Traditional anti-tumor therapies have been recently supplemented with substances inhibiting the growth of blood vessels. The rationale for such an approach was the Judah Folkman’s hypothesis from the beginnings of 70ies of the last century. He suggested that the growth of tumour  is dependent on the process of angiogenesis and proposed that treatment of tumours can be achieved by inhibition of the capillaries growth. Therapy of breast, lung, intestine and kidney cancer was recently improved by introduction of Avastin, the antibody specifically binding the vascular endothelial growth factor. The studies on small molecular weight inhibitors of growth factors receptors are underway, but they reveal the new previously unknown problems. Development of efficient means of inhibition of complex angiogenic activity of tumour cells and strategies allowing. tumour cells to change the mechanisms of angiogenesis during the therapy will be crucial for increasing the effectiveness of current and future anti-angiogenic drugs. During the lecture the own results of studies on mechanisms of angiogenesis regulated by HIF and Nrf2 transcription factors will be discussed.

• Legal notice:
  

  Copyright (c) Pielaszek Research, all rights reserved.
  The above materials, including auxiliary resources, are subject to Publisher's copyright and the Author(s) intellectual rights. Without limiting Author(s) rights under respective Copyright Transfer Agreement, no part of the above documents may be reproduced without the express written permission of Pielaszek Research, the Publisher. Express permission from the Author(s) is required to use the above materials for academic purposes, such as lectures or scientific presentations.
  In every case, proper references including Author(s) name(s) and URL of this webpage: https://science24.com/paper/23040 must be provided.

1. HO-1 regulates expression of human MMP-1 and murine MMP-13 in vitro.
2. Effects of heme oxygenase-1 on proliferation, cell cycle regulation and susceptibility of the primary murine fibroblasts to oxidative stress.
3. Overexpression of biliverdin reductase enhances heme oxygenase expression, activates ERK1, JNK1 and p38 kinases and ensure partial protection against cellular stress