2014  0,718
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 51(2017) N 5 p. 740-747; DOI 10.1134/S0026893317050107 Full Text

G.S. Krasnov1, G.A. Puzanov1, A.V. Kudryavtseva1, A.A. Dmitriev1, A.D. Beniaminov1, T.T. Kondratieva2, V.N. Senchenko1*

Differential expression of an ensemble of the key genes involved in cell-cycle regulation in lung cancer

1Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia
2Cancer Research Center, Russian Academy of Medical Sciences, Moscow, 115478 Russia

Received - 2017-05-03; Accepted - 2017-05-19

Targeted cancer therapy directed at individual targets is often accompanied by the rapid development of drug resistance. The development of a new generation of antitumor drugs involves the search for many targets simultaneously to block or, conversely, restore their activity. In this regard, simultaneous analysis of gene expression in a complex network of interactions, primarily cell cycle control elements, is relevant for the search of specific molecular markers for the differential diagnosis of adenocarcinoma (ADC) and squamous cell lung cancer (SCC), as well as new targets for therapy. In this paper we performed an extended quantitative analysis of the expression of two suppressor genes, CTDSPL and its target RB1, as well as 84 genes of the main participants of the p16INK4A-Cdk/cyclin D1-Rb and p53/p21Waf1 signaling pathways in the histological types of non-small-cell lung cancer (NSCLC), i.e., ADC and SCC, using the special panel of the Human Cell Cycle Regulation Panel. The expression profile of some genes shows the specificity to the histological type of NSCLC and the presence of metastases. The genes with a significantly increased expression that affect the activity of Rb (cyclins, cyclin-dependent kinases, their activators, inhibitors, etc.) can serve as potential targets for combined therapy of both ADC and SCC.

non-small-cell lung cancer, adenocarcinoma, squamous cell lung cancer, cell cycle, suppressor genes, gene expression