Professor Jerry Adams

Professor Jerry Adams



Professor Jerry Adams outside the lab



BSc Emory PhD Harvard

Joint Division Head

Impaired cell death is now recognised as an important step towards cancer. Defects in cell death (apoptosis) are also a major barrier to effective anti-cancer therapy. The discoveries on apoptosis by our team have galvanised the search for drugs that directly engage the cell’s apoptotic machinery, as a new way to treat cancer.

One major goal of our research is to determine how drugs that promote cell death can be used most effectively to improve cancer treatment. We also aim to clarify further how apoptosis is controlled and how the control goes awry in cancer.

Research interest

Impaired apoptosis is critical for tumorigenesis and a barrier to effective therapy. This concept arose from my laboratory’s seminal discovery that the Bcl-2 gene, known to be translocated in certain lymphomas, imposes cell survival. Our subsequent research with institute colleagues has helped to establish that interactions between proteins related to Bcl-2 determine whether a cell lives or commits suicide in response to diverse damage signals. These discoveries have galvanized the development of novel potential anti-cancer agents (‘BH3 mimetics’) that directly switch on apoptosis by engaging Bcl-2-like proteins.

The further advancement of BH3 mimetics requires a deeper understanding of how the apoptotic switch operates and how it is impaired in cancer. Those are the prime objectives of our current and proposed research.

Our research thus aims to:

  • Clarify apoptotic mechanisms.
  • Establish how the Bcl-2 family affects anti-cancer drug responses
  • Identify better ways to use BH3 mimetic drugs. 

Professor Jerry Adams delivers the 2014 Macfarlane Burnet Lecture