Berberine / Casp3 Cancer Research Results

BBR, Berberine: Click to Expand ⟱
Features:

Berberine — Berberine is a protoberberine/isoquinoline alkaloid natural product found in plants such as Coptis, Berberis, and Phellodendron. It is a small-molecule phytochemical with pleiotropic metabolic, anti-inflammatory, and anticancer signaling effects rather than a single highly selective target profile. Its standard abbreviation is BBR. In oncology it is best classified as a multitarget natural-product lead compound and adjunct-sensitizer candidate, with strong preclinical evidence but no established standard anticancer regulatory use. Its translational profile is shaped by very low conventional oral bioavailability, extensive first-pass metabolism, broad tissue distribution, and substantial context dependence between cancer-cell pro-death effects and normal-cell cytoprotective redox effects.

Primary mechanisms (ranked):

  1. AMPK-centered metabolic stress with mitochondrial dysfunction, ATP depletion, and apoptosis/autophagy induction
  2. Suppression of aerobic glycolysis and hypoxia signaling, including HIF-1α, GLUT1, HK2, LDHA, and PKM2-linked tumor metabolism
  3. Anti-proliferative cell-cycle control with cyclin/CDK suppression and tumor suppressor reactivation
  4. Inhibition of PI3K/AKT, MAPK/ERK, JAK/STAT, and NF-κB inflammatory-survival signaling
  5. Anti-metastatic and anti-EMT activity via Wnt/β-catenin, TGF-β/Smad, FAK/RhoA/ROCK, MMPs, and CXCR4-related programs
  6. Pro-oxidant mitochondrial ROS elevation and ER-stress/caspase signaling in many cancer models, with opposite antioxidant/NRF2-supportive effects in some normal-cell and non-cancer settings
  7. Context-dependent chemosensitization and radiosensitization, including effects on hypoxia signaling and DNA-repair competence
  8. Emerging ferroptosis-related activity in some tumor models, but not a universal dominant mechanism across berberine biology

Bioavailability / PK relevance: Conventional oral berberine has poor systemic bioavailability, often cited as below 1% in animal studies, because of limited absorption, P-glycoprotein efflux, first-pass intestinal/hepatic metabolism, and self-aggregation. Human exposure is usually in the low ng/mL plasma range with conventional dosing, while multiple metabolites may contribute to activity. Tissue distribution can exceed plasma levels, but PK remains a major clinical translation constraint.

In-vitro vs systemic exposure relevance: Many anticancer in-vitro studies use roughly 10–100 µM, commonly around 20–50 µM, which usually exceeds readily achievable conventional plasma exposure after standard oral dosing. Therefore, direct translation of cell-culture potency to systemic monotherapy expectations is limited unless local gut exposure, tissue accumulation, metabolite contribution, formulation enhancement, or combination use is specifically relevant.

Clinical evidence status: Strong preclinical and mechanistic evidence; limited early human oncology/chemoprevention evidence; no established phase III anticancer efficacy standard and no mainstream regulatory approval as an anticancer drug. Current clinical relevance is best viewed as investigational and adjunct-oriented rather than proven standalone oncology therapy.

Berberine is a chemical found in some plants like European barberry, goldenseal, goldthread, Oregon grape, phellodendron, and tree turmeric. Berberine is a bitter-tasting and yellow-colored chemical.
Coptis (commonly referring to Coptidis Rhizoma, a traditional Chinese medicinal herb) contains bioactive alkaloids (most notably berberine and coptisine) that have been studied for their pharmacological effects—including their influence on reactive oxygen species (ROS) and related pathways.

– Berberine is known for its relatively low oral bioavailability, often cited at less than 1%. This low bioavailability is mainly due to poor intestinal absorption and active efflux by transport proteins such as P-glycoprotein.
– Despite the low bioavailability, berberine is still pharmacologically active, and its metabolites may also contribute to its overall effects.

• Effective Dosage in Studies
– Many clinical trials or preclinical studies use dosages in the range of 500 to 1500 mg per day, typically administered in divided doses.
– Therefore, to obtain a bioactive dose of berberine, supplementation in a standardized extract form is necessary.

-IC50 in cancer cell lines: Approximately 10–100 µM (commonly around 20–50 µM in many models)
-IC50 in normal cell lines: Generally higher (often above 100 µM), although this can vary with cell type
- In vivo studies: Dosing regimens in animal models generally range from about 50 to 200 mg/kg
- very effective AChE inhibitor (Alzheimers)
- Berberine may enhance the effects of blood-thinning medications like warfarin and aspirin.


-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi1↓, CD133↓, β-catenin↓, n-myc↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, α↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 AMPK → mTOR axis ↑ AMPK / ↓ mTOR signaling Metabolic stress + growth suppression In vivo/in vitro colon tumorigenesis model: berberine activates AMPK, inhibits mTOR signaling and reduces proliferation/tumorigenesis, growth suppression, autophagy, HIF-1α ↓, glycolysis ↓, berberine’s known mitochondrial/energetic effects (ref)
2 Mitochondrial dysfunction / ROS generation ↑ ROS / mitochondrial stress Upstream metabolic trigger Berberine inhibits mitochondrial function, increases ROS, and contributes to AMPK activation and downstream apoptosis (ref)
3 Mitochondrial apoptosis (cytochrome c release) ↑ cytochrome c release Intrinsic death signaling Oral cancer model: berberine reduces mitochondrial membrane potential, releases cytochrome c, activates caspase-3 (ref)
4 Intrinsic apoptosis (caspase-3 activation) ↑ caspase-3 activation Programmed cell death Same oral cancer study documents caspase-3 activation as a key execution marker (ref)
5 NF-κB signaling (p65 activation) ↓ NF-κB activation Reduced pro-survival transcription Colon cancer model reports inhibition of p65 phosphorylation; interpreted as secondary to metabolic/redox stress (ref)
6 Cell cycle control ↑ G1 arrest Proliferation blockade Prostate cancer model: berberine induces G1-phase cell cycle arrest and caspase-3–dependent apoptosis (ref)
7 Hypoxia / glycolysis signaling (HIF-1α) ↓ HIF-1α protein Warburg / glycolysis suppression Berberine suppresses mTOR and reduces HIF-1α protein expression downstream of AMPK activation (ref)
8 Angiogenesis signaling (HIF-1α → VEGF axis) ↓ VEGF signaling Reduced vascular support Lung cancer study: berberine suppresses VEGF signaling alongside HIF-1α inhibition (ref)
9 PI3K–AKT–mTOR signaling ↓ PI3K / AKT / mTOR Survival pathway suppression Gastric cancer paper: berberine represses PI3K/AKT/mTOR signaling and improves chemosensitivity (ref)
10 Migration / invasion programs ↓ migration & invasion Anti-metastatic phenotype Tongue SCC model: berberine suppresses migration and invasion with associated signaling changes (ref)
11 Telomerase (hTERT) / immortalization axis ↓ hTERT-related signaling Reduced proliferative capacity Lung cancer study includes AP-2/hTERT regulatory axis modulation by berberine (ref)
12 In vivo tumor suppression ↓ tumorigenesis Demonstrated anti-tumor effect Colon tumorigenesis model confirms reduced proliferation and tumor burden with berberine (ref)


Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
Scientific Papers found: Click to Expand⟱
2700- BBR,    Cell-specific pattern of berberine pleiotropic effects on different human cell lines
- in-vitro, GBM, U343 - in-vitro, GBM, MIA PaCa-2 - in-vitro, Nor, HDFa
selectivity↑, TumCCA↑, Casp3↑, TumCI↓, TumCMig↓, N-cadherin?, DNMT1↑,
2691- BBR,    Berberine induces FasL-related apoptosis through p38 activation in KB human oral cancer cells
- in-vitro, Oral, KB
tumCV↓, DNAdam↑, Casp3↑, Casp7↑, FasL↑, Casp8↑, Casp9↑, PARP↑, BAX↑, BAD↑, APAF1↑, MMP2↓, MMP9↓, p‑p38↑, ERK↑, MAPK↑,
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, IL6↓, MCP1↓, COX2↓, PGE2↓, MMP2↓, MMP9↓, DNAdam↑, eff↝, Telomerase↓, Bcl-2↓, AMPK↑, ROS↑, MMP↓, ATP↓, p‑mTORC1↓, p‑S6K↓, ERK↓, PI3K↓, PTEN↑, Akt↓, Raf↓, MEK↓, Dose↓, Dose↑, selectivity↑, TumCCA↑, eff↑, EGFR↓, Glycolysis↓, Dose?, p27↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycE/CCNE↓, Bax:Bcl2↑, Casp3↑, Casp9↑, VEGFR2↓, ChemoSen↑, eff↑, eff↑, PGE2↓, JAK2↓, STAT3↓, CXCR4↓, CCR7↓, uPA↓, CSCs↓, EMT↓, Diff↓, CD133↓, Nestin↓, n-MYC↓, NOTCH↓, SOX2↓, Hif1a↓, VEGF↓, RadioS↑,
5179- BBR,    Regulation of Cell Signaling Pathways by Berberine in Different Cancers: Searching for Missing Pieces of an Incomplete Jig-Saw Puzzle for an Effective Cancer Therapy
- Review, Var, NA
AMPK↑, Casp3↑, cl‑PARP↑, Mcl-1↓, cFLIP↓, β-catenin/ZEB1↓, Wnt↓, STAT3↓, mTOR↓, Hif1a↓, NF-kB↓, SIRT1↑, DNMT1↓, DNMT3A↓, miR-29b↓, IGFBP1↑, eff↑, chemoPv↑, BioAv↓,
5178- BBR,    Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumCP↑, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, P21↑, p27↑, Apoptosis↑, Bax:Bcl2↑, MMP↓, Casp9↑, Casp3↑, PARP↑, DNAdam↑, selectivity↑, Cyt‑c↑,
5177- BBR,    Berberine induces apoptosis in human HSC-3 oral cancer cells via simultaneous activation of the death receptor-mediated and mitochondrial pathway
- in-vitro, Oral, HMC3
TumCCA↑, Apoptosis↑, TumCG↓, Casp3↑, TumCCA↑, ROS↑, Ca+2↑, MMP↓, ER Stress↑, Cyt‑c↑,
5176- BBR,    Berberine regulates AMP-activated protein kinase signaling pathways and inhibits colon tumorigenesis in mice
- vitro+vivo, CRC, HCT116 - in-vitro, CRC, SW480 - in-vitro, CRC, LoVo
TumVol↓, Ki-67↓, COX2↓, AMPK↑, mTOR↓, NF-kB↓, cycD1/CCND1↓, survivin↓, P53↑, cl‑Casp3↑, TumCP↓, Inflam↓, COX2↓, ACC↑,
1394- BBR,  DL,    Synergistic Inhibitory Effect of Berberine and d-Limonene on Human Gastric Carcinoma Cell Line MGC803
- in-vitro, GC, MGC803
eff↑, ROS↑, MMP↓, Casp3↑, Bcl-2↓, TumCCA↑,
1393- BBR,  EPI,    Berberine promotes antiproliferative effects of epirubicin in T24 bladder cancer cells by enhancing apoptosis and cell cycle arrest
- in-vitro, Bladder, T24/HTB-9
ChemoSen↑, TumCCA↑, Apoptosis↑, cl‑Casp3↑, cl‑Casp9↑, BAX↑, P53↑, P21↑, Bcl-2↓, ROS↑,
1390- BBR,  Rad,    Berberine Inhibited Radioresistant Effects and Enhanced Anti-Tumor Effects in the Irradiated-Human Prostate Cancer Cells
- in-vitro, Pca, PC3
RadioS↑, Apoptosis↑, ROS↑, eff↑, BAX↑, Casp3↑, P53↑, p38↑, JNK↑, Bcl-2↓, ERK↓, HO-1↓,
1382- BBR,    Berberine increases the expression of cytokines and proteins linked to apoptosis in human melanoma cells
- in-vitro, Melanoma, SK-MEL-28
Apoptosis↑, necrosis↑, DNAdam↑, TumCCA↑, ROS↑, Casp3↑, p‑P53↑, ERK↑,
1378- BBR,    Berberine induces non-small cell lung cancer apoptosis via the activation of the ROS/ASK1/JNK pathway
- in-vitro, Lung, NA
Apoptosis↑, Casp3↑, Cyt‑c↑, MMP↓, p‑JNK↑, eff↓,
1374- BBR,  PDT,    Berberine associated photodynamic therapy promotes autophagy and apoptosis via ROS generation in renal carcinoma cells
- in-vitro, RCC, 786-O - in-vitro, RCC, HK-2
ROS↑, TumAuto↑, Apoptosis↑, Casp3↑, eff↑,
1030- BBR,    Berberine diminishes cancer cell PD-L1 expression and facilitates antitumor immunity via inhibiting the deubiquitination activity of CSN5
- in-vitro, Lung, H460
PD-L1↓, TumCG↓, Ki-67↓, cl‑Casp3↑,
2681- BBR,  PDT,    Berberine-photodynamic induced apoptosis by activating endoplasmic reticulum stress-autophagy pathway involving CHOP in human malignant melanoma cells
- in-vitro, Melanoma, NA
Apoptosis↑, cl‑Casp3↑, LC3s↑, ER Stress↑, ROS↑, CHOP↑,
1404- BBR,    Berberine-induced apoptosis in human prostate cancer cells is initiated by reactive oxygen species generation
- in-vitro, Pca, PC3
Apoptosis↑, *Apoptosis∅, MMP↓, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, ROS↑, eff↓, Cyt‑c↑,
1402- BBR,    Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction
- in-vitro, GBM, T98G
tumCV↓, ROS↑, Ca+2↑, ER Stress↑, eff↓, Bax:Bcl2↑, MMP↓, Casp9↑, Casp3↑, cl‑PARP↑,
1398- BBR,    Berberine inhibits the progression of renal cell carcinoma cells by regulating reactive oxygen species generation and inducing DNA damage
- in-vitro, Kidney, NA
TumCP↓, TumCMig↓, ROS↑, Apoptosis↑, BAX↑, BAD↑, Bak↑, Cyt‑c↑, cl‑Casp3↑, cl‑Casp9↑, E-cadherin↑, TIMP1↑, γH2AX↑, Bcl-2↓, N-cadherin↓, Vim↓, Snail↓, RAD51↓, PCNA↓,
1403- SDT,  BBR,    From 2D to 3D In Vitro World: Sonodynamically-Induced Prooxidant Proapoptotic Effects of C60-Berberine Nanocomplex on Cancer Cells
- in-vitro, Cerv, HeLa - in-vitro, Lung, LLC1
eff↑, tumCV↓, ATP↓, ROS↑, Casp3↑, Casp7↑, mtDam↑,

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   ROS↑, 12,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MEK↓, 1,   MMP↓, 7,   mtDam↑, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↑, 1,   AMPK↑, 3,   Glycolysis↓, 1,   p‑S6K↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 10,   BAD↑, 2,   Bak↑, 1,   BAX↑, 4,   Bax:Bcl2↑, 3,   Bcl-2↓, 5,   Casp3↑, 13,   cl‑Casp3↑, 6,   Casp7↑, 2,   Casp8↑, 1,   Casp9↑, 4,   cl‑Casp9↑, 3,   cFLIP↓, 1,   Cyt‑c↑, 5,   FasL↑, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↑, 1,   Mcl-1↓, 1,   necrosis↑, 1,   p27↑, 2,   p38↑, 1,   p‑p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 3,  

Autophagy & Lysosomes ⓘ

LC3s↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 4,   DNMT1↓, 1,   DNMT1↑, 1,   DNMT3A↓, 1,   P53↑, 3,   p‑P53↑, 1,   PARP↑, 2,   cl‑PARP↑, 3,   PCNA↓, 1,   RAD51↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 2,   CDK4↓, 2,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 2,   P21↑, 2,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CSCs↓, 1,   Diff↓, 1,   EMT↓, 1,   ERK↓, 2,   ERK↑, 2,   IGFBP1↑, 1,   mTOR↓, 2,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 2,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   Ki-67↓, 2,   miR-29b↓, 1,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin?, 1,   N-cadherin↓, 1,   Snail↓, 1,   TIMP1↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumCP↑, 1,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 2,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

CCR7↓, 1,   COX2↓, 3,   CXCR4↓, 1,   IL6↓, 1,   Inflam↓, 2,   JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   PD-L1↓, 1,   PGE2↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   eff↓, 3,   eff↑, 8,   eff↝, 1,   RadioS↑, 2,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   IL6↓, 1,   Ki-67↓, 2,   PD-L1↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   TumVol↓, 1,  
Total Targets: 127

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Apoptosis∅, 1,  
Total Targets: 1

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
19 Berberine
2 Photodynamic Therapy
1 D-limonene
1 epirubicin
1 Radiotherapy/Radiation
1 SonoDynamic Therapy UltraSound
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#:41  Target#:42  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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