Axonal injury, induced in the white matter by expansion of early tumour cells, is a key driver of glioblastoma progression.

Researchers discovered that NASP, a key protein involved in chromatin organization, plays a surprising role in resistance to PARP inhibitors. Targeting NASP offers a new therapeutic strategy for cancer treatment.

PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

The emergence of poly(ADP-ribose) polymerase inhibitors (PARPi) as a transformative therapy for homologous recombination-deficient tumors has significantly altered the landscape of cancer treatment. These drugs exploit synthetic lethality to selectively kill tumor cells harboring defects in DNA repair pathways, particularly BRCA1 and BRCA2 mutations. However, the clinical utility of PARPi is frequently hampered by the development of resistance, posing a formidable challenge for long-term therapeutic success.