ABSTRACT
In this seminar, Dr Buchert will present two vignettes highlighting his group’s research in gastric cancer. The first one will centre on the serine/threonine kinase and suspected cancer driver DCLK1 and reveals the cell intrinsic and extrinsic mechanisms by which this kinase promotes gastric cancer. The second one investigates the crosstalk between epithelial tuft cells and type 2 innate lymphoid cells (ILC2s) in the gastric mucosa and how this pathway promotes gastritis, gastric metaplasia and tumour formation.

BIOGRAPHY
Michael is a trained Molecular Biologist who obtained his PhD from the University of Zürich (Switzerland) in 1998. During his two stints as a postdoctoral fellow in Melbourne (1999-2002) and in Montpellier (2002-2007), he investigated the role of tight junction proteins in GI tumourigenesis.

In 2007, he returned to Melbourne and joined the group of Prof Matthias Ernst at the Ludwig Institute for Cancer Research (LICR) in Parkville as an Assistant Investigator and his work there aimed at dissecting the contributions of canonical Wnt/beta-catenin and Jak/Stat3 signalling pathways to GI tumourigenesis.

Via a three-year pit stop at the WEHI from 2012-2015, he then came to the newly opened Olivia-Newton-John Cancer Research Institute in Melbourne in 2016 where he set up his own research group with a general focus on stomach cancer.  

One of his projects centres on understanding the role of the tuft cell/ILC2 crosstalk during gastritis and gastric tumourigenesis while another project aims at working out how the suspected cancer driver doublecortin-like kinase 1 (DCLK1) promotes gastric cancer.  He leverages complex genetically modified mouse strains and preclinical mouse models of gastric cancer to dissect the contributions of genes and signalling pathways to the genesis, maintenance and progression of this disease with an aim of identifying therapeutic targets.