Zobrazeno 1 - 6
of 6
pro vyhledávání: '"E Sh, Solomko"'
Autor:
D. A. Khochenkov, M. I. Volkova, I. V. Timofeev, A. S. Olshanskaya, Yu. A. Khochenkova, E. Sh. Solomko, S. A. Ashuba, V. B. Matveev
Publikováno v:
Сибирский онкологический журнал, Vol 20, Iss 4, Pp 64-72 (2021)
Purpose: to study the expression of vascular endothelial growth factor (vegf-a) and its receptors (vegfr-1 and vegfr-2) in renal cell carcinoma (rcc) cells and assess the effect of the expression levels of these markers on the tumor characteristics a
Externí odkaz:
https://doaj.org/article/e766d839f4ab44a8afc121bf20a6ba39
Autor:
Yu. A. Khochenkova, I. G. Dyrda, Yu. S. Machkova, E. Sh. Solomko, T. A. Sidorova, D. A. Khochenkov, E. A. Avilova
Publikováno v:
Успехи молекулярной онкологии, Vol 6, Iss 4, Pp 69-74 (2019)
Background. The incidence of brain gliomas firmly occupies a leading position among all central nervous system tumors – 40–50 % of the cases detected, more than half of them are glioblastoma. Existing cell lines and cultivation methods do not ref
Externí odkaz:
https://doaj.org/article/71b239b4d09340f9bb783e3ceaf9f178
Publikováno v:
Russian Journal of Biotherapy. 19:38-45
Introduction.The molecular basis of radio- and photodynamic therapy (PDT), the mechanism of action of a number of antitumor chemotherapy drugs is oxidative stress (OS). The enzyme hemoxygenase-I (НO-1), a molecular marker of OS, is a key participant
Autor:
M. I. Volkova, A. S. Olshanskaya, I. V. Tsimafeyeu, N. L. Vashakmadze, Yu. A. Khochenkova, E. Sh. Solomko, S. A. Ashuba, D. A. Khochenkov, V. B. Matveev
Publikováno v:
Onkourologiâ, Vol 16, Iss 1, Pp 17-26 (2020)
Objective: to assess the expression and prognostic value of vascular endothelial growth factor A (VEGF-A), fibroblast growth factor 2 (FGF-2) and their receptors VEGFR-1, -2; FGFR-1, -2, as well as platelet-derived growth factor receptors (PDGFR-α,
Publikováno v:
Molecular Biology. 52:398-405
Publikováno v:
Molekuliarnaia biologiia. 52(3)
The discovery of B-RAF activating mutations in malignant melanoma cells has led to the development of a number of targeted drugs, which block exclusively the mutant B-RAF protein. Tumor cells often acquire resistance to B-RAF inhibitors via activatio