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Prof. Pieter Eichhorn

Professor
Diagnostic and Therapeutic Sciences

Experimental Therapeutics Group

Professor Pieter Eichhorn is a cancer biologist whose research focuses on the genetic and molecular mechanisms driving tumour development and treatment resistance. He completed his PhD at the University of Newcastle upon Tyne under Professor Tom Strachan, followed by postdoctoral research at the Netherlands Cancer Institute with Professor Rene Bernards, where he helped pioneer RNAi screening in mammalian cells. He later worked with Professor José Baselga at the Vall d’Hebron Institute of Oncology in Barcelona, identifying key pathways involved in drug resistance, including PI3K hyperactivation in Lapatinib resistance. As Dean of Research Infrastructure at Curtin, he continues to advance cancer research and support the development of world-class research capability across the university.  

About

Professor Eichhorm earned his Bachelor of Science in Human Genetics from the University of Western Ontario and completed his PhD at the University of Newcastle upon Tyne under Professor Tom Strachan, where he cloned the gene responsible for Cornelia de Lange syndrome. During his postdoctoral work with Professor Rene Bernards at the Netherlands Cancer Institute, he helped pioneer RNA interference (RNAi) screening in mammalian cells to identify genes driving cancer progression.

At the Vall d’Hebron Institute of Oncology in Barcelona, he worked with Professor José Baselga to identify novel cancer-related genes and pathways, including PI3K hyperactivation as a mechanism of Lapatinib resistance. His later research at Massachusetts General Hospital and Harvard Medical School uncovered Cyclin E and RSK4 as key mediators of resistance to Trastuzumab and PI3K inhibitors.

Before joining Curtin University, Professor Eichhorn led a research group at the Cancer Science Institute in Singapore. His current work at Curtin investigates adaptive resistance mechanisms, ubiquitin-modifying enzymes, and non-coding RNAs that reshape cancer signalling networks under treatment pressure, with the goal of developing more durable, combination-based cancer therapies.

 

Email: Pieter.Eichhorn@curtin.edu.au
Tel: +61 (08) 9266 1239
ORCID
Google Scholar
Curtin Staff Profile

Research Focus

Professor Eichhorn’s research focuses on understanding the mechanisms by which cancer cells develop resistance to targeted therapies, with a particular emphasis on breast cancer and melanoma. Although targeted treatments have significantly improved patient outcomes, most responses are short-lived due to primary or acquired resistance. His team investigates how these adaptive responses enable tumour cells to reactivate key oncogenic pathways, such as MAPK and PI3K, often through the suppression of negative feedback mechanisms.

Using a range of preclinical and clinical models, including patient-derived xenografts, organoids (PDXOs), and CRISPR/Cas9-edited cell lines, the group studies how cancer cells evade therapeutic inhibition. A central area of focus is the role of ubiquitin-modifying enzymes—such as SMURF2, USP9X, USP28, and USP15—in regulating these feedback loops and driving drug resistance.

The lab also explores the contribution of long non-coding RNAs (lncRNAs) to resistance, revealing how they influence ubiquitin pathways and reshape cellular signalling networks under drug pressure.

In addition, Professor Eichhorn’s research examines the link between adaptive resistance and tumour-immune interactions, investigating how reactivation of MAPK and PI3K pathways affects immune evasion mechanisms, including PD-L1 expression and antigen presentation. This work aims to guide the integration of targeted and immune-based therapies to overcome resistance and improve long-term outcomes for cancer patients.

 

Research Team

Dr Christopher Witham

Research Associate

Stephanie Bridgeman

Research Assistant

Sona Bassi

PhD Student

Alicia Dixon

Student

Publications

Kumari, N., S. C. E. Wright, C. M. Witham, L. Monserrat, M. Palafox, J. L. C. Richard, C. Costa, M. Elkabets, M. Agostino, T. Klemm, and 27 more contributors. 2026. USP10/GSK3β-mediated inhibition of PTEN drives resistance to PI3K inhibitors in breast cancer.Journal of Clinical Investigation 136 (1)
ABSTRACT

Activating mutations in PIK3CA, the gene encoding the catalytic p110α subunit of PI3K, are some of the most frequent genomic alterations in breast cancer. Alpelisib, a small-molecule inhibitor that targets p110α, is a recommended drug for patients with PIK3CA-mutant advanced breast cancer. However, clinical success for PI3K inhibitors (PI3Kis) has been limited by their narrow therapeutic window. The lipid phosphatase PTEN is a potent tumor suppressor and a major negative regulator of the PI3K pathway. Unsurprisingly, inactivating mutations in PTEN correlate with tumor progression and resistance to PI3K inhibition due to persistent PI3K signaling. Here, we demonstrate that PI3K inhibition leads rapidly to the inactivation of PTEN. Using a functional genetic screen, we show that this effect is mediated by a USP10-GSK3β signaling axis, in which USP10 stabilizes GSK3β, resulting in GSK3β-mediated phosphorylation of the C-terminal tail of PTEN. This phosphorylation inhibits PTEN dimerization and thus prevents its activation. Downregulation of GSK3β or USP10 resensitizes PI3Ki-resistant breast cancer models and patient-derived organoids to PI3K inhibition and induces tumor regression. Our study establishes that enhancing PTEN activity is a new strategy to treat PIK3CA mutant tumors and provides a strong rationale for pursuing USP10 inhibitors in the clinic.

Kumari, N., S. C. E. Wright, C. M. Witham, L. Monserrat, M. Palafox, J. L. C. Richard, C. Costa, M. Elkabets, M. Agostino, T. Klemm, and 27 more contributors. 2025. Aa href="https://www.jci.org/articles/view/180927">USP10/GSK3β-mediated inhibition of PTEN drives resistance to PI3K inhibitors in breast cancer.Journal of Clinical Investigation 135 (22)

Identification & characterisation of molecular drivers of therapeutic resistance

Prof. Pieter Eichhorn

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