 (Cipher ЕУ12/2017/39/4) Notes : Bibliogr. at the end of the art. MeSH-main: ЛЕЙКОЗ ЛИМФОЦИТАРНЫЙ ХРОНИЧЕСКИЙ B-КЛЕТОЧНЫЙ -- LEUKEMIA, LYMPHOCYTIC, CHRONIC, B-CELL ТРАНСФОРМИРУЮЩИЙ ФАКТОР РОСТА БЕТА2 -- TRANSFORMING GROWTH FACTOR BETA2 ГЕННОЙ ЭКСПРЕССИИ ПРОФИЛИРОВАНИЕ -- GENE EXPRESSION PROFILING БИОИНЖЕНЕРИЯ -- BIOENGINEERING СТАТИСТИЧЕСКАЯ ОБРАБОТКА ДАННЫХ -- DATA INTERPRETATION, STATISTICAL Annotation: To study the status of the tumor growth factor beta (TGFB) pathway in chronic lymphocytic leukemia (CLL) cells and to uncover molecular details underlying CLL cell genesis. Objects and Methods: The study was conducted on peripheral blood samples of patients with CLL using the following methods: RNA isolation, analysis of expression of transcription factors using RT2 profiler assay, bioinformatics analysis of publicly available data bases on expression. Results: We have shown that the TGFB — SMAD canonical pathway is not active in CLL cells. SMAD-responsive genes, such as BCL2L1 (BCL-XL), CCND2 (Cyclin D2), and MYC, are down-regulated in CLL cells compared with peripheral blood B cells of healthy donors. Conclusions: The TGFB-mediated signaling is not active in CLL cells due to low (or absent) expression of SMAD1, -4, -5, -9, and ATF-3. Expression and phosphorylation status of SMAD2 and -3 should be further elucidated in the future studies Additional Access Points: Matveeva, A. Kovalevska, L. Kholodnyuk, I. Ivanivskaya, T. Kashuba, E.