Date Fruit Extract / P53 Cancer Research Results

DFE, Date Fruit Extract: Click to Expand ⟱
Features:
Dates (the fruit of Phoenix dactylifera) have been increasingly studied for their potential anticancer and cancer-preventive properties, mainly due to their rich phytochemical content and strong antioxidant activity.
Dates contain a broad spectrum of bioactive compounds linked to cancer prevention:
-Phenolic acids – e.g., ferulic acid, gallic acid, caffeic acid, and p-coumaric acid
-Flavonoids – e.g., quercetin, luteolin, apigenin
-Carotenoids – e.g., β-carotene, lutein
-Tannins, saponins, and sterols
-Dietary fiber and polysaccharides
These compounds have antioxidant, anti-inflammatory, and antiproliferative effects.

Date fiber and polyphenols foster beneficial gut bacteria (e.g., Bifidobacterium, Lactobacillus) that produce short-chain fatty acids (SCFAs), which protect the colon and may lower colon cancer risk.

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Nrf2 / ARE antioxidant response Context-dependent modulation Nrf2 ↑; antioxidant enzymes ↑ R, G Redox buffering Polyphenol-driven antioxidant response is the dominant mechanistic theme in non-malignant systems.
2 ROS / oxidative stress modulation ROS ↓ (generally); pro-oxidant effects not dominant Oxidative stress ↓ P, R Antioxidant effect Most studies describe antioxidant protection rather than tumor-selective ROS elevation.
3 NF-κB inflammatory signaling NF-κB ↓ (reported in limited models) Inflammation tone ↓ R, G Anti-inflammatory modulation Observed in inflammatory and oxidative injury systems; tumor-specific evidence is limited.
4 Intrinsic apoptosis (mitochondrial; limited data) Apoptosis ↑ (reported in some in-vitro studies) ↔ G Conditional cytotoxicity Cytotoxic effects generally mild and concentration-dependent; not comparable to strong pro-oxidants.
5 Cell-cycle arrest Cell-cycle modulation ↑ (limited evidence) ↔ G Cytostasis (weak) Evidence exists but is inconsistent and often extract-dependent.
6 PI3K → AKT signaling Limited data; possible ↓ (reported in some systems) ↔ R, G Survival pathway modulation Not a consistently demonstrated primary mechanism.
7 Angiogenesis signaling (VEGF) Limited data; possible ↓ ↔ G Potential anti-angiogenic effect Evidence sparse compared to stronger polyphenols like gallic or caffeic acid.
8 Invasion / metastasis (MMPs) Limited evidence ↔ G Uncertain tumor relevance Not well characterized mechanistically in oncology models.
9 Metabolic modulation Indirect via anti-inflammatory and antioxidant tone Metabolic support ↑ R, G Systemic metabolic effect Better supported in cardiometabolic contexts than direct anticancer contexts.
10 Extract variability / compositional heterogeneity Activity varies by cultivar, processing, solvent — — Translation constraint Whole fruit extracts differ significantly in phenolic profile and potency.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (rapid antioxidant interactions)
  • R: 30 min–3 hr (acute transcriptional shifts)
  • G: >3 hr (gene-regulatory and phenotype-level outcomes)
P53, P53-Guardian of the Genome: Click to Expand ⟱
Source: TCGA
Type: Proapototic
TP53 is the most commonly mutated gene in human cancer. TP53 is a gene that encodes for the p53 tumor suppressor protein ; TP73 (Chr.1p36.33) and TP63 (Chr.3q28) genes that encode transcription factors p73 and p63, respectively, are TP53 homologous structures.
p53 is a crucial tumor suppressor protein that plays a significant role in regulating the cell cycle, maintaining genomic stability, and preventing tumor formation. It is often referred to as the "guardian of the genome" due to its role in protecting cells from DNA damage and stress.
TP53 gene, which encodes the p53 protein, is one of the most frequently mutated genes in human cancers.
Overexpression of MDM2, an inhibitor of p53, can lead to decreased p53 activity even in the presence of wild-type p53.
In some cancers, particularly those with mutant p53, there may be an overexpression of the p53 protein.
Cancers with overexpression: Breast, lung, colorectal, overian, head and neck, Esophageal, bladder, pancreatic, and liver.
Scientific Papers found: Click to Expand⟱
4455- DFE,    Ajwa Date (Phoenix dactylifera L.) Extract Inhibits Human Breast Adenocarcinoma (MCF7) Cells In Vitro by Inducing Apoptosis and Cell Cycle Arrest
- in-vitro, BC, MCF-7 - in-vitro, Nor, 3T3
TumCCA↑, P53↑, BAX↑, Casp3↑, MMP↓, Fas↑, FasL↑, Bcl-2↓, Apoptosis↑, TumCP↓, TUNEL↑, eff↑, selectivity↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Fas↑, 1,   FasL↑, 1,   TUNEL↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: P53, P53-Guardian of the Genome
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:371  Target#:236  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page