Cancer therapy articles from across Nature Portfolio

Pharmacological targeting of missense TP53 mutations has traditionally failed owing to the mutant heterogeneity, gain-of-function oncogenic properties and paradoxical stability of mutant p53 protein. A ‘p53-conditional’ proximity strategy promises to eradicate TP53 missense mutant-driven cancer by exploiting its abundance.

Dormant tumour cells that survive initial therapy can awaken years later to seed metastases. New data from a phase II trial indicate that intercepting this dormancy by targeting autophagy and mTOR signalling might prevent breast cancer relapse before it begins, opening a path towards proactive prevention disease recurrence.

Two seminal studies report a bioengineering approach to modeling CAR-T cell therapy of solid human tumors.

Melanoma cells lacking SOX10 are tolerant to MAPK inhibition (MAPKi) due to elevated TAZ-driven TEAD signaling. Here, the authors develop two inhibitors of TEAD, capable of resensitising SOX10 knockout melanoma cells to MAPKi and offering a strategy to overcome drug tolerance and improve treatment response.

Pharmacological targeting of missense TP53 mutations has traditionally failed owing to the mutant heterogeneity, gain-of-function oncogenic properties and paradoxical stability of mutant p53 protein. A ‘p53-conditional’ proximity strategy promises to eradicate TP53 missense mutant-driven cancer by exploiting its abundance.

Dormant tumour cells that survive initial therapy can awaken years later to seed metastases. New data from a phase II trial indicate that intercepting this dormancy by targeting autophagy and mTOR signalling might prevent breast cancer relapse before it begins, opening a path towards proactive prevention disease recurrence.