NOS2 Cancer Research Results

NOS2, nitric oxide synthase 2: Click to Expand ⟱

Source:

Type:

Also known as NOS2A, INOS
Nitric Oxide Synthase 2 (NOS2, also known as inducible NOS or iNOS) in cancer.
elevated NOS2 has been shown to predict poor outcome in cancer such as ER- breast cancer, glioma, melanoma, cervical, liver, ovarian, and pancreatic. Taken together, NOS2 may be one of the most powerful biomarker and predictors of poor prognosis and an ideal target for cancer therapy.
Many cancers exhibit upregulated NOS2 expression as part of the tumor-associated inflammatory response.

– Examples include colorectal, breast, lung, and some head and neck cancers, where the inflammatory microenvironment can drive NOS2 induction.

Scientific Papers found: Click to Expand⟱

5470-

AF,

Exploring a Therapeutic Gold Mine: The Antifungal Potential of the Gold-Based Antirheumatic Drug Auranofin

Review,

Var,

TrxR↓, mechanism of action of auranofin was correlated with thioredoxin reductase inhibition,
other↝, but other modes of action such as interference with mitochondrial protein import and NADH kinase were also described and discussed
IL6↑, Conversely, auranofin stimulated IL-6 and IL-8 secretion in monocytes,
IL8↑,
NK cell⇅, NK activation was only observed at low doses of auranofin, while high doses inhibited NK activity
COX2↓, suppression of pro-inflammatory factors such as COX-2 (cyclooxygenase-2), NOS (nitric oxide synthase), NF-κB (nuclear factor-κB), and TrxR, as well as on the activation of peroxyredoxin-1 and Nrf2 (nuclear factor erythroid 2-related factor 2) [19].
NOS2↓,
NRF2↑,
Prx↑,
Half-Life↑, plasma half-lives of 15–25 days [24]
Dose↝, To avoid frequently occurring diarrhea, oral doses of 3–6 mg per day, or below, should also be considered when repurposing auranofin for the treatment of other human diseases.
ROS↑, Imbalances in this system lead to the accumulation of cytotoxic ROS.
NF-kB↓, Auranofin can bind to IKK, which ultimately leads to NF-κB inhibition

1503-

EGCG,

Epigenetic targets of bioactive dietary components for cancer prevention and therapy

Review,

NA,

IC50 values ranging from 0.21 to 0.47 μM

selectivity↑, EGCG has been shown to induce apoptosis and cell cycle arrest in many cancer cells without affecting normal cells
DNMT1↓, inhibition of DNMT1 leading to demethylation and reactivation of methylation-silenced genes.
RECK↑, EGCG-induced epigenetic reactivation of RECK
MMPs↓, negatively regulates matrix metalloproteinases (MMPs)
TumCI↓, inhibits tumor invasion, angiogenesis, and metastasis
angioG↓,
TumMeta↓,
HATs↓, EGCG has strong HAT inhibitory activity
IκB↑, increases the level of cytosolic IκBα
NF-kB↓, suppresses tumor necrosis factor α-induced NF-κB activation
IL6↓,
COX2↓,
NOS2↓,
ac‑H3↑, increased the levels of acetylated histone H3 (LysH9/18) and H4 levels
ac‑H4↑,
eff↑, EGCG may synergize with the HDAC inhibitory action of vorinostat to help de-repress silenced tumor suppressor genes regulating key functions such as proliferation and cell survival

3779-

FA,

A review on ferulic acid and analogs based scaffolds for the management of Alzheimer’s disease

Review,

AD,

*antiOx↑, antioxidant, neuroprotection, Aβ aggregation modulation, and anti-inflammatory.
*neuroP↑,
*Aβ↓,
*Inflam↓,
*COX2↓, , FA inhibits various cytotoxic enzymes’ upregulation, including cyclooxygenase (COX), caspases, and nitric oxide synthase.
*Casp↓,
*NOS2↓,
*HO-1↑, It also upregulates different cytoprotective enzymes such as threonine kinase and heme oxygenase-1 [79].
*AChE∅, recent research work from our laboratory have strongly implicated that FA does not effectively interact with AChE and BChE (<20% inhibition of AChE and BChE at 20 mM)
*BChE∅,
*memory↑, FA to the transgenic mouse model of AD could enhance learning and memory and reduce the toxic Aβ fibrils level

1780-

MEL,

Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing

Review,

Var,

*antiOx↑, Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy.
*toxicity↓,
ChemoSen↑,
*eff↑, melatonin was superior in preventing free radical destruction compared to other antioxidants, vitamin E, β-carotene, vitamin C, and garlic oil
*mitResp↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ATP↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ROS↓, most attractive property of melatonin is that its metabolites also regulate the mitochondrial redox status by scavenging ROS and RNS
*CardioT↓, melatonin has a protective effect on the heart without affecting DOX's antitumor activity,
*GSH↑, improving the de novo synthesis of glutathione (GSH) by promoting the activity of gamma-glutamylcysteine synthetase
*NOS2↓, melatonin inhibits the production of nitric oxide synthase (NOS)
*lipid-P↓, lipid peroxidation was reduced after melatonin treatment (role in induces organ failure)
eff↑, but it also enhances its antitumor activity more than vitamin E
*HO-1↑, melatonin upregulates heme oxygenase-1 (HO-1) (role in induces organ failure)
*NRF2↑, decreased bladder injury and apoptosis due to the upregulation of Nrf2 and nuclear transcription factor NF-κB expression
*NF-kB↑,
TumCP↓, significantly reduced cell proliferation
eff↑, Pretreatment with melatonin effectively preserved the ovaries from cisplatin-induced injury
neuroP↑, Melatonin has neuroprotective roles in oxaliplatin-induced peripheral neuropathy

3807-

mushLions,

Searching for a Longevity Food, We Bump into Hericium erinaceus Primordium Rich in Ergothioneine: The “Longevity Vitamin” Improves Locomotor Performances during Aging

*AntiAge↑, Hericium erinaceus (He) has been demonstrated to display a variety of physiological effects, including anti-aging properties.
*other↑, H. erinaceus primordium (He2) extract contains a high amount of Ergothioneine (ERGO), the longevity vitamin.
*NOS2↓, This effect was accompanied by a significant decrease in some oxidative stress markers (NOS2, COX2) paralleled by an increase in P53,
*COX2↓,
*P53↑,
*neuroP↑, emonstrated the neuro-protective and preventive effects of He2 extract during aging,

3251-

PBG,

The Antioxidant and Anti-Inflammatory Effects of Flavonoids from Propolis via Nrf2 and NF-κB Pathways

Review,

AD,

Review,

Diabetic,

Review,

Var,

in-vitro,

Nor,

H9c2

To induce oxidative stress, H9c2 cells were exposed to multiple H2O2 concentrations (0, 50, 100, 150, 200, and 250 μM) for 1 h

*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

3597-

PI,

Chronic diseases, inflammation, and spices: how are they linked?

Review,

AD,

Review,

Park,

Review,

Var,

*NF-kB↓, downregulation of inflammatory pathways such as NF-κB, MAPK, AP-1, COX-2, NOS-2, IL-1β, TNF-α, PGE2, STAT3
*MAPK↓,
*AP-1↓,
*COX2↓,
*NOS2↓,
*IL1β↓, Parkinson’s disease ↓IL-1β, ↓TNF-α
*TNF-α↓,
*PGE2↓,
*STAT3↓,
*IL10↑, Arthritis ↑IL-10
*IL4↓, Asthma ↓IL-4, -5, ↓NF-κB
*IL5↓,
P53↑, Breast cancer ↑p53, ↓MMP-9,-2, ↓c-Myc, ↓VEGF
MMP9↓,
MMP2↓,
cMyc↓,
VEGF↓,
STAT3↓, Gastric cancer ↓STAT3
survivin↓, Triple negative breast cancer ↓Survivin, ↓p65
p65↓,

76-

QC,

Multifaceted preventive effects of single agent quercetin on a human prostate adenocarcinoma cell line (PC-3): implications for nutritional transcriptomics and multi-target therapy

in-vitro,

Pca,

PC3

 100, 150 uM

aSmase↝, Figure 3b shows that quercetin treatment caused a dose-dependent augmentation in mRNA levels of Diablo and FAS
Diablo↑,
Fas↓,
Hsc70↓, coupled with a dose-responsive reduction in transcriptional activity of HSC70, HIF1A, Mcl-1, Hsp90 and BIRC4.
Hif1a↓,
Mcl-1↓,
HSP90↓,
FLT4↓, A dose-dependent drop in mRNA levels of FLT4, EPHB4, DNAPK, PARP1, ATM, perlecan, GnTV and heparanase genes was observed after treatment of PC-3 cells with quercetin
EphB4↓,
DNA-PK↓,
PARP1↓,
ATM↓,
XIAP↝,
PLC↓,
GnT-V↝,
heparanase↝,
NM23↑, quercetin significantly exerted a dose-responsive rise in transcriptional levels of NM23 and CSR1 genes
CSR1↑,
SPP1↓, coupled with an expressive lowering in mRNA levels of SPP1, DNMT1, HDAC4, CXCR4, b-catenin and NHE1.
DNMT1↓,
HDAC4↓,
CXCR4↓,
β-catenin/ZEB1↓,
FBXW7↝,
AMACR↓,
cycD1/CCND1↓,
IGF-1R↓, down-regulation of mRNA levels of AMACR, cyclin D1, NOS2A, IGF1R, IMPDH1, IMPDH2 and HEC1
IMPDH1↓,
IMPDH2↓,
HEC1↓,
NHE1↓,
NOS2↓,

3194-

SFN,

Sulforaphane impedes mitochondrial reprogramming and histone acetylation in polarizing M1 (LPS) macrophages

in-vitro,

Nor,

*OXPHOS↑, suggesting that OXPHOS activity is needed for maximal inhibition of M1 marker expression by Sfn
*M1↓,
*IL1β↓, Consistent with our previous study [40], presence of Sfn significantly diminished mRNA expression of il1β, il6, nos2, and tnfα in M1 (LPS) cells
*IL6↓,
*NOS2↓,
*TNF-α↓,
*ROS↓, 0 and 10 μM, impaired M1 marker expression, ROS or NO production and preserved respiratory activity after LPS exposure
*NO↓,
*ACC↑, Sfn prevents the drop of nuclear and cytosolic acetyl-CoA in LPS-stimulated macrophages

5904-

TV,

Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Obesity,

Review,

AD,

Review,

Arthritis,

*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol

4838-

Uro,

The Therapeutic Potential of Urolithin A for Cancer Treatment and Prevention

Review,

Var,

BioAv↑, Urolithin A is better absorbed in the gastrointestinal tract than its parent substances.
Inflam↓, Urolithin A attenuated the pro-inflammatory factors production (IL-6, IL-1β, NOS2 and others) in vitro studies.
IL6↓,
IL1β↓,
NOS2↓,
p53 Wildtype↑, figure 1
MDM2↑,
Snail↓,
E-cadherin↑,
N-cadherin↓,
Vim↓,
NF-kB↓,
mTOR↓, Urolithin A can downregulate several oncogenes such as mTOR and Kirsten-rat sarcoma viral oncogenehomolog (KRAS) and upregulate tumor suppressor genes such as p53
p‑Akt↓, At molecular level urolithin A dose-dependently decreased phosphorylation of AKT
selectivity↑, At the same time, it isimportant to note that urolithin A has minimal impact on normal pancreatic epithelial cells such as humanpancreatic epithelial nestin-expressing cells (HPNE) and HPNE-KRAS
EMT↓, Urolithin A (10 mcM) inhibits epithelial-mesenchymal transition (EMT) in lung cancer cells

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 4, Catalase↑, 2, GPx↑, 2, GSH↑, 3, GSTs↑, 1, H2O2↓, 1, HDL↑, 1, HO-1↑, 3, lipid-P↓, 1, MDA↓, 2, NADH↓, 1, NRF2↓, 1, NRF2↑, 3, OXPHOS↑, 1, RNS↓, 1, ROS↓, 4, ROS⇅, 1, SOD↑, 3,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, mitResp↑, 1, mtDam↓, 1,

Core Metabolism/Glycolysis ⓘ

ACC↑, 1, LDL↓, 1,

Cell Death ⓘ

Casp↓, 1, MAPK↓, 1,

Transcription & Epigenetics ⓘ

other↓, 1, other↑, 2,

DNA Damage & Repair ⓘ

P53↑, 1,

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,

Migration ⓘ

AntiAg↑, 1, AP-1↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 3,

Barriers & Transport ⓘ

GastroP↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 4, IL10↑, 1, IL1β↓, 3, IL4↓, 1, IL5↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 3, M1↓, 1, NF-kB↓, 2, NF-kB↑, 1, p65↓, 1, PGE2↓, 1, TNF-α↓, 3,

Synaptic & Neurotransmission ⓘ

AChE↓, 1, AChE∅, 1, BChE↓, 1, BChE∅, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 3, BioAv↝, 1, eff↑, 2, Half-Life↝, 1,

Clinical Biomarkers ⓘ

BP↓, 1, IL6↓, 1, NOS2↓, 7,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiDiabetic↑, 1, cardioP↑, 1, CardioT↓, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 2, Obesity↓, 1, toxicity↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 72

Scientific Paper Hit Count for: NOS2, nitric oxide synthase 2

1 Auranofin
1 EGCG (Epigallocatechin Gallate)
1 Ferulic acid
1 Melatonin
1 Mushroom Lion’s Mane
1 Propolis -bee glue
1 Piperine
1 Quercetin
1 Sulforaphane (mainly Broccoli)
1 Thymol-Thymus vulgaris
1 Urolithin

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#:%  Target#:409  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

NOS2 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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