Inhibiting Bcl-2 proteins for cancer therapy

Project Description

In many types of cancers, the rogue malignant cells are long-lived because, unlike normal cells, they cannot be readily killed. This characteristic often renders them highly resistant to anti-cancer drugs, thereby causing treatment failure or disease relapse.

An attractive approach to overcome this problem is to directly activate the normal cell death machinery that eliminates excess, unwanted or damaged cells. One way to directly induce the killing of tumor cells is to target specialised proteins belonging to the Bcl-2 family that normally act to keep cells alive.

In order to do this, we need to have a detailed map of how they can be targeted. The aim of this project is to provide such a comprehensive picture so that we know what the requirements are to target critical survival factors such as Bcl-2 itself. Our previous studies indicate that it will be feasible and desirable to target only the survival factor pertinent for maintaining the viability of a particular cancer cell type.

This will also spare normal tissues, thus minimising the harmful and undesirable side-effects commonly seen with many anti-cancer agents. The studies are important for developing a new class of anti-cancer agents that promises much by targetting a critical molecular defect in most tumours.

Annual Lay Report 

Year

2007-2009

Researchers

Dr Walter Fairlie, Dr David Huang

Institution

Walter and Eliza Hall Institute

Funding

$70,000 per annum

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