We don’t begin
with techniques.
We begin with biological questions—and then build the experiments needed to answer them.
Why is GM2 overexpressed in cancer?
How is B4GALNT1/GM2-synthase transcriptionally deregulated? How do transcription factors and chromatin regulators reshape the glycosphingolipid landscape of a tumour cell?
What does excess GM2 do?
How does a GM2-rich membrane alter receptor-associated signalling, EMT, migration, invasion, anchorage-independent growth and metastatic behaviour—and how does shed GM2 communicate with the tumour microenvironment?
We Don’t Begin With Techniques
We begin with core biological questions—and then build the systematic experimental frameworks needed to answer them.
Why is GM2 overexpressed in cancer?
How is B4GALNT1/GM2-synthase transcriptionally deregulated? How do transcription factors and chromatin regulators reshape the glycosphingolipid landscape of a tumour cell?
What does excess GM2 do?
How does a GM2-rich membrane alter receptor-associated signalling, epithelial-to-mesenchymal transition (EMT), cell migration, invasion, anchorage-independent growth, and metastatic behaviour? How does shed GM2 communicate with and remodel the surrounding tumour microenvironment?