My name is Tony Burgess.
I'm a Laboratory Head at the Walter and Eliza Hall Institute in Melbourne.
My talk today will be about the EGF receptor family targets for improving cancer therapy.
This talk will cover a set of mutations relevant to the EGF receptor,
that drive cancer biology.
We will focus on the EGF receptor family and its ligands,
how they were discovered to be involved in cancer and then
some of the modern aspects of EGF receptor biology,
such as the way the receptor moves on the cell surface to provide
the intracellular signaling for driving cells into proliferation.
We will also be looking at the targeting,
the EGF receptor family members so we can improve cancer treatment,
in particular, how the different EGF receptor pathway
targeting drugs should be able to work together to improve outcomes for cancer patients.
Most colon cancers are initiated by mutations to the tumor suppressor genes, APC and p53.
These mutations are followed by several other mutations to signaling molecules,
in particular, the ras oncogene, integrins,
intracellular matrix overproduction, DNA repair enzymes such as MLH1,
and in our case, the EGF receptor,
which is sometimes over-expressed through amplification,
and at other times activated by truncation of
the N-terminus or mutations in the kinase domain.
All of these perturbations combine to drive cancer cells from
normal proliferation to abnormal lifetime and cell production in tissues.