tbResList Print — DFE Date Fruit Extract

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Product

DFE Date Fruit Extract
Description: <b>Dates</b> (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.<br>
Dates contain a broad spectrum of bioactive compounds linked to cancer prevention:<br>
-Phenolic acids – e.g., ferulic acid, gallic acid, caffeic acid, and p-coumaric acid<br>
-Flavonoids – e.g., quercetin, luteolin, apigenin<br>
-Carotenoids – e.g., β-carotene, lutein<br>
-Tannins, saponins, and sterols<br>
-Dietary fiber and polysaccharides<br>
These compounds have antioxidant, anti-inflammatory, and antiproliferative effects.<br>
<br>
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.<br>
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<!-- Date Fruit Extract (DFE) — Cancer-Oriented Time-Scale Flagged Pathway Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer / Tumor Context</th>
<th>Normal Tissue Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>Nrf2 / ARE antioxidant response</td>
<td>Context-dependent modulation</td>
<td>Nrf2 ↑; antioxidant enzymes ↑</td>
<td>R, G</td>
<td>Redox buffering</td>
<td>Polyphenol-driven antioxidant response is the dominant mechanistic theme in non-malignant systems.</td>
</tr>

<tr>
<td>2</td>
<td>ROS / oxidative stress modulation</td>
<td>ROS ↓ (generally); pro-oxidant effects not dominant</td>
<td>Oxidative stress ↓</td>
<td>P, R</td>
<td>Antioxidant effect</td>
<td>Most studies describe antioxidant protection rather than tumor-selective ROS elevation.</td>
</tr>

<tr>
<td>3</td>
<td>NF-κB inflammatory signaling</td>
<td>NF-κB ↓ (reported in limited models)</td>
<td>Inflammation tone ↓</td>
<td>R, G</td>
<td>Anti-inflammatory modulation</td>
<td>Observed in inflammatory and oxidative injury systems; tumor-specific evidence is limited.</td>
</tr>

<tr>
<td>4</td>
<td>Intrinsic apoptosis (mitochondrial; limited data)</td>
<td>Apoptosis ↑ (reported in some in-vitro studies)</td>
<td>↔</td>
<td>G</td>
<td>Conditional cytotoxicity</td>
<td>Cytotoxic effects generally mild and concentration-dependent; not comparable to strong pro-oxidants.</td>
</tr>

<tr>
<td>5</td>
<td>Cell-cycle arrest</td>
<td>Cell-cycle modulation ↑ (limited evidence)</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis (weak)</td>
<td>Evidence exists but is inconsistent and often extract-dependent.</td>
</tr>

<tr>
<td>6</td>
<td>PI3K → AKT signaling</td>
<td>Limited data; possible ↓ (reported in some systems)</td>
<td>↔</td>
<td>R, G</td>
<td>Survival pathway modulation</td>
<td>Not a consistently demonstrated primary mechanism.</td>
</tr>

<tr>
<td>7</td>
<td>Angiogenesis signaling (VEGF)</td>
<td>Limited data; possible ↓</td>
<td>↔</td>
<td>G</td>
<td>Potential anti-angiogenic effect</td>
<td>Evidence sparse compared to stronger polyphenols like gallic or caffeic acid.</td>
</tr>

<tr>
<td>8</td>
<td>Invasion / metastasis (MMPs)</td>
<td>Limited evidence</td>
<td>↔</td>
<td>G</td>
<td>Uncertain tumor relevance</td>
<td>Not well characterized mechanistically in oncology models.</td>
</tr>

<tr>
<td>9</td>
<td>Metabolic modulation</td>
<td>Indirect via anti-inflammatory and antioxidant tone</td>
<td>Metabolic support ↑</td>
<td>R, G</td>
<td>Systemic metabolic effect</td>
<td>Better supported in cardiometabolic contexts than direct anticancer contexts.</td>
</tr>

<tr>
<td>10</td>
<td>Extract variability / compositional heterogeneity</td>
<td>Activity varies by cultivar, processing, solvent</td>
<td>—</td>
<td>—</td>
<td>Translation constraint</td>
<td>Whole fruit extracts differ significantly in phenolic profile and potency.</td>
</tr>

</table>

<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (rapid antioxidant interactions)</li>
<li><b>R</b>: 30 min–3 hr (acute transcriptional shifts)</li>
<li><b>G</b>: &gt;3 hr (gene-regulatory and phenotype-level outcomes)</li>
</ul>

Pathway results for Effect on Cancer / Diseased Cells

Redox & Oxidative Stress

ROS↑, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 4,  

Cell Death

Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Fas↑, 1,   FasL↑, 1,   TumCD↑, 1,   TUNEL↑, 1,  

DNA Damage & Repair

P53↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 4,  

Migration

TumCP↓, 1,  

Drug Metabolism & Resistance

eff↑, 1,   selectivity↑, 2,  
Total Targets: 16

Pathway results for Effect on Normal Cells

Redox & Oxidative Stress

antiOx↑, 1,   GSH↑, 1,   MDA↓, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis

ALAT↓, 1,  

Drug Metabolism & Resistance

BioAv↑, 1,  

Clinical Biomarkers

ALAT↓, 1,   Albumin↑, 1,  

Functional Outcomes

AntiCan↑, 1,   hepatoP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 13

Research papers

Year Title Authors PMID Link Flag
2019Cytostatic and Anti-tumor Potential of Ajwa Date Pulp against Human Hepatocellular Carcinoma HepG2 CellsSahabjada SiddiquiPMC6341075https://pmc.ncbi.nlm.nih.gov/articles/PMC6341075/0
2018Induction of apoptosis and cell cycle arrest by ethyl acetate fraction of Phoenix dactylifera L. (Ajwa dates) in prostate cancer cellsMuqtadir Baig Mirza29476962https://pubmed.ncbi.nlm.nih.gov/29476962/0
2016Ajwa Date (Phoenix dactylifera L.) Extract Inhibits Human Breast Adenocarcinoma (MCF7) Cells In Vitro by Inducing Apoptosis and Cell Cycle ArrestFazal KhanPMC4956039https://pmc.ncbi.nlm.nih.gov/articles/PMC4956039/0
2023A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino ratsGhada Nady OuaisPMC10714081https://pmc.ncbi.nlm.nih.gov/articles/PMC10714081/0