Haematological Malignancies
Early but mechanistically distinct apigenin data in leukaemia, myeloma, and neuroblastoma models.
Why this cancer type is a plausible fit
Haematological cancers often depend heavily on BCL-2 family proteins for survival. Apigenin has been studied as a chemosensitiser in leukaemia and as a ferroptosis inducer in multiple myeloma.
The topoisomerase inhibitor sensitisation data in leukaemia are among the most mechanistically detailed combination findings in the apigenin literature.
Cell data
Leukaemia
Apigenin sensitises leukaemia cells to topoisomerase II inhibitors, increasing apoptosis beyond either agent alone.
Apigenin causes cell-cycle arrest and also sensitises leukaemia cells to vincristine.
These effects fit with broader BCL-2 family suppression and cell-cycle disruption.
Multiple myeloma
Apigenin-induced ferroptosis has been confirmed in
NCI-H929myeloma cells.Rescue with ferrostatin-1 supports ferroptosis as a true mechanism rather than nonspecific toxicity.
Neuroblastoma
Apigenin enhanced etoposide activity in neuroblastoma cells by retaining p53 in the nucleus and increasing DNA-damage-driven apoptosis.
Animal data
No direct haematological cancer animal studies were identified in the current review. Most evidence in this category remains cell-line based.
Human data
No human oncology data exist.
Clinical positioning
This is early, but mechanistically distinct.
Leukaemia is a plausible setting because of topoisomerase inhibitor dependence and BCL-2 family signalling. The myeloma ferroptosis signal is novel and worth following. This remains one of the thinner areas for in vivo evidence.