Dandelion Root / Inflam 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
Inflam, inflammation: Click to Expand ⟱
Source:
Type:
Cancer and inflammation are closely linked, with chronic inflammation contributing to the development and progression of cancer. Various inflammatory mediators and cells are involved in this process.
Scientific Papers found: Click to Expand⟱
6350- DRE,    Tracking Evidences of Dandelion for the Treatment of Cancer: From Chemical Composition, Bioactivity, Signaling Pathways in Cancer Cells to Perspective Study
- Review, Var, NA
AntiCan↑, *Bacteria↓, *Inflam↓, *antiOx↑, TumCCA↑, Apoptosis↑, MOMP↑, Cyt‑c↑, APAF1↑, Casp9↑, Casp3↑, MMP↓, Bcl-2↓, TumCMig↓, TumCI↓, Wnt↓, β-catenin/ZEB1↓, MMP2↓, MMP9↓, TumAuto↑, mTOR↓, 4E-BP1↓, Glycolysis↓, angioG↓,
6353- DRE,  Cisplatin,    Insights Into Protective Mechanisms of Dandelion Leaf Extract Against Cisplatin-Induced Nephrotoxicity in Rats: Role of Inhibitory Effect on Inflammatory and Apoptotic Pathways
- in-vivo, Nor, NA
*antiOx↑, *Inflam↓, *Apoptosis↓, *NF-kB↓, *Cyt‑c↓, *DNAdam↓, *GSH↑, *SOD↑, *Albumin↝, *creat↓, *BUN↓, *RenoP↑, *lipid-P↓, *TNF-α↓, *Casp3↓, *Casp9↓, *chemoP↑,
6357- DRE,    New Perspectives on the Effect of Dandelion, Its Food Products and Other Preparations on the Cardiovascular System and Its Diseases
- Review, Nor, NA
*cardioP↑, *Dose↝, *Dose↝, *toxicity∅, *toxicity↓, *BP↓, *Inflam↓, *Bacteria↓, *Imm↑, *lipid-P↓, *AST↓, *ALAT↓, *AntiAg↑, *ROS↓, *AntiThr↑,
6359- DRE,    Natural Health Products (NHP’s) and Natural Compounds as Therapeutic Agents for the Treatment of Cancer; Mechanisms of Anti-Cancer Activity of Natural Compounds and Overall Trends
- Review, Var, NA
*antiOx↑, *Inflam↓, Dose↝, PI3K↓, Akt↓, NF-kB↓,
6363- DRE,    Therapeutic Potential of Dandelion (Taraxacum officinale) Root Extract in Colon Cancer: A Comprehensive Review
- in-vitro, CRC, NA
Apoptosis↑, *Inflam↓, TLR4↓, NF-kB↓, *GutMicro↑, mtDam↑, *ROS↓, Casp1↑, TNF-α↑, Bcl-2↓, PARP↓, MMP↓, Cyt‑c↓, Casp3↑, TumVol↓, COX2↓, iNOS↓, ROS↑, selectivity↑, TumCMig↓, TumCI↓, ER Stress↑, PERK↑, eIF2α↑, ATF4↑, CHOP↑, TumCCA↑, cycD1/CCND1↓, P21↓, P53↑, BioAv↝, Half-Life↝,
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↓,
6319- DRE,    Efficient induction of extrinsic cell death by dandelion root extract in human chronic myelomonocytic leukemia (CMML) cells
- in-vitro, AML, MV411 - in-vitro, AML, HL-60
Apoptosis↑, TumAuto↑, *toxicity↓, selectivity↑, Casp8↑, MMP↓, *Inflam↓, *antiOx↑, *AntiCan↑, DNAdam↑, cl‑Casp3↑, tumCV↓, ROS↑,
6343- DRE,    Dandelion root extract affects ESCC progression via regulating multiple signal pathways
- vitro+vivo, ESCC, NA
*Inflam↓, TumCG↓, TumCP↓, TumCMig↓, TumCI↓, Apoptosis↓, TumCG↓, PI3K↓, p‑Akt↓, RAS↓, Raf↓, p‑ERK↓, Bcl-2↓, BAX↑,
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↑,
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 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 3,   mtDam↑, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 5,   BAX↑, 1,   Bcl-2↓, 3,   Casp1↑, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 1,   iNOS↓, 1,   JNK↓, 1,   MOMP↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

4E-BP1↓, 1,   Diff↑, 1,   EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   mTOR↓, 1,   PI3K↓, 3,   RAS↓, 1,   TumCG↓, 2,   Wnt↓, 2,  

Migration ⓘ

MMP2↓, 3,   MMP9↓, 2,   MMP9↑, 1,   TumCI↓, 3,   TumCMig↓, 4,   TumCP↓, 2,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1↑, 1,   IL1β↑, 1,   NF-kB↓, 2,   TLR4↓, 1,   TNF-α↑, 3,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Dose↝, 2,   eff↑, 2,   Half-Life↝, 1,   selectivity↑, 3,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

diuretic↑, 2,  

Redox & Oxidative Stress ⓘ

antiOx↑, 7,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 3,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   BUN↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3↓, 1,   proCasp3↓, 1,   Casp9↓, 1,   Cyt‑c↓, 1,  

Transcription & Epigenetics ⓘ

AntiThr↑, 1,   other↝, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Migration ⓘ

AntiAg↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Imm↑, 3,   Inflam↓, 10,   NF-kB↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   Albumin↝, 1,   AST↓, 1,   BP↓, 1,   creat↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 2,   AntiTum↑, 1,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 3,   neuroP↑, 2,   RenoP↑, 2,   toxicity↓, 2,   toxicity∅, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 44

Scientific Paper Hit Count for: Inflam, inflammation
10 Dandelion Root
1 Cisplatin
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#:953  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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