Journal of Molecular Biology

Year	IMPACT-FACTOR
2023	1,500
2022	1,200
2021	1,540
2020	1,374
2019	1,023
2018	0,932
2017	0,977
2016	0,799
2015	0,662
2014	0,740
2013	0,739
2012	0,637
2011	0,658
2010	0,654
2009	0,570
2008	0,849
2007	0,805
2006	0,330
2005	0,435
2004	0,623
2003	0,567
2002	0,641
2001	0,490
2000	0,477
1999	0,762
1998	0,785
1997	0,507
1996	0,518
1995	0,502

Vol 49(2015) N 5 p. 638-648; DOI 10.1134/S0026893315050118

G.S. Krasnov^1,2,3*, A.A. Dmitriev^1,2, A.F. Sadritdinova¹, N.N. Volchenko², E.N. Slavnova², T.V. Danilova², A.V. Snezhkina¹, N.V. Melnikova¹, M.S. Fedorova¹, V.A. Lakunina¹, A.A. Belova¹, K.M. Nyushko², B.Y. Alekseev², A.D. Kaprin², A.V. Kudryavtseva^1,2

Molecular genetic mechanisms of drug resistance in prostate cancer
¹Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991, Russia
²Herzen Moscow Cancer Research Institute, Ministry of Health of the Russian Federation, Moscow, 125284, Russia
³Orekhovich Institute of Biomedical Chemistry, Russian Academy of Medical Sciences, Moscow, 119121, Russia

^*gskrasnov@mail.ru
Received - 2014-12-25; Accepted - 2015-03-07

Drug resistance and especially cross-resistance are the most important problems of therapy of prostate cancer. Drug resistance mechanisms, including ligand-dependent (requiring the presence of androgens in the cell) and independent (not requiring androgens) ones, are reviewed. The mechanisms are mainly based on mutations of the androgen receptor (AR) gene, expression of aberrant constitutively active AR splice variants, and upregulation of androgen synthesis genes.

prostate cancer, drug resistance, androgen receptor, androgens, abiraterone, enzalutamide, mutations, splice variants