How cancer spreads throughout the body

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FAU researchers identify mechanism that causes particularly aggressive types of cancer to develop

Fast metastasis and resistance to treatment are characteristic of aggressive types of cancer such as pancreatic cancer and certain kinds of breast cancer. They are also the main causes of cancer-related death, as there is currently no specific treatment available that is able to stop tumors spreading throughout the whole body. Researchers at FAU have recently made a discovery that could change this. They have discovered a mechanism that promotes metastasis and causes tumors to become resistant to treatment. Based on these findings they have identified a gene set that suggests a particularly bad prognosis in case of breast cancer. The researchers’ findings have recently been published in the journal Nature Communications.

Two key characteristics must be activated in tumor cells in order for them to metastasize: the ability to spread throughout the body and the ability to form new tumors – metastases – in other remote parts of the body.  In addition, such tumor cells must be especially resilient – a characteristic that also makes them more resistant to treatment.

The team led by Prof. Dr. T. Brabletz from the Chair of Experimental Medicine I has now proven that these characteristics are activated when two fundamental embryonic signaling pathways, the EMT pathway and the HIPPO pathway, interact. When the key molecules of the two pathways, ZEB1 and YAP, interact with one another directly they activate a range of genes that are required for aggressive tumor growth. The team was able to identify a set of eight genes from among this range that, when activated, is associated with particularly aggressive tumor growth in case of breast cancer.  They now aim to use these findings to identify biological markers for aggressive tumors – known as prognostic markers – to confirm the clinical relevance of the mechanism that they have discovered.

As the fatal potential of the two key molecules ZEB1 and YAP is only activated when they are combined, the team also aims to search for inhibitors that can block this interaction, with the long-term goal to develop new treatment concepts for aggressive types of cancer.

Original publication

Further information

Prof. Dr. Thomas Brabletz
Phone: +49 9131 8529104