Dandelion Root / hepatoP Cancer Research Results

DRE, Dandelion Root: Click to Expand ⟱
Features:
Dandelion root (Taraxacum officinale)
-Various phytochemicals, including flavonoids and phenolic compounds, which have antioxidant properties.
-Root extract can induce apoptosis
-Anti-inflammatory properties
-Immune System Support
Dosage: dried root 2-8g/d. Extract 250-500mg/d Tea 1-2g, 1-3x/d
aqueous Dandelion flower extracts (DFE), dandelion leaf extract (DLE), and dandelion root extract (DRE) may have different effects.
Common Names: Blowball, Puffball, Lion's tooth, Pu gong ying, Swine snout, Wild endive
Taraxacum officinale is rich in flavonoids (e.g., luteolin, quercetin glycosides), phenolic acids (chicoric, chlorogenic, and caffeic acids), terpenoids (taraxasterol, taraxerol), sesquiterpene lactones (taraxinic acid β-D-glucopyranosyl ester), and phytosterols (β-sitosterol, cycloartenol)

Dandelion Root — Dandelion root is the root material or root extract of Taraxacum officinale, a polychemical botanical preparation containing phenolic acids, flavonoids, sesquiterpene lactones, triterpenes, inulin-type carbohydrates, and other phytochemicals. It is formally classified as a botanical dietary supplement or herbal extract rather than a defined single-molecule oncology drug. Standard abbreviations include DRE for dandelion root extract and T. officinale for the plant species. Current oncology relevance is mainly preclinical, with repeated in-vitro and xenograft signals but no completed convincing human cancer efficacy trial.

Primary mechanisms (ranked):

  1. Selective programmed cell death induction in cancer cells, especially extrinsic caspase-8 signaling with downstream mitochondrial destabilization and caspase execution.
  2. Mitochondrial stress and pro-death autophagy, including loss of mitochondrial integrity and context-dependent mitochondrial ROS involvement.
  3. Multi-pathway growth suppression through cell-cycle disruption, PI3K-Akt/JAK-STAT/PPAR pathway modulation, and reduced survival signaling.
  4. Anti-invasive and anti-metastatic signaling, including reduced migration/invasion phenotypes and reduced MMP-9/IL-1β expression in some models.
  5. Chemosensitization or adjunctive enhancement in preclinical models, especially with taxol and mitoxantrone in prostate cancer models.
  6. Anti-inflammatory and antioxidant effects in non-cancer contexts; these are biologically relevant but not the central cancer-killing mechanism.

Bioavailability / PK relevance: Dandelion root extract is not a standardized single active agent, so formal human PK is not well established. Oral use is plausible as a botanical preparation, but systemic exposure to the same complex extract composition used in cell culture is unknown. Inulin-rich root material may also act partly through gastrointestinal or microbiome-facing exposure rather than direct plasma-equivalent exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use crude extract concentrations in the mg/mL range and exposure windows of 24–96 hours. These concentrations should not be assumed to be systemically achievable after oral use. Colorectal and gastrointestinal tumor models may have relatively better luminal-exposure plausibility than distant solid-tumor systemic exposure, but clinical translation remains unproven.

Clinical evidence status: Preclinical. Evidence includes cell-line studies, some xenograft studies, and case-report-level human observations. A phase I cancer trial effort was reported as Health Canada-approved/recruiting, but there is no clear completed trial demonstrating cancer efficacy. It should not be treated as an established anticancer therapy.

Safety / deployment status: Dandelion is widely marketed as a food/herbal dietary supplement and is generally considered likely safe at food-level intake, but concentrated medicinal doses have less safety evidence. Important constraints include possible allergy in Asteraceae-sensitive individuals, theoretical interactions with antidiabetic, anticoagulant/antiplatelet, lithium, diuretic, and other medications, and uncertainty in pregnancy or breastfeeding. Hormone-sensitive cancer caution is reasonable because some preclinical evidence suggests estrogenic activity and possible stimulation of hormone-sensitive breast cancer models.

Dandelion Root Cancer Mechanism Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Extrinsic apoptosis and caspase activation ↑ caspase-8, ↑ Annexin V positivity, ↑ programmed cell death ↔ or lower toxicity in tested PBMCs, fibroblasts, colon mucosa, and mammary epithelial cells G Selective cancer-cell apoptosis Most central recurring anticancer signal across melanoma, leukemia, colorectal, pancreatic, prostate, and breast models; strongest evidence remains in vitro.
2 Mitochondrial destabilization ↓ mitochondrial integrity, ↓ mitochondrial membrane potential, ↑ downstream death signaling ↔ or relatively spared in several comparator normal-cell models G Amplifies intrinsic death execution Mitochondrial injury appears downstream of extrinsic death signaling in some leukemia models and more direct in melanoma/pancreatic models.
3 Pro-death autophagy ↑ autophagy with apoptosis linkage ↔ uncertain G Contributes to programmed cell death Reported in CMML and pancreatic cancer studies; autophagy direction should be interpreted as pro-death in those models, not automatically cytoprotective.
4 Cell cycle arrest ↑ S phase and G2/M accumulation, ↓ proliferation ↔ or less affected in tested normal mammary epithelial cells G Restricts proliferation Best supported in newer breast cancer fractionation/proteomics work; extract-specific and concentration-dependent.
5 PI3K-Akt and JAK-STAT survival signaling ↓ PI3K/Akt-related survival proteins, ↓ JAK/STAT-associated signaling markers (model-dependent) ↔ uncertain G Reduces survival signaling Mechanistic support is strongest in MDA-MB-231 fraction studies; requires caution because crude extracts and fractions differ substantially.
6 Mitochondrial ROS increase secondary ↑ ROS (context-dependent), ↑ oxidative mitochondrial stress ↔ uncertain; antioxidant effects may occur in normal inflammatory injury models R/G Stress-mediated death amplification ROS is not uniformly the primary DRE mechanism; in prostate work, DRE apoptosis was described as caspase-dependent while lemongrass was more ROS-dependent.
7 Migration invasion and metastasis markers ↓ migration, ↓ invasion, ↓ MMP-9, ↓ IL-1β, ↑ KAI1 (model-dependent) ↔ uncertain G Anti-invasive phenotype Observed in breast and pediatric/neuroblastoma models; translational strength is lower than the apoptosis signal.
8 Chemosensitization ↑ taxol-induced apoptosis, ↑ mitoxantrone-induced apoptosis, ↓ xenograft tumor burden with oral extract in prostate models ↔ or reduced toxicity signal in selected comparator normal-cell assays G Adjunctive enhancement Preclinical adjunct signal only; drug interaction risk means this should not be assumed safe with chemotherapy without oncology supervision.
9 Inflammation and NF-κB linked signaling ↓ inflammatory signaling markers (context-dependent) ↓ inflammatory injury markers in non-cancer models G Anti-inflammatory modulation Relevant to tumor microenvironment hypotheses but less directly established as a dominant cancer-cell killing mechanism for root extract.
10 NRF2 antioxidant axis ↔ insufficient direct cancer-specific evidence for root extract ↑ antioxidant defense may occur in injury/metabolic models (context-dependent) G Not a core cancer axis Do not tag NRF2 as a primary DRE anticancer mechanism unless a specific study directly supports it in the target cancer model.
11 Clinical Translation Constraint High in-vitro extract concentrations; variable extract chemistry; no validated human anticancer exposure target Food-level safety generally favorable but concentrated-dose interaction and allergy concerns remain G Limits clinical inference Evidence is promising but mostly preclinical; oral dosing cannot be translated directly from mg/mL cell-culture exposure.

TSF legend: P: 0–30 min; R: 30 min–3 hr; G: >3 hr
hepatoP, L,hepatoprotective: Click to Expand ⟱
Source:
Type:
Hepatoprotective is the ability of a chemical substance to prevent damage to the liver.

Grapefruit:
-hepatoprotective potential has emerged from the study of naringenin and naringin.
Blueberries/cranberries:
-proanthocyanidins
Grape:
Nopal (Cactus pear) and tuna (Cactus pear fruit) “Opuntia ficus-indica”:
Chamomile (Matricaria chamomilla or Chamomilla recutita):
Silymarin (Silybum marianum):
Blue green algae spirulina :
Propolis (bee glue):

POLYSACCHARIDES
β-glucans
Scientific Papers found: Click to Expand⟱
6354- DRE,    Taraxacum officinale L. in leukemia and lymphoma: current knowledge and prospects for horticulture
- Review, AML, NA
ROS↑, mt-Apoptosis↑, TumCCA↑, PI3K↓, Akt↓, STAT3↓, Dose↝, *hepatoP↑, Casp8↑, mtDam↑, TumCD↑, selectivity↑, DNAdam↑, BAX↑, P53↑, Bcl-2↓, CSCs↓, *toxicity↓, tumCV↓, Imm↑, FAK↓, mTOR↓, ChemoSen↑, eff↝, eff↑,
6365- DRE,    AN OVERVIEW OF THERAPEUTIC POTENTIALS OF TARAXACUM OFFICINALE (DANDELION): A TRADITIONALLY VALUABLE HERB WITH A REACH HISTORICAL BACKGROUND
- Review, Var, NA
*Inflam↓, *AntiTum↑, *Imm↑, *antiOx↑, *AntiDiabetic↑, *diuretic↑, *RenoP↑, *hepatoP↑, *neuroP↑, AntiTum↑, TNF-α↑, IL1β↑, Apoptosis↑, MMP2↓, MMP9↑, eff↑, Diff↑, *ROS↓, *HO-1↑, *NRF2↑, *lipid-P↓,
6366- DRE,    A comprehensive review of the benefits of Taraxacum officinale on human health
- Review, Var, NA
*diuretic↑, *hepatoP↑, *Imm↑, *Bacteria↓, *AntiArt↑, *AntiDiabetic↑, *Obesity↓, *antiOx↓, *AntiCan↑, Dose?,
6344- DRE,    Dandelion: Purported Benefits, Side Effects & More
- Review, Var, NA
*other↝, *hepatoP↑, *ALAT↓, *MDA↓, *TNF-α↓, *IL6↓, *antiOx↑, *Inflam↓, *proCasp3↓, Casp3↑, tumCV↓, TNF-α↑, IL1↑,
6347- DRE,    Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure
*hepatoP↑, *AST↓, *ALAT↓, *ALP↓, *Bil↓, *creat↓, *TOS↑,
6348- DRE,    New prospects in oncotherapy: bioactive compounds from Taraxacum officinale
- Review, Var, NA
Dose↝, TumCP↓, toxicity↓, *AntiDiabetic↑, *antiOx↑, *hepatoP↑, *diuretic↑, *Inflam↓, *neuroP↑, *Imm↑, eff↑, Apoptosis↑, tumCV↓, selectivity↑, TumCMig↓, EMT↓, MMP2↓, MMP9↓, Wnt↓, β-catenin/ZEB1↓, PI3K↓, Akt↓, JNK↓, ERK↓,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   mt-Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   JNK↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   Diff↑, 1,   EMT↓, 1,   ERK↓, 1,   mTOR↓, 1,   PI3K↓, 2,   STAT3↓, 1,   Wnt↓, 1,  

Migration ⓘ

FAK↓, 1,   MMP2↓, 2,   MMP9↓, 1,   MMP9↑, 1,   TumCMig↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL1↑, 1,   IL1β↑, 1,   Imm↑, 1,   TNF-α↑, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose?, 1,   Dose↝, 2,   eff↑, 3,   eff↝, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

AntiTum↑, 1,   toxicity↓, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 1,   diuretic↑, 3,  

Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 3,   Bil↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   TOS↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,  

Cell Death ⓘ

proCasp3↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Imm↑, 3,   Inflam↓, 3,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   ALP↓, 1,   AST↓, 1,   Bil↓, 1,   creat↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 3,   AntiTum↑, 1,   hepatoP↑, 6,   neuroP↑, 2,   Obesity↓, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 33

Scientific Paper Hit Count for: hepatoP, L,hepatoprotective
6 Dandelion Root
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#:222  Target#:1179  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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