mtDam Cancer Research Results
mtDam, mitochondrial damage: Click to Expand ⟱
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Mitochondrial damage can lead to a shift from oxidative phosphorylation to glycolysis, a process known as the Warburg effect. This shift can provide cancer cells with a selective advantage, allowing them to grow and proliferate more rapidly.
Mitochondrial Damage can also lead to cell death of cancer cells.
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Scientific Papers found: Click to Expand⟱
*cardioP↑, Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation - PMC
*MitoP↑, The mechanism included promotion of mitophagy, which reduced generation of mitochondrial ROS and accumulation of damaged mitochondria[31].
*ROS↓, AS-IV can reduce ROS-mediated autophagosome accumulation and myocardial injury caused by I/R[21]
*mtDam↓,
*neuroP↓, Ischemic stroke MCAO in SD rats; OGD/R in HT22 cells A neuroprotective role (-) apoptosis (+) autophagy
TumAuto↓, For NSCLC cells treated with cisplatin, AS-IV inhibited the increased autophagy of proteins Beclin1 and LC3 I/II
*AntiDiabetic↑, Protective effect of AS-IV on diabetes
*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.
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in-vitro, |
Park, |
SH-SY5Y |
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*neuroP↑, Neuroprotective effects of Withania somnifera
*Inflam↓, including inflammation and oxidative stress reduction, memory and cognitive function improvement.
*ROS↓,
*cognitive↑,
*memory↑,
*GPx↑, significantly increased glutathione peroxidase activity
*Prx↓, KSM-66, had peroxiredoxin-1 and VGF levels significantly lower than the untreated control
*ATP↑, rescue of mitochondria with 0.5 mg/ml KSM-66 extract showed an increase in ATP levels.
*Vim↓, Pre-treatment with KSM-66 decreased level of vimentin
*mtDam↓, KSM-66 attenuates 6-OHDA-induced mitochondrial dysfunction in SH-SY5Y cells
*eff↑, BA significantly improved post‐ischemic cardiac function, reduced infarct size and apoptotic cell death, decreased oxidative stress, and improved the mitochondrial state.
*ROS↓,
*mtDam↓,
*AMPK↑, Furthermore, BA markedly increased AMPK activation, Nrf2 nuclear translocation, and the levels of NAD(P)H quinone dehydrogenase and heme oxygenase‐1.
*NRF2↑,
*NADPH↑,
*HO-1↑,
*cardioP↑, berbamine (BA)‐induced cardioprotective effects
*mtDam↓, CAP ameliorated mitochondrial damage, facilitated the nuclear translocation of NRF2, thereby promoting the expression of downstream antioxidant response elements, HO-1, Trx, GSS and NQO1 in GES-1 cells.
*NRF2↑,
*HO-1↑,
*Trx↑,
*GSS↑,
*NQO1↑,
*Keap1↓, CAP could directly bind to KEAP1 and inhibit the interaction between KEAP1 and NRF2.
*ROS↓, Capsaicin protects GES-1 from oxidative stress
*PKM2↓, Previous studies have demonstrated that CAP can directly bind to and inhibit the activity of PKM2 and LDHA, subsequently attenuating inflammatory response
*LDHA↓,
*Inflam↓,
*antiOx↑, hydrogen has shown great anti-oxidative stress and anti-inflammatory effect in many cerebral disease models
*Inflam↓,
*AMPK↑, hydrogen-rich water can stimulate AMPK-Sirt1-FoxO3a pathway which could play a role in anti-oxidative
stress,
*SIRT1↑,
*FOXO↑,
*mtDam↓, diminishing mitochondrial damage and acting as a neuroprotective agent, and neutralize ROS induced by Aβ
*neuroP↑,
*ROS↓,
*p38↓, hydrogen water
could suppress the activation of phospho-p38 and JNK
*cognitive↑, Currently, Hou et al.50 reported that hydrogen-rich water could improve cognition function in female transgenic AD mice by reducing the decline in brain estrogen levels
*BDNF↑, reducing the decline in brain estrogen levels, estrogen receptor (ER) β, and the expression of brain-derived neuro-trophic factor (BDNF)
*memory↑, Li et al.71 found that hydrogen-rich saline could reduce
learning and memory impairments and neural inflammation
which were induced by Aβ in rats
*lipid-P↓, Moreover, hydrogen-rich saline suppressed lipid peroxidation products, inflammatory factor like interleukin-6 and TNF-α, and the activation of astrocytes
*IL6↓,
*TNF-α↓,
*JNK↓, protective effect of hydrogen-rich saline may be due to inhibition of the activation of JNK
and NF-κB
*NF-kB↓,
*NLRP3↓, Hydrogen-rich water inhibit NLRP3, and weaken the oestrogen-ERβ-BDNF signalling pathway.
*Inflam↓, Hydrogen therapy AD: inflammation, energy regulation, prevents neuronal damage.
*neuroP↑,
*toxicity↓, Hydrogen therapy's low side effects make it a complement to AD treatment. Even at high concentrations, hydrogen gas is still non-toxic, and has been widely used in the diving field.
*antiOx↑, hydrogen’s role as a natural antioxidant,
*ROS↓, Hydrogen has been shown to mitigate the amount of ROS released from mitochondria, thereby reducing mitochondrial DNA peroxidation and inhibiting the expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), caspase-1, and I
*NLRP3↓,
*IL1β↓,
*mtDam↓, curtail mitochondrial damage, thereby bolstering ATP synthesis and fortifying the electron transport chain within mitochondria
*ATP↑,
*AMPK↑, activating AMPK and amplifying the downstream antioxidant response of forkhead box O3a (FOXO3
*FOXO3↑,
*SOD1↑, It elevates the levels of intracellular antioxidant enzymes, notably superoxide dismutase 1 (SOD1) and catalase (CAT), thereby serving as a neuroprotective agent that diminishes the risk and progression of AD
*Catalase↑,
*NRF2↑, Hydrogen slows AD progression by activating the cellular endogenous antioxidant system Nrf2;
*NO↓, Reduced inflammatory markers such as ROS, Nitric oxide (NO) and Malondialdehyde (MDA)
*MDA↓,
*lipid-P↓, drinking HRW significantly reduced lipid peroxidation in the brain of SAMP8 mice.
*memory↑, HRW inhibited the decline of learning and memory impairment
*ER(estro)↓, Decreased hormone levels, estrogen receptor (ER) β, and BDNF expression improve cognitive function in female transgenic AD mice.
*BDNF↑, upsurge in BDNF levels, which further ameliorated the cognitive impairments observed in mice affected by sepsis.
*cognitive↑,
*APP↓, The expression of APP, BACE1, and SAPPβ was proficiently suppressed, thereby curtailing the overproduction of Aβ in Alzheimer's
*BACE↓,
*Aβ↓,
*BP∅, inhaling hydrogen gas has no effect on blood pressure and other blood parameters (such as pH, body temperature, etc.),
*BBB↑, efficiently crossing the blood-brain barrier to perform their functions.
*NRF2↑, After LYC intervened in the body, it activated Nrf2 nuclear translocation and its downstream HO-1 and NQO1 antioxidant signaling pathways
*HO-1↑, Lycopene activates Nrf2-HO-1 antioxidant pathway to inhibit oxidative stress injury induced by AAI exposure in NRK52E cells
*NQO1↑,
*ROS↓, LYC inhibited ROS production by renal tubular epithelial cells, and alleviated mitochondrial damage.
*mtDam↓,
*Bcl-2↑, LYC was able to up-regulate the expression of Bcl-2, down-regulate Bax expression and inhibit the activation of cleaved forms of Caspase-9 and Caspase-3, which finally attenuated the apoptosis
*BAX↓,
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*RenoP↑, Interestingly, there was a significant improvement in damaged renal tissue in mice with AAN after lycopene intervention
*lipid-P↓, lycopene significantly decreased the expression of AAI-induced lipid peroxidation product (MDA), and increased the expression of antioxidant enzyme systems (T-AOC, SOD, and GSH-PX)
*SOD↑,
*GPx↑,
*Inflam↓, Lycopene improves inflammatory responses in the kidneys of AAN mice
*TNF-α↓, TNF-α, IL-6, IL-10, was increased and the expression of IL-12 was decreased in the kidneys of model mice compared with the control group. However, LYC intervention reversed the expression of these genes in a dose-dependent manner
*IL6↓,
*IL10↓,
*Inflam↓, main activity profile of lycopene includes antiatherosclerotic, antioxidant, anti-inflammatory, antihypertensive, antiplatelet, anti-apoptotic, and protective endothelial effects, the ability to improve the metabolic profile, and reduce arterial stif
*antiOx↑, It is a much more potent antioxidant than alpha-tocopherol (10 × more potent) or beta-carotene (twice as potent)
*AntiAg↑, lycopene, protecting against myocardial infarction and stroke, is its antiplatelet activity
*cardioP↑, favorable effect in patients with subclinical atherosclerosis, metabolic syndrome, hypertension, peripheral vascular disease, stroke and several other cardiovascular disorders
*SOD↑, Lycopene modulates also the production of antioxidant enzymes, such as superoxide dismutase and catalase
*Catalase↑,
*ROS↓, By reducing oxidative stress and reactive oxygen species, lycopene increases the bioavailability of nitric oxide (NO), improves endothelium-dependent vasodilation and reduces protein, lipids, DNA, and mitochondrial damage (
*mtDam↓,
*cardioP↑, Lycopene exerts a cardioprotective effect against atrazine induced cardiac injury due to its anti-inflammatory effect, by blocking the NF-kappa B pathway and NO production
*NF-kB↓,
*NO↓,
*COX2↓, downregulation of cyclooxygenase 2,
*LDL↓, significant reductions in total and LDL cholesterol were revealed only at doses of, at least, 25 mg lycopene/day
*eff↑, It was noticed that lycopene can potentiate the antiplatelet effect of aspirin, which requires low lycopene diet
*ER Stress↓, Lycopene protects the cardiomyocytes by relieving ERS
*BioAv↑, Lycopene is very bioavailable in the presence of oil, especially in monounsaturated oils, other dietary fats and processed tomato products
*eff↑, Lycopene can increase the antioxidant properties of vitamin C, E, polyphenols and beta-carotene in a synergistic way
*MMPs↓, figure 3, secretion of MMPs
*COX2↓,
*RAGE↓,
*antiOx↑, Lycopene is an antioxidant protecting from oxidative stress-induced cell damage
*ROS↓, Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells.
*NF-kB↓,
*neuroP↑, Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration.
*MMP↓, As shown in Figure 3C, amyloid-β increased the ratio of green to red fluorescence in the cells, which reflects a decrease in MMP in amyloid β-stimulated cells
*mtDam↓, Lycopene suppressed decrease in OCR in amyloid-β-stimulated cell, suggesting that lycopene prevents mitochondrial damage induced by amyloid-β in the cells.
*OCR↓, In the present study, lycopene significantly inhibited amyloid-β-induced mitochondrial dysfunction, which was proven by its protective effect in reducing both MMP and OCR.
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Review, |
Nor, |
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AD, |
NA |
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NA, |
Diabetic, |
NA |
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NA, |
Stroke, |
NA |
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NA, |
LiverDam, |
NA |
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NA, |
Park, |
NA |
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*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,
*ER Stress↓, 4-PBA attenuated ER stress and mitochondrial dysfunction induced by Dex in MC3T3-E1 cells.
*mtDam↓,
*Apoptosis↓, 4-PBA reduces apoptosis induced by Dex and ER stressors in osteoblast cells
eff↑, inhibiting ER stress. This new discovery is of great significance for molecular intervention against GC-induced osteoporosis.
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Review, |
AD, |
NA |
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Review, |
Diabetic, |
NA |
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Review, |
Var, |
NA |
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in-vitro, |
Nor, |
H9c2 |
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*antiOx↑, In this study, the antioxidant and anti-inflammatory effects of the main flavonoids of propolis (chrysin, pinocembrin, galangin, and pinobanksin) and propolis extract were researched.
*Inflam↓,
*ROS↓, ROS levels were decreased; SOD and CAT activities were increased; and the expression of HO-1 protein was increased by chrysin.
*SOD↑,
*Catalase↑,
*HO-1↑,
*NO↓, The results demonstrated that NO (Nitric Oxide), NOS (Nitric Oxide Synthase), and the activation of the NF-κB signaling pathway were inhibited in a dose-dependent manner
*NOS2↓,
*NF-kB↓,
*NRF2↑, it is possible that phytochemicals activate the Nrf2 pathway and inhibited the NF-κB (Nuclear factor kappa B) pathway.
*hepatoP↑, propolis has antioxidant, anti-inflammatory, anti-cancer, anti-bacterial, and hepatoprotective properties.
*MDA↓, chrysin reduced the cytotoxicity, MDA levels, and lysosomal and mitochondrial damage induced by AlP in a dose-dependent manner and increased the GSH activity induced by AlP i
*mtDam↓,
*GSH↑,
*p65↓, Similarly, galangin at 15, 30, and 60 mg/kg inhibited the expression of NF-κB p65, NOS, TNF-α, and IL-1β in a dose-dependent manner
*TNF-α↓,
*IL1β↓,
*NRF2↑, Nrf2 translocation from the cytoplasm to the nucleus was up-regulated (chrysin range of 5 μM–10 μM, pinocembrin range of 5 μM–40 μM, and propolis-extract range of 5 μg/mL–40 μg/mL)
*NRF2↓, and then down-regulated (chrysin range of 15 μM–25 μM, pinocembrin range of 40 μM–60 μM, and propolis-extract range of 40 μg/mL–100 μg/mL) following treatments with chrysin, pinocembrin, and propolis extract
*ROS⇅, Secondly, chrysin, pinocembrin, galangin, pinobanksin, and propolis extract exhibited antioxidant and pro-oxidant effects in a dose-dependent manner.
*BioAv↓, bioavailability values of galangin and chrysin in propolis extracts were determined in a study, and they were at 7.8% and 7.5%, respectively
*BioAv↑, Moreover, propolis extract has a higher bioavailability than single-flavonoid standards
*AntiAge↑, Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK)
*IGF-1↓,
*AMPK↑,
*CRM↑, resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways.
*PGC-1α↑, activated receptor- γ coactivator 1α (PGC-1α) activity, increased mitochondrial number, and improved motor function.
*mtDam↓,
*motorD↑, Surprisingly, the resveratrol-fed HC mice steadily improved their motor skills as they aged
*hepatoP↑, At 18 months of age it was apparent that the high-calorie diet greatly increased the size and weight of livers and that resveratrol prevented these changes
*Dose↝, this study shows that an orally available small molecule at doses achievable in humans can safely reduce many of the negative consequences of excess caloric intake, with an overall improvement in health and survival.
*AMPK↑, In muscle, resveratrol activated AMPK, increased SIRT1 and PGC-1α protein levels,
*SIRT1↑, Resveratrol, which was discovered in a small-molecule screen as a potent SIRT1 activator
*PGC-1α↑,
*BP↓, Systolic blood pressure dropped and HOMA index improved after resveratrol.
*CRM↑, 30 days of resveratrol supplementation induces metabolic changes in obese humans, mimicking the effects of calorie restriction.
*Dose↝, resveratrol (150 mg/day (99%); resVida™)
*mtDam↓, Resveratrol increases AMPK activity, increases mitochondrial efficiency and respiration on fatty acid substrates.
*ALAT↓, paralleled by lower plasma ALAT values, as mentioned before, both indicating improved liver function.
*hepatoP↑,
*NLRP3↓, inhibits NLRP3 inflammasome-derived IL-1β secretion and pyroptosis in macrophages.
*mtDam↓, Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage
*p38↑, Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol.
TumCD↑, urolithin A markedly induced cell death of OSCC via the induction of endoplasmic reticulum stress and subsequent inhibition of AKT and mTOR signaling as evidenced by decreased levels of phosphorylated mTOR and 4EBP1.
ER Stress↑,
Akt↓,
mtDam↓,
p‑mTOR↓,
*BioAv↝, The bioavailability of urolithins widely varies with inter individual gut microbiome composition depending on the presence of several identified species like Clostridium coccoides and Eggerthellacae family
ROS↑, remarkable anticancer effect on progressive Oral squamous cell carcinoma cells due to their ability to induce ER stress, ROS, cell cycle arrest and increased apoptosis through the preferential inhibition of AKT/mTOR/ERK signaling pathway.
TumCCA↑,
Apoptosis↑,
ERK↓,
Showing Research Papers: 1 to 17 of 17
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↓, 1, ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
mtDam↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 1, TumCD↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↓, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, p‑mTOR↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Total Targets: 12
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 6, Catalase↑, 3, GPx↑, 2, GSH↑, 1, GSS↑, 1, HO-1↑, 4, Keap1↓, 1, lipid-P↓, 4, MDA↓, 2, NQO1↑, 2, NRF2↓, 1, NRF2↑, 6, Prx↓, 1, ROS↓, 11, ROS⇅, 1, SOD↑, 3, SOD1↑, 1, Trx↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 2, ATP∅, 1, MMP↓, 2, mtDam↓, 16, OCR↓, 1, PGC-1α↑, 2,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 5, CRM↑, 2, LDH↓, 1, LDHA↓, 1, LDL↓, 1, NADPH↑, 1, PKM2↓, 1, SIRT1↑, 3,
Cell Death ⓘ
Apoptosis↓, 3, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, JNK↓, 1, p38↓, 1, p38↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 2,
Autophagy & Lysosomes ⓘ
MitoP↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
FOXO↑, 1, FOXO3↑, 1, IGF-1↓, 1,
Migration ⓘ
AntiAg↑, 1, APP↓, 1, Ca+2↝, 1, MMPs↓, 1, RAGE↓, 1, Vim↓, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 3,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL10↓, 1, IL1β↓, 2, IL6↓, 2, Inflam↓, 7, NF-kB↓, 4, p65↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission ⓘ
BDNF↑, 2,
Protein Aggregation ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 3,
Hormonal & Nuclear Receptors ⓘ
ER(estro)↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv↝, 2, Dose↝, 3, eff↑, 6,
Clinical Biomarkers ⓘ
ALAT↓, 1, BG↓, 1, BP↓, 1, BP∅, 1, creat↓, 1, IL6↓, 2, LDH↓, 1, NOS2↓, 1, RAGE↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, cardioP↑, 5, cognitive↑, 4, hepatoP↑, 4, memory↑, 3, motorD↑, 1, neuroP↓, 1, neuroP↑, 5, OS↑, 1, RenoP↑, 1, toxicity↓, 1,
Total Targets: 95
Scientific Paper Hit Count for: mtDam, mitochondrial damage
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
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