Timur R. Samatov
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Timur R. Samatov has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Alexander Grigorievich Tonevitsky
Faculty of Biology and Biotechnology, HSE University, Moscow, Russia
5 shared publications - Maxim Yurievich Shkurnikov
National Research University Higher School of Economics, Moscow, Russia
3 shared publications - Andrei Dmitrievich Kaprin
National Medical Research Radiological Centre of the Ministry of Health of the Russian Federation, Koroleva St. 4, 249036 Obninsk, Russia
2 shared publications Svetlana A. Tonevitskaya
Moscow State University of Mechanical Engineering,Moscow,Russia
2 shared publications- Udo Schumacher
Institute of Anatomy and Experimental Morphology, Center for Experimental Medicine, University Cancer Center, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany
2 shared publications - Vladimir V. Galatenko
Evotec International GmbH
2 shared publications
Latest Publications
- 2 June 2017
- Published by Springer Nature in BioChip Journal
- Vol. 11 (4) , 262-269
miRNA-mediated expression switch of cell adhesion genes driven by microcirculation in chip
- 2 June 2017
- Published by Springer Nature in BioChip Journal
- Vol. 11 (4) , 262-269
miRNA-mediated expression switch of cell adhesion genes driven by microcirculation in chip
- Open Access
- 1 August 2016
- Published by Elsevier in Progress in Histochemistry and Cytochemistry
- Vol. 51 (2) , 25-32
L1CAM: Cell adhesion and more
- 1 August 2016
- Published by Elsevier in Progress in Histochemistry and Cytochemistry
- Vol. 51 (2) , 25-32
Open AccessL1CAM: Cell adhesion and more
- Open Access
- 8 October 2015
- Published by Springer Nature in Scientific Reports
- Vol. 5 (1) , 14967
Highly informative marker sets consisting of genes with low individual degree of differential expression
Genes with significant differential expression are traditionally used to reveal the genetic background underlying phenotypic differences between cancer cells. We hypothesized that informative marker sets can be obtained by combining genes with a relatively low degree of individual differential expression. We developed a method for construction of highly informative gene combinations aimed at the maximization of the cumulative informative power and identified sets of 2–5 genes efficiently predicting recurrence for ER-positive breast cancer patients. The gene combinations constructed on the basis of microarray data were successfully applied to data acquired by RNA-seq. The developed method provides the basis for the generation of highly efficient prognostic and predictive gene signatures for cancer and other diseases. The identified gene sets can potentially reveal novel essential segments of gene interaction networks and pathways implied in cancer progression.
- 8 October 2015
- Published by Springer Nature in Scientific Reports
- Vol. 5 (1) , 14967
Open AccessHighly informative marker sets consisting of genes with low individual degree of differential expression
Genes with significant differential expression are traditionally used to reveal the genetic background underlying phenotypic differences between cancer cells. We hypothesized that informative marker sets can be obtained by combining genes with a relatively low degree of individual differential expression. We developed a method for construction of highly informative gene combinations aimed at the maximization of the cumulative informative power and identified sets of 2–5 genes efficiently predicting recurrence for ER-positive breast cancer patients. The gene combinations constructed on the basis of microarray data were successfully applied to data acquired by RNA-seq. The developed method provides the basis for the generation of highly efficient prognostic and predictive gene signatures for cancer and other diseases. The identified gene sets can potentially reveal novel essential segments of gene interaction networks and pathways implied in cancer progression.
- 1 January 2015
- Published by Elsevier in Progress in Histochemistry and Cytochemistry
- Vol. 49 (4) , 21-29
Modelling the metastatic cascade by in vitro microfluidic platforms
- 1 January 2015
- Published by Elsevier in Progress in Histochemistry and Cytochemistry
- Vol. 49 (4) , 21-29
Modelling the metastatic cascade by in vitro microfluidic platforms
- Open Access
- 4 December 2014
- Published by Springer Nature in BMC Research Notes
- Vol. 7 (1) , 871
miRNome of inflammatory breast cancer
Inflammatory breast cancer (IBC) is an extremely malignant form of breast cancer which can be easily misdiagnosed. Conclusive prognostic IBC molecular biomarkers which are also providing the perspectives for targeted therapy are lacking so far. The aim of this study was to reveal the IBC-specific miRNA expression profile and to evaluate its association with clinicopathological parameters.
- 4 December 2014
- Published by Springer Nature in BMC Research Notes
- Vol. 7 (1) , 871
Open AccessmiRNome of inflammatory breast cancer
Inflammatory breast cancer (IBC) is an extremely malignant form of breast cancer which can be easily misdiagnosed. Conclusive prognostic IBC molecular biomarkers which are also providing the perspectives for targeted therapy are lacking so far. The aim of this study was to reveal the IBC-specific miRNA expression profile and to evaluate its association with clinicopathological parameters.
- Open Access
- 1 January 2013
- Published by Springer Nature in Molecular Cancer
- Vol. 12 (1) , 107
Epithelial-mesenchymal transition: focus on metastatic cascade, alternative splicing, non-coding RNAs and modulating compounds
Epithelial-mesenchymal transition (EMT) is a key process in embryonic development and metastases formation during malignant progression. This review focuses on transcriptional regulation, non-coding RNAs, alternative splicing events and cell adhesion molecules regulation during EMT. Additionally, we summarize the knowledge with regard to the small potentially druggable molecules capable of modulating EMT for cancer therapy.
- 1 January 2013
- Published by Springer Nature in Molecular Cancer
- Vol. 12 (1) , 107
Open AccessEpithelial-mesenchymal transition: focus on metastatic cascade, alternative splicing, non-coding RNAs and modulating compounds
Epithelial-mesenchymal transition (EMT) is a key process in embryonic development and metastases formation during malignant progression. This review focuses on transcriptional regulation, non-coding RNAs, alternative splicing events and cell adhesion molecules regulation during EMT. Additionally, we summarize the knowledge with regard to the small potentially druggable molecules capable of modulating EMT for cancer therapy.