Apigenin Evidence by Cancer Type
Cancer settings with the strongest dedicated apigenin signals, plus shorter notes on thinner evidence areas.
This page maps the cancer types where apigenin has enough independent evidence to justify closer review. Additional pages can be added as the literature grows.
Dedicated pages
Cancer Type | Why It Matters | Evidence Level |
|---|---|---|
Colorectal Cancer | PKM2 glycolysis, BCL-2 family pressure, | One of the strongest settings |
Hepatocellular Carcinoma |
| Strong in vivo signal |
Prostate Cancer | Akt inactivation, | One of the most mechanistically developed settings |
Ovarian Cancer |
| Clinically interesting |
Haematological Malignancies | Topoisomerase inhibitor sensitisation in leukaemia, ferroptosis in myeloma | Early, but mechanistically distinct |
Dedicated page links
Other cancer types overview
Several additional tumour types show consistent cell-line signals but do not yet justify standalone pages:
Lung cancer (
NSCLC):TRAILpotentiation,PI3K/AKTeffects, and early anti-metastatic signals in animal modelsMelanoma:
PD-L1suppression,STAT3involvement, and one of the strongest immune-oncology signals across the apigenin literatureBreast cancer: p53-dependent apoptosis, SASP suppression, and
IL-1α/NF-κBrelevance. This could justify a dedicated page if the evidence base continues to grow.Endometrial cancer: ferroptosis and autophagy data. Early, but mechanistically interesting.
Pancreatic cancer: gemcitabine sensitisation and NK-cell cytotoxicity data. Very early and still thin.