PROF Jerry Adams

PROF Jerry Adams

Positions

  • Genetic basis of cancer and cell death control (Molecular Biology, Drug Discovery)

Overview

OverviewText1

  • www.wehi.edu.au/people/jerry-adams

    Lab focus: Genetic basis of cancer and cell death control

    Impaired cell death is now recognised as an important step towards cancer, and a major barrier to effective anti-cancer therapy. Our team's discoveries on apoptosis have galvanised the search for drugs that directly engage the cell’s apoptotic machinery, as a new way to treat cancer. One such drug has been approved for an aggressive form of leukaemia and is under trial for many other malignancies.

    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.

    Our primary focus is better understanding of cell death mechanisms, which should expedite the search for better ways to control cell death to improve therapy.   

Publications

Selected publications

Awards

Education and training

  • PhD, Harvard University
  • BSc, Institution not known

Awards and honors

  • Macfarlane Burnet Lecture and Medal, Australian Academy of Science, 2014
  • Fellow of the Royal Society, 2004
  • Fellow of the Australian Academy of Science, 1986

Supervision

Available for supervision

  • N

Supervision Statement

  • 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.