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OSCC arises from tobacco/areca-nut carcinogenesis compounded by chronic inflammation and oxidative stress. The literature converges on NF-κB, STAT3, Nrf2/KEAP1 and EGFR as central druggable nodes. Phytochemical chemoprevention evidence is strongest for polyphenols and flavonoids, with reproducible apoptosis and tumour-burden reduction in cell and animal models.
EGCG, curcumin, resveratrol · antioxidant & anti-inflammatory mechanisms.
NF-κB / STAT3 / Nrf2 mechanistic dissection.
Nanoemulsion, oral films, exosomes.
Small-cohort chemoprevention studies.
8-OHdG, Ki-67, p53 status.
| Extracted claim | Model | Effect | Confidence |
|---|---|---|---|
| EGCG induces apoptosis via caspase-3/9 in OSCC lines | In-vitro | ↑ apoptosis | |
| EGCG upregulates Nrf2/HO-1 cytoprotective axis | In-vitro | ↑ Nrf2 | |
| Nimbolide suppresses NF-κB nuclear translocation | In-vivo | ↓ NF-κB | |
| Curcumin plasma levels sub-therapeutic orally | Clinical | ↓ bioavail. |
Highly-cited hub (gold) anchors the EGCG-OSCC literature; recent nodes (teal) branch into delivery and combination work.
Topics sized by 3-year citation acceleration. Green = fastest-rising white-space worth entering now.