Quercetin / cognitive Cancer Research Results

QC, Quercetin: Click to Expand ⟱
Features:
Plant pigment (flavonoid) found in red wine, onions, green tea, apples and berries.
Quercetin is thought to contribute to anticancer effects through several mechanisms:
-Antioxidant Activity:
-Induction of Apoptosis:modify Bax:Bcl-2 ratio
-Anti-inflammatory Effects:
-Cell Cycle Arrest:
-Inhibition of Angiogenesis and Metastasis: (VEGF)

Cellular Pathways:
-PI3K/Akt/mTOR Pathway: central to cell proliferation, survival, and metabolism.
-MAPK/ERK Pathway: influencing cell proliferation, differentiation, and apoptosis.
-NF-κB Pathway: downregulate NF-κB
-JAK/STAT Pathway: interfere with the activation of STAT3
-Apoptotic Pathways: intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways

Quercetin has been used at doses around 500–1000 mg per day
Quercetin’s bioavailability from foods or standard supplements can be low.
EMIQ bioavialability is about 3X that of Quercetin (Example Natural Factors brand)
Isoquercitrin is high bioaviability and efficiacy but at this time does not seem available as supplement.

-Note half-life 11 to 28 hours.
BioAv low 1-10%, poor water-solubility, consuming with fat may improve bioavialability. also piperine or VitC.
Pathways:
- induce ROS production in cancer cells (higher dose). Typicallys Lowers ROS in normal cells(unless it is high dose?)or depends on Redox status?. "quercetin paradox"
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Confusing info about Lowering AntiOxidant defense in Cancer Cells: NRF2↓(some contrary), TrxR↓**, SOD↓(contrary), GSH↓ Catalase↓(contrary), HO1↓(some contrary), GPx↓(some contrary)
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓,
- some indication of inhibiting Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD24↓, β-catenin↓, Notch2↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS Conditional Driver Biphasic redox modulation Quercetin exhibits pro-oxidant behavior in cancer cells while protecting normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction is a central apoptosis route in cancer cells
3 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Driver Growth and survival inhibition AKT/mTOR suppression is a consistently reported upstream effect in cancer models
4 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Reduced survival and inflammatory transcription NF-κB inhibition contributes to chemosensitization and apoptosis susceptibility
5 MAPK signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-mediated apoptosis signaling MAPK activation supports apoptosis downstream of redox stress
6 Cell cycle regulation ↑ G1/S or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects disruption of growth signaling
7 HIF-1α hypoxia signaling ↓ HIF-1α ↔ minimal Secondary Reduced hypoxia tolerance Quercetin interferes with hypoxia-driven transcriptional programs
8 NRF2 antioxidant response ↑ NRF2 (adaptive, context-dependent) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 induction reflects redox buffering rather than primary cytotoxicity


cognitive, cognitive: Click to Expand ⟱
Source:
Type:
Cognitive


Scientific Papers found: Click to Expand⟱
3336- QC,    Neuroprotective Effects of Quercetin in Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
*Aβ↓,
*Inflam↓,
*BBB↝, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
*iNOS↓,
*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
*cognitive↑,
*AChE↓, Quercetin administration resulted in the inhibition of AChE
*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
*ROS↓,
*ATP↑,
*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation

3607- QC,    Mechanisms of Neuroprotection by Quercetin: Counteracting Oxidative Stress and More
- Review, AD, NA - Review, Park, NA
*neuroP↑, supportive evidence for neuroprotective effects of quercetin
*NRF2↑, nduction of Nrf2-ARE and induction of the antioxidant/anti-inflammatory enzyme paraoxonase 2 (PON2).
*PONs↑,
*antiOx↑,
*Inflam↓,
*SIRT1↑, quercetin has been shown to activate sirtuins (SIRT1), to induce autophagy, and to act as a phytoestrogen, all mechanisms by which quercetin may provide its neuroprotection.
*eff↑, Additionally, coadministration of quercetin and alpha-tocopherol has been shown to increase the transport of quercetin across the blood-brain barrier
*ROS↓, was shown to protect rodents from oxidative stress
*cognitive↑, quercetin ameliorates Alzheimer's disease pathology and related cognitive deficits in an aged triple transgenic Alzheimer's disease mouse model
*eff↑, combined oral supplementation of quercetin and fish oil enhanced neuroprotection in rats exposed to 3-nitropropionic acid
*lipid-P↓, Decreased lipid perox. in hippocampus;
*GSH↑, Decreased reduction of GSH, GPx (5, 50 mg/kg)
*GPx↑,
*SOD↑, Diminished reduction of DA levels, SOD, and GPx
*NRF2↑, Quercetin has been shown to counteract oxidative stress-induced cellular damage by activating the Nrf2-ARE pathway

3604- QC,    Quercetin enrich diet during the early-middle not middle-late stage of alzheimer’s disease ameliorates cognitive dysfunction
- in-vivo, AD, NA
*cognitive↑, early-middle stage of AD pathological development period ameliorates cognitive dysfunction and the protection effect was mainly related to increased Aβ clearance and reduced astrogliosis.
*Aβ↓, Quercetin enrich diet prevented cognitive dysfunction through increasing Aβ clearance and astrocyte function. has been demonstrated that it could inhibit the aggregation of Aβ
*neuroP↑, quercetin may have neuro-protective effects and slow down the progression of degenerative diseases
*BACE/β-secretase↓, The results showed that the protein level of CTFβ and BACE1 was decreased
*p‑SMAD2↓, protein level of p-Smad2 and p-STAT3 were decreased in quercetin enrich diet
*p‑STAT3↓,
*SPARC↓, quercetin enrich diet (1 month-9 months) significantly reduced the mRNA and protein level of Hevin and SPARC compared with normal diet.

3602- QC,    The flavonoid quercetin ameliorates Alzheimer's disease pathology and protects cognitive and emotional function in aged triple transgenic Alzheimer's disease model mice
- in-vivo, AD, NA
*BACE/β-secretase↓, significant reduction in the paired helical filament (PHF), β-amyloid (βA) 1–40 and βA 1–42 levels and a decrease in BACE1-mediated cleavage of APP (into CTFβ).
*cognitive↑, protects cognitive and emotional function in aged 3xTg-AD mice.
*ROS↓, These potential uses may be due to its high oxygen radical scavenging activity or its ability to inhibit xanthine oxidase and lipid peroxidation in vitro
*lipid-P↓,
*iNOS↓, inhibiting iNOS (Martinez-Florez et al., 2005) and regulating the expression of COX-2
*COX2/PTGS2↓,
*BBB↑, ability to penetrate the blood brain barrier
*neuroP↑, n addition to neuroprotection, quercetin has been suggested to exert other beneficial effects on the central nervous system (CNS), such as anti-anxiety and cognitive enhancement, by stimulating or inhibiting enzyme activities/signal transduction path
*other↓, remarkable reduction in the βA 1–40 and βA 1–42 levels in the hippocampus of the quercetin-treated 3xTg-AD mice compared to the vehicle-treated 3xTg-AD mice
*memory↑, Quercetin improves the spatial learning and memory task performance of 3xTg-AD mice

3601- QC,    Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid
- Review, Var, NA - Review, AD, NA
*Inflam↓, known for its anti-inflammatory, antihypertensive, vasodilator effects, antiobesity, antihypercholesterolemic and antiatherosclerotic activities
*cardioP↑, beneficial effects include cardiovascular protection, anticancer, antitumor, anti-ulcer, anti-allergy, anti-viral, anti-inflammatory activity, anti-diabetic, gastroprotective effects, antihypertensive, immunomodulatory, and anti-infective.
AntiCan↑,
AntiTum↑,
*neuroP↑, The consumption of flavonoids rich food limits neurodegeneration and to reverse age-dependent loss in cognitive performance.
*cognitive↑,
*ROS↓, It is known to protect brain cells against the oxidative stress, which damages tissue leading to Alzheimer and other neurological conditions
*BP↓, Quercetin supplementation (150 mg/day) reduced systolic blood pressure and plasma oxidized LDL concentrations in overweight subjects
*LDL↓,

4297- QC,    Quercetin attenuates tau hyperphosphorylation and improves cognitive disorder via suppression of ER stress in a manner dependent on AMPK pathway
- in-vitro, AD, SH-SY5Y
*AMPK↑, administration of quercetin enhanced AMPK activity, inhibited IRE1α and PERK phosphorylation, NLRP3 expression and tau phosphorylation
*IRE1↓,
*p‑PERK↓,
*p‑tau↓,
*cognitive↑, and improved cognitive disorder in mice exposed to high fat diets
*antiOx↑, exert anti-oxidative, anti-ER stress, anti-inflammatory activities and regulating glucose homeostasis, which can prevent neurodegenerative disorders, diabetes, and obesity
*ER Stress↓,
*Inflam↓,
*neuroP↑,
*TXNIP↓, Quercetin and quercetin-3-O-glucuronide suppressed ER stress with decreased phosphorylation of IRE1α and PERK, thereby inhibited TXNIP and NLRP3 inflammasome activation,
*NLRP3↓, effectively protected neuronal cells from inflammatory insult by blocking ER stress/NLRP3 inflammasome activation.

7826- QC,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA - Review, Stroke, NA - Review, Park, NA
*Stroke↓, quercetin improved AD, ischemic stroke, and Parkinson’s disease, as well as aging, neuroinflammation, and daily intakes of advanced glycation end products (AGEs) or alumimum-induced cognitive impairments.62
*Inflam↓,
*AGEs↓,
*cognitive↑, quercetin (100 mg/kg, intragastrically, i.g.) to 6 month old 3xTg-AD mice for one year significantly prevented cognitive impairments, β-amyloidosis, and tauopathy.
*memory↑, clinical trial indicated that the memory recall improved in the early stage AD patients who consume quercetin-enriched onion powder
*Dose↝, (containing 80 mg quercetin aglycone) daily for 4 weeks compare to those who take white onion powder (containing less than 5 mg quercetin aglycone),
*neuroP↑, implying its great neuroprotective potentials in AD.65
*p‑tau↓, quercetin inhibited tau hyperphosphorylation in a cell model induced by okadaic acid
*GSK‐3β↓, through suppressing tau phosphorylationrelated kinases, such as GSK-3β and CDK5
*CDK5↓,

3347- QC,    Recent Advances in Potential Health Benefits of Quercetin
- Review, Var, NA - Review, AD, NA
*antiOx↑, Its strong antioxidant properties enable it to scavenge free radicals, reduce oxidative stress, and protect against cellular damage.
*ROS↓,
*Inflam↓, Quercetin’s anti-inflammatory properties involve inhibiting the production of inflammatory cytokines and enzymes,
TumCP↓, exhibits anticancer effects by inhibiting cancer cell proliferation and inducing apoptosis.
Apoptosis↑,
*cardioP↑, cardiovascular benefits such as lowering blood pressure, reducing cholesterol levels, and improving endothelial function
*BP↓, Quercetin‘s ability to reduce blood pressure was also supported by a different investigation
TumMeta↓, The most important impact of quercetin is its ability to inhibit the spread of certain cancers including those of the breast, cervical, lung, colon, prostate, and liver
MDR1↓, quercetin decreased the expression of genes multidrug resistance protein 1 and NAD(P)H quinone oxidoreductase 1 and sensitized MCF-7 cells to the chemotherapy medication doxorubicin
NADPH↓,
ChemoSen↑,
MMPs↓, Inhibiting CT26 cells’ migration and invasion abilities by inhibiting their expression of tissue inhibitors of metalloproteinases (TIMPs) inhibits their invasion and migration abilities
TIMP2↑,
*NLRP3↓, inhibited NLRP3 by acting on this inflammasome
*IFN-γ↑, quercetin significantly upregulates the gene expression and production of interferon-γ (IFN-γ), which is obtained from T helper cell 1 (Th1), and downregulates IL-4, which is obtained from Th2.
*COX2/PTGS2↓, quercetin is known to decrease the production of inflammatory molecules COX-2, nuclear factor-kappa B (NF-κB), activator protein 1 (AP-1), mitogen-activated protein kinase (MAPK), reactive nitric oxide synthase (NOS), and reactive C-protein (CRP)
*NF-kB↓,
*MAPK↓,
*CRP↓,
*IL6↓, Quercetin suppressed the production of inflammatory cytokines such as IL-6, TNF-α, and IL-1β via upregulating TLR4.
*TNF-α↓,
*IL1β↓,
*TLR4↑,
*PKCδ↓, Quercetin employed suppression on the phosphorylation of PKCδ to control the PKCδ–JNK1/2–c-Jun pathway.
*AP-1↓, This pathway arrested the accumulation of AP-1 transcription factor in the target genes, thereby resulting in reduced ICAM-1 and inflammatory inhabitation
*ICAM-1↓,
*NRF2↑, Quercetin overexpressed Nrf2 and targeted its downstream gene, contributing to increased HO-1 levels responsible for the down-regulation of TNF-α, iNOS, and IL-6
*HO-1↑,
*lipid-P↓, Quercetin acts as a potent antioxidant by scavenging ROS, inhibiting lipid peroxidation, and enhancing the activity of antioxidant enzymes
*neuroP↑, This helps to counteract oxidative stress and protect against neurodegenerative processes that contribute to AD
*eff↑, rats treated with chronic rotenone or 3-nitropropionic acid showed enhanced neuroprotection when quercetin and fish oil were taken orally
*memory↑, Both memory and learning abilities in the test animals increased
*cognitive↑,
*AChE↓, The increase in AChE activity brought on by diabetes was prevented in the cerebral cortex and hippocampus by quercetin at a level of 50 mg/kg body weight.
*BioAv↑, consumption of fried onions compared to black tea, suggesting that the form of quercetin present in onions is better absorbed than that in tea
*BioAv↑, This suggests that dietary fat can increase the absorption of quercetin [180]
*BioAv↑, potential of liposomes to enhance the bioactivity and bioavailability of quercetin has been the subject of several investigations
*BioAv↑, several emulsion types that may be employed to encapsulate quercetin, but oil-in-water (O/W) emulsions are the most widely utilized.
*BioAv↑, the kind of oil (triglyceride oils made up of either long-chain or medium-chain fatty acids) affected the bioaccessibility of quercetin and gastrointestinal stability, emphasizing the significance of picking a suitable oil phase

3367- QC,    Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments
- Review, Stroke, NA - Review, AD, NA
*NRF2↑, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus.
*neuroP↑,
*motorD↑, Que protected the blood-brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction.
*Inflam↓, (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex
*cognitive↑, (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1-4, antioxidant activity, and Nrf2 levels in the brain.

6058- SeNPs,  RES,  QC,  CAR,    Engineered nanoplatforms for brain-targeted co-delivery of phytochemicals in Alzheimer's disease: Rational design, blood-brain barrier penetration, and multi-target therapeutic synergy
- Review, AD, NA
*DDS↑, This review systematically examines the rational design and recent advancements in engineered nanoplatforms for brain-targeted co-delivery of phytochemicals in AD.
*cognitive↑, nanodrug delivery systems demonstrate substantial cognitive improvement in AD animal models through synergistic multi-pathway effects: inhibiting Aβ aggregation, modulating Tau phosphorylation,
*Aβ↓,
*tau↓,
*Inflam↓, reducing neuroinflammation, and enhancing antioxidant activity, often at markedly reduced doses compared to free drugs.
*antiOx↑,
*BioAv↑, A novel RSV–selenium nanoparticle (RSV–SeNP) system was developed by combining RSV with SeNPs, substantially improving the bioavailability and stability of RSV.
*BioAv↑, A nanodelivery system based on arabic gum and polysorbate 80-modified Qu-loaded selenium nanoparticles (P80-Qu@Se NCs) substantially improved the water solubility and stability of Qu
*neuroP↑, Cur/Se–PLGA nanospheres: Dual action: anti–Aβ aggregation & neuroprotection. High biocompatibility and sustained drug release.
*BioAv↑, The nanoemulsion particle size and monodispersity ensured efficient BBB penetration, with brain drug concentrations increasing eight-fold compared to free carvacrol.
*AChE↓, carvacrol nanoemulsions improved ACh signaling by reducing brain AChE activity.


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:


Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

Migration(tgid=13) ⓘ

MMPs↓, 1,   TIMP2↑, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   MDR1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiTum↑, 1,  
Total Targets: 10

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 5,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 4,   NRF2↑, 4,   ROS↓, 5,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   LDL↓, 1,   NADPH↓, 1,   PONs↑, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 2,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,   IRE1↓, 1,   p‑PERK↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GSK‐3β↓, 1,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   CDK5↓, 1,   PKCδ↓, 1,   p‑SMAD2↓, 1,   SPARC↓, 1,   TXNIP↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   BBB↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   CRP↓, 1,   ICAM-1↓, 1,   IFN-γ↑, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 8,   NF-kB↓, 2,   TLR4↑, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3,   tau↓, 1,   p‑tau↓, 3,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 3,   BACE/β-secretase↓, 2,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 8,   DDS↑, 1,   Dose↝, 1,   eff↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 2,   CRP↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   cognitive↑, 10,   memory↑, 4,   motorD↑, 1,   neuroP↑, 10,  
Total Targets: 61

Scientific Paper Hit Count for: cognitive, cognitive
10 Quercetin
1 Mung Bean Sprouts
1 Selenium NanoParticles
1 Resveratrol
1 Carvacrol
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#:140  Target#:557  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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