National Repository of Grey Literature 2 records found  Search took 0.01 seconds. 
Oncoretroviruses: tumor transformation mechanisms of hematopoietic cells resulting in leukaemia
Gašpareková, Mária ; Bendová, Michaela (advisor) ; Mrvová, Silvia (referee)
HTLV-1 and FeLV are retroviruses, which are able to transform host cells and cause cancer, mostly leukemia, in infected organism. Belonging to Retroviridae family and both using very similar genome, these viruses developed different ways to reach transformation of infected cells. While FeLV uses insertional activation close to cellular proto-oncogenes in order to regulate transcription of these genes or carries cellular oncogene in its genome, HTLV-1 codes viral proteins which are able to regulate many processes of the cell. One of these proteins is Tax, which regulates many events in the cell, such as signalization, cell cycle, apoptosis and others. Another protein responsible for oncogenesis is HBZ, which is transcribed from antisense strand of proviral DNA. In the end HTLV-1 and FeLV strategies causing cancer are compared with some other leukemic retroviruses in order to show, that molecular strategies described on examples of HTLV-1 and FeLV are more or less common also for other oncogenic retroviruses. Key words: HTLV-1, FeLV, transformation, leukaemia, tumor, oncogene
The effect of Crk SH3domain inhibition in invasiveness of cells
Tomášová, Lea ; Rösel, Daniel (advisor) ; Vomastek, Tomáš (referee)
Protooncogene Crk was found to be upregulated in tumours with aggressive and invasive potential. The adaptor protein Crk has an important role in cell signaling: it integrates signals from activated integrins and growth factors receptors via its SH2 domain and transmits the signal to its SH3 domain binding partners that activate the small GTPases Rac1, Rap1 and Ras. This leads to regulation of cell migration, proliferation and survival. The aim of this thesis project was to inhibit the Crk dependent signaling by a competitive inhibition of the Crk SH3 domain, using a high affinity CrkSH3 binding peptoid. Binding of the inhibitor to the Crk SH3 domain prevents binding of cellular Crk SH3 interaction partners and the corresponding signal transmission is impaired. In this thesis project the effect of the Crk SH3 inhibition on the invasiveness of cancer cells was analyzed. The observed inhibitory effect on cell invasion as well as on anchorage independent growth provides a proof of therapeutical relevance of targeting CrkSH3N domain by peptoide-based inhibitors. Powered by TCPDF (www.tcpdf.org)

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