Dr Marco Herold

Dr Marco Herold

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Dr Marco Herold in the laboratory

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Dr
Marco
Herold

Dip Biol PhD Wuerzburg

Laboratory Head

Lab focus: CRISPR/Cas9 for identifying cancer drivers

My laboratory aims to identify how cancer cell survival is controlled. Human cancers frequently express high levels of pro-survival proteins. They also harbour defects in processes that inhibit tumour growth, so-called tumour suppressor genes. Importantly, these abnormalities render the tumour cells resistant to many standard chemotherapeutics. 

The ultimate goal of my research is to develop drugs that kill chemo-resistant tumour cells to improve the outcome for cancer patients.

Research interest

Our laboratory is interested in the molecular regulation of apoptotic cell death. We study how this contributes to the development and growth of cancer cells.

One focus of our research is the BH3 mimetic drugs which inhibit pro-survival Bcl-2 family proteins. We are collaborating with industry colleagues to develop new BH3 mimetics that target the pro-survival protein Mcl-1. 

We are also investigating the role of another pro-survival protein, A1, in cancer. In conjunction with teams from the Structural Biology and Chemical Biology divisions, we are developing BH3 mimetics that specifically inhibit A1, with a goal of producing clinically useful agents.

Another project in my laboratory aims to identify novel tumour suppressor genes. We are using in vivo whole genome CRISPR library screening and gene deletion technologies to systematically inactivate putative tumour suppressor genes. This project is revealing exciting new candidate tumour suppressors. We are currently defining their biochemical functions. The ultimate aim of these studies is to identify novel drug targets for cancer therapy.

 

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Dr Marco Herold speaks to ABC TV’s Catalyst program about new ways to fight cancer with CRISPR and Cas9

Our researchers have discovered a promising strategy for treating cancers that are caused by one of the most common cancer-causing changes in cells.