Thomas R. Cox, Jan 2020
We are pleased to announce that Kaitlin Wyllie has just joined the Matrix & Metastasis team as a Research Assistant.
Kaitlin recently completed her Master of Research (M.Res.) at the Department of Molecular Sciences at Macquarie University.
Kaitlin will join our projects looking at the role of the ECM in breast cancer therapy and our efforts to develop novel targeting approaches.
Thomas R. Cox, Aug 2019
The Mini‐Organo: A rapid high‐throughput 3D coculture organotypic assay for oncology screening and drug development
Just published in Cancer Reports is our new protocol paper detailing the development of a rapid high-throughput (96wp) 3D organotypic coculture assay that is optimised for screening cancer cell and cancer-associated fibroblast response to drugs in physiologically relevant matrices.
Thomas R. Cox, Mar 2019
Targeting promiscuous heterodimerization overcomes innate resistance to ERBB2 dimerization inhibitors in breast cancer
We have just published a new paper in Breast Cancer Research in collaboration with lead researcher Dr. David Croucher from the Garvan Institute, looking at how and why ERBB2 (HER2) positive breast cancer cells develop resistance to targeted therapies such as trastuzumab (Herceptin™).
Thomas R. Cox, Jan 2019
The extracellular matrix as a key regulator of intracellular signalling networks
Our latest review in collaboration with Dr. David Croucher and Dr. Dirk Fey on ‘The extracellular matrix as a key regulator of intracellular signalling networks‘ has just been published as part of a special series on ‘Translating the Matrix’ in the British Journal of Pharmacology.
Computational model of the interplay between the ECM and drug activated MAPK‐JNK signalling network.
At their simplest, cells follow a set of rules governed by their genetic code. These rules, which are executed by the protein‐based signalling networks that the genes encode, control the assimilation of information and decision‐making processes that shape a cell’s response to their surroundings.
Thomas R. Cox, Jan 2019
The Matrix and Metastasis group is excited to be welcoming two new Honours students to the team for 2019.
Yordanos Setargew (left) and Shivanjali Ratnaseelan (right) will both be joining us to spend the next 10 months in the lab as part of their UNSW Sydney, School of Medical Sciences (SoMS) Honours Program.
Yordanos will be looking at new ways to target the lysyl oxidase (LOX) family in pancreatic cancer, and Shivanjali will be looking at how the biomechanical properties of the tumour microenvironment alter breast cancer cell sensitivity to chemotherapy.
Thomas R. Cox, Oct 2018
Cancer cell ability to mechanically adjust to extracellular matrix stiffness correlates with their invasive potential
Just published in Molecular Biology of the Cell is our recent paper looking at the effect of extracellular matrix stiffness on the intrinsic biomechanical properties of cancer cells. Led by Professors Janine Erler (Biotech Research & Innovation Centre) and Lene Oddershede (Niels Bohr Institute) both from the University of Copenhagen, the study combines optical tweezers–based microrheology and deformability cytometry with 3D biological models to dissect how cancer cells biomechanically interact with and respond to the stiffness of the microenvironment they are within.
Optical Tweezers Schematic for measuring intracellular viscosity
The results show that invasive cancer cells adjust their intracellular and overall viscoelasticity to ECM density, and that cancer cell viscosity increases during invasion into 3D collagen matrices.
Thomas R. Cox, Sep 2018
The lab is excited to be welcoming our first Ph.D. student Michael Papanicoloau who has just started in the lab. Michael joins us after completing his Honours degree in Biomedical Science at UTS and the Woolcock Institute of Medical Research.
Having been awarded a prestigious UTS Research Excellence Scholarship, Michael’s Ph.D. will focus on understanding how the extracellular matrix changes over time in solid tumours, in particular breast cancer, and how these changes feed into the pathological progression of the disease at both primary and secondary sites.