VitC, Vitamin C (Ascorbic Acid): Click to Expand ⟱
Features:
High-dose vitamin C: Some studies have suggested that high-dose vitamin C may be effective in treating certain types of cancer, such as ovarian cancer and pancreatic cancer.
Symptoms of vitamin C deficiency include fatigue, weakness, poor wound healing, ecchymoses, xerosis, lower extremity edema, and musculoskeletal pain—most of them are often observed in end-stage cancer patients. -Vitamin C is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function.
-Ascorbic Acid, Different levels in different Organs
Homeostasis ranging from about 0.2 mM in the muscle and heart, and up to 10 mM in the brain and adrenal gland. -(Note the Oncomagnetic success in the brain also was then under conditions of high Vitamin C)

-Ascorbic acid is an electron donor
Ascorbic Acid, can be a Pro-oxidant
"The pro-oxidative activity of ascorbic acid (Figure 2) is associated with the interaction with transition metal ions (especially iron and copper). Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals."
Ascorbic Acid, formation of H2O2 (Hydrogen Peroxide)
Many studies indicate the toxicity of ascorbate to cancer cells. Much evidence indicates that the underlying phenomenon is the pro-oxidative activity of ascorbate, which induces the formation of H2O2 and oxidative stress.
"ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2)"
-High dose VitC therapy may not be for those with kidney problems
-Oral supplement up to 10g/day?
-Direct regulator of TET">TET↑
-caution for (G6PD-) deficient patients receiving vitamin C infusions

-Note plasma half-life 30mins to 1hr, 1.5-2hr elimination half-life.
oral BioAv water soluble, but has limitiations as 100mg yeilds 60uM/L in plasma, but 1000mg only yeilds 85uM/L. mM concentration are required for effectiveness on cancer cells. Hence why IV administration is common. Boosting HIF increases the intracellular uptake of oxidized VitC
Pathways:
- high dose induces ROS production in cancer cells. Otherwise well known antioxidant in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Caspases↑, DNA damage↑, cl-PARP↑,
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- 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↓, VEGF↓, NF-κB↓,
- reactivate genes thereby inhibiting cancer cell growth : P53↑, TET">TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓,
- Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
271- ALA,  VitC,  LDN,    The Long-Term Survival of a Patient With Stage IV Renal Cell Carcinoma Following an Integrative Treatment Approach Including the Intravenous α-Lipoic Acid/Low-Dose Naltrexone Protocol
OS↑, >9 years
Weight↑, up 30 lbs
TumVol↓, PET/CT scan

2580- ART/DHA,  VitC,    Effects of Antioxidants and Pro-oxidants on Cytotoxicity of Dihydroartemisinin to Molt-4 Human Leukemia Cells
- in-vitro, AML, NA
eff↓, Compared to control, ascorbate and H 2 O 2 both caused a significant decrease in cell count both at 24-h (p<0.05 and p<0.0001 for ascorbate and H 2 O 2 , respectively)
other↝, Vitamin C, a common supplement, has been shown to act as both a ROS generator in the presence of iron and copper (15) and as an antioxidant
ROS↑, From our results, we can postulate that ROS generation is causing cell death independently and in combination with DHA
eff↓, Ascorbate can convert ferric iron into ferrous iron (18), the active form that reacts with artemisinin, generating short lived free radicals.
eff↓, If this happens in the stomach of a person who is consuming artemisinin along with ascorbate, ascorbate will convert ferric iron in foods to the ferrous form, which may react with artemisinin locally, making the therapy less effective

1846- dietFMD,  VitC,    A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer
- Study, Var, NA
TumCG↓, FMDs delay tumor progression
ChemoSen↑, potentiate chemotherapy efficacy
ChemoSideEff↓, while protecting healthy tissues from chemo-associated side effects in different cancer models
ROS↑, presence of metals, and particularly iron, high dose of vitamin C exerts a pro-oxidant action by generating hydrogen peroxide and hydroxyl radicals via Fenton chemistry
Fenton↑,
H2O2↑,
eff↑, we show that FMD cycles potentiate high-dose vitamin C anti-cancer effects in a range of cancer types
HO-1↓, KRAS-mutant cancer cells respond to vitamin C treatment by up-regulating HO-1, and consequently limiting vitamin C pro-oxidant action. FMD is able to revert HO-1 up-regulation
DNAdam↑, increase in free reactive iron and oxygen species causing DNA damage and cell death
eff↑, we found that the nontoxic FMD + vitamin C combination therapy is as effective as oxaliplatin + vitamin C in delaying tumor progression while the triple FMD, vitamin C and chemotherapy combination treatment is the most effective.

1847- dietFMD,  VitC,    Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers
- in-vitro, PC, PANC1
TumCG↓, Fasting-mimicking diets delay tumor progression
ChemoSen↑, sensitize a wide range of tumors to chemotherapy
eff↑, vitamin C anticancer activity is limited by the up-regulation of the stress-inducible protein heme-oxygenase-1. The fasting-mimicking diet selectivity reverses vitamin C-induced up-regulation of heme-oxygenase-1
HO-1↓, FMD reverses the effect of vitamin C on HO-1(downregulating HO-1)
Ferritin↓,
Iron↑, consequently increasing reactive iron, oxygen species, and cell death
ROS↑, Vitamin C’s pro-oxidant action is strictly dependent on metal-ion redox chemistry. In particular, free iron was shown to be a key player in vitamin C-induced cytotoxic effects
TumCD↑,
IGF-1↓, effects on the insulin-like growth factor 1 (IGF-1)
eff↓, When cancer cells were grown under STS conditions before and during treatment, vitamin C-mediated toxicity was strongly enhanced
eff↓, Conversely, KRAS-wild-type CRC (SW48, HT29), prostate cancer (PC-3), ovarian cancer (COV362) cell lines and a normal colon cell line (CCD841CoN) were resistant to vitamin C when used both as a single agent and in combination with STS

1914- Fer,  VitC,  TMZ,  Rad,    Pharmacologic Ascorbate and Ferumoxytol Combined with Temozolomide and Radiation Therapy for the Treatment of Newly Diagnosed Glioblastoma
- Trial, GBM, NA
eff↑, Adding pharmacologic ascorbate and ferumoxytol to standard temozolomide and radiation therapy may work better in treating glioblastoma compared to giving temozolomide and radiation therapy alone

3152- H2,  VitC,  Rad,    Hydrogen and Vitamin C Combination Therapy: A Novel Method of Radioprotection
- in-vitro, Nor, HUVECs - in-vivo, NA, NA
AntiTum↑, Hydrogen also has direct and indirect antitumor effects, which could be useful for the treatment of cancer patients. Hydrogen therapy improves overall survival, quality of life, blood parameters, and tumor reduction.
OS↑,
QoL↑,
TumVol↓,
radioP↑, In addition, hydrogen attenuates the risk of carcinogenesis induced by radiation.
Dose↑, Patients begin hydrogen inhalation 10 minutes prior to vitamin C injection. Patients are treated with high-dose vitamin C injection while inhaling simultaneous hydrogen
Dose↝, patients also performed the hydrogen and vitamin C combination therapy at home on their own as much as possible
eff↑, These results suggest that in normal cells, the combination of 1 mM vitamin C and hydrogen is the most effective radioprotective agent.

1721- Lyco,  RES,  VitC,    Lycopene, resveratrol, vitamin C and FeSO4 increase damage produced by pro-oxidant carcinogen 4-nitroquinoline-1-oxide in Drosophila melanogaster: Xenobiotic metabolism implications.
- in-vitro, Pca, PC3 - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Liver, HepG2
ROS↑, We propose that the basal levels of the XM's enzymes in the ST cross interacted with a putative pro-oxidant activity of the compounds added to the pro-oxidant effects of 4-NQO.

585- MF,  VitC,    Impact of pulsed magnetic field treatment on enzymatic inactivation and quality of cloudy apple juice
other↓, significant decreases of ascorbic acid were observed at the intensity of 7 T with 5–30 pulses.

590- MF,  VitC,    Sub-millitesla magnetic field effects on the recombination reaction of flavin and ascorbic acid radicals
- in-vitro, NA, NA
RPM↑,

592- MF,  VitC,    Alternative radical pairs for cryptochrome-based magnetoreception
RPM↑,

582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, boost, Ascorbic acid (AA, C6H8O6) can act as an electron-donor
Ferroptosis↑, HCSVs and MF efficiently inhibited TRAMP-C1 growth through ferroptosis-mediated cell death.
ROS↑, The generated ferrous ions, inducing stronger Fenton-like oxidation than ferric ions, triggered the higher accumulation of ROS, and finally inhibited tumor cell growth
TumCG↓, Collectively, it was proved that the exogenous magnetic field-boosted Fenton reaction efficiently inhibit tumor growth.
Iron↑, after 10-min MF treatment, the increase of ferrous ions was found in 0.1 h
GPx4↓, combination treatment of MF and HCSVs downregulated GPX4

594- MF,  VitC,    Static Magnetic Field Effect on the Fremy's Salt-Ascorbic Acid Chemical Reaction Studied by Continuous-Wave Electron Paramagnetic Resonance
- Analysis, NA, NA
RPM↑,

587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑,
SOD↓,
other↓, ascorbic acid content decreased

595- MFrot,  VitC,    The Effect of Alternating Magnetic Field Exposure and Vitamin C on Cancer Cells
- in-vitro, PC, MIA PaCa-2 - in-vitro, CRC, SW-620 - in-vitro, NA, HT1080 - in-vitro, Pca, PC3 - in-vitro, OS, U2OS - in-vitro, BC, MCF-7 - in-vitro, Nor, CCD-18Co
TumCD↑, An 80 percent cell death (20 percent survival) was achieved with 160 mg/dL of vitamin C in the magnetic field treatment group. It required 360 mg/dL to achieve the same effect with vitamin C only treatment group.
eff↑, vitamin C combined with low frequency magnetic field or rotating magnetic field reduces the amount of vitamin C to induce 50 percent inhibition of tumor cells.
*TumCG∅, For normal cell line of colon fibroblast magnetic field did not potentiate inhibition of cell growth. These are all mono-layer cell culture.

786- Mg,  VitC,    A narrative review on the role of magnesium in immune regulation, inflammation, infectious diseases, and cancer
Risk↓, boasts a significant anti-cancer effect.
*VitD↑, Mg is also essential for the synthesis and distribution of vitamin D
*pH↝, Additionally, the presence of Mg2+ plays a crucial role in regulating the levels of "intracellular free Ca2+ and intracellular pH"
*ROS↓, mitochondrial ROS inhibition (study in frail elderly patients)
TumCG↓, Mg in the diet slowed tumor development in young male rats
eff↑, Mg can enhance the anti-cancer effects of AA. (related to SVCT2 expression)

1254- PI,  VitC,    Piperlongumine combined with vitamin C as a new adjuvant therapy against gastric cancer regulates the ROS–STAT3 pathway
- in-vivo, GC, NA
STAT3⇅, PL effectively suppressed STAT3 activation while VC caused abnormal activation of STAT3.
eff↑, combination of PL and VC exhibited a stronger apoptotic effect compared with either agent alone
ROS↑, PL and VC effectively induced apoptosis of GC cells through oxidative stress.
Apoptosis↑, 15 µM PL and 3 mM VC caused more than 60% apoptosis in two GC cell lines.

918- QC,  CUR,  VitC,    Anti- and pro-oxidant effects of oxidized quercetin, curcumin or curcumin-related compounds with thiols or ascorbate as measured by the induction period method
- Analysis, NA, NA
ROS↑, CUR enhances the prooxidant activity of ascorbate(vit C)
ROS↑, Under anaerobic conditions, QUE, with a catechol ring, may be more prooxidant than CUR, with a phenol ring.

3111- VitC,    https://pmc.ncbi.nlm.nih.gov/articles/PMC4492638/
- Trial, Nor, NA
Inflam↓, Vitamin C (500 mg twice daily) has potential effects in alleviating inflammatory status by reducing hs-CRP, IL-6, and FBG in hypertensive and/or diabetic obese patients.
CRP↓,
IL6↓,

3121- VitC,  immuno,    Ascorbic acid induced TET2 enzyme activation enhances cancer immunotherapy efficacy in renal cell carcinoma
- in-vivo, RCC, A498 - in-vitro, RCC, 786-O
TET2↑, Ascorbic acid induced TET2 enzyme activation enhances cancer immunotherapy efficacy in renal cell carcinoma
eff↑, Therefore, we speculated that restoring 5hmC levels in RCC promoting TET2 activity may have a synergistic effect with immune checkpoint therapy.
eff↑, Vitamin C sensitizes renal cell carcinoma to anti-PD-L1 treatment

3112- VitC,    Antioxidative and Anti-Inflammatory Activity of Ascorbic Acid
- Review, Nor, NA
*ROS↓, ascorbate as a free radical scavenger but also summarizes its antioxidant action
*antiOx↑,
*SOD↑, activation of antioxidant enzymes, such as superoxide dismutase, catalase, or glutathione peroxidase.
*Catalase↑,
*GPx↑,
*NRF2↑, ascorbate promotes the activity of transcription factors (Nrf2, Ref-1, AP-1), which enables the expression of genes encoding antioxidant proteins
*AP-1↑,
*Inflam↓, Thus, through its antioxidant properties, the molecule prevents inflammation mediated by lipid peroxidation.
*CRP↓, CRP level in human plasma is significantly reduced by ascorbate supplementation
IFN-γ↓,

3113- VitC,    Vitamin C enhances NF-κB-driven epigenomic reprogramming and boosts the immunogenic properties of dendritic cells
- in-vitro, Nor, NA
TET2↑, intravenous vitamin C treatment in mice abrogates cancer progression through direct TET2 function restoration in cancer cells
NF-kB↑, Vitamin C triggers extensive demethylation at NF-κB/p65 binding sites

3114- VitC,    Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression
- in-vitro, AML, NA
TET2↑, Treatment with vitamin C, a cofactor of Fe2+ and α-KG-dependent dioxygenases, mimics TET2 restoration by enhancing 5-hydroxymethylcytosine formation in Tet2-deficient mouse HSPCs
eff↑, enhances the efficacy of PARP inhibition in suppressing leukemia progression.
ROS↑, High levels of vitamin C can lead to reactive oxygen species (ROS) production via the Fenton reaction
Fenton↑,
Hif1a↓, One study suggested that vitamin C decreases viability of human leukemia cell lines by promoting downregulation of HIF1α and the anti-apoptotic genes, BCL2, BCL2L1, and MCL1

3115- VitC,    The NF-κB Transcriptional Network Is a High-Dose Vitamin C-Targetable Vulnerability in Breast Cancer
- in-vitro, BC, NA
NF-kB↓, vitamin C can regulate the activation of NF-κB by inhibiting specific NF-κB-dependent genes and multiple stimuli.
Hif1a↓, Vitamin C activates enzymes that are able to inhibit NF-κB and HIF-1α as well as their target genes.
P53↑, vitamin C was reported to decrease NF-κB function and increase p53 overexpression and stability

3116- VitC,    Vitamin C Inhibits NF-kB Activation by TNF Via the Activation of p38 Mitogen-Activated Protein Kinase
- in-vitro, Nor, ECV304 - in-vitro, Nor, HUVECs
*NF-kB↓, vitamin C inhibited TNF-mediated NF-kB activation in a dose-dependent manner,
*p38↑, Vitamin C potently activates p38 MAPK
*MAPK↑,

3117- VitC,    Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells
- in-vitro, Nor, mESC
TET1↑, Here we report that addition of vitamin C to mouse ES cells promotes Tet activity, leading to a rapid and global increase in 5hmC.
eff↝, Importantly, vitamin C, but not other antioxidants, enhances the activity of recombinant Tet1 in a biochemical assay

3118- VitC,    Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
- Trial, Nor, NA
TET2↑, vitamin C reinforces the DNA demethylation cascade,

3119- VitC,    Ascorbic acid–induced TET activation mitigates adverse hydroxymethylcytosine loss in renal cell carcinoma
- in-vitro, RCC, NA
TET2↑, Ascorbic acid–induced TET activation
TumCG↓, Pharmacologic AA treatment led to reduced growth of ccRCC in vitro and reduced tumor growth in vivo, with increased intratumoral 5hmC.
tumCV↓, We observed acute loss in viability with high-dose AA that was reversed in the presence of catalase cotreatment, suggesting that the acute cytotoxicity with short-term exposure of high-dose AA (millimolar concentration) is primarily mediated by H2O2

3120- VitC,    Upregulation of TET activity with ascorbic acid induces epigenetic modulation of lymphoma cells
- in-vitro, lymphoma, NA
TET2↑, ascorbic acid (AA) is a cofactor for TET with a binding site at the catalytic domain, and enhances TET activity
Smad1↑, AA treatment increased the expression of SMAD1, a tumor suppressor gene known to be suppressed by methylation, and increased chemosensitivity of lymphoma cells.
ChemoSen↑,
other↝, AA treatment produced a progressive decrease in DNA methylation and an increase in the hydroxymethylation fraction in a dose-dependent manner, correlating with the increase in TET activity

3110- VitC,    Vitamin C Attenuates Oxidative Stress, Inflammation, and Apoptosis Induced by Acute Hypoxia through the Nrf2/Keap1 Signaling Pathway in Gibel Carp (Carassius gibelio)
- in-vivo, Nor, NA
*IL2↑, Moreover, the levels of the inflammatory cytokines (tnf-α, il-2, il-6, and il-12) were increased by enhancing the Nrf2/Keap1 signaling pathway
*IL6↑,
*IL12↑,
*NRF2↑,
*Catalase↑, Upregulation of the antioxidant enzymes activity (CAT, SOD, and GPx); T-AOC;
*SOD↑,
*GPx↑,
*GRP78/BiP↓, The expression of GRP78 protein in the liver and endoplasmic reticulum stress and apoptosis induced by hypoxia were inhibited by VC.
*ER Stress↓,

3109- VitC,    Vitamin C Inhibited Pulmonary Metastasis through Activating Nrf2/HO-1 Pathway
- in-vitro, Lung, H1299
TumMeta↓, intraperitoneal injection of Vc inhibits pulmonary metastasis through up-regulating the expression of Nrf2, HO-1, cleaved caspases 3 and 9, and causing DNA damage and apoptosis
NRF2↑,
HO-1↑,
cl‑Casp3↑,
cl‑Casp9↑,
DNAdam↑,
Apoptosis↑,
other↑, Meanwhile, oral administration of Vc up-regulates the expression of p53, directly activates Nrf2/HO-1 pathway, increases expression of cleaved caspases 3 and 9, and ultimately inhibits pulmonary metastasis
selectivity↑, has little cytotoxic effects on normal cells.

3108- VitC,  QC,    The role of quercetin and vitamin C in Nrf2-dependent oxidative stress production in breast cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, Lung, A549
NRF2↓, significant decrease in the expression of Nrf2 mRNA and protein levels following the treatment of breast cancer cells with VC and Q
HO-1↓, In the MDA-MB 231 and MCF-7 cell lines, HO1 was significantly suppressed following treatment with VC and Q
ROS↑, It was demonstrated that ROS levels significantly increased in tumor cells treated with VC and Q.
NRF2⇅, it was demonstrated that treatment of MDA-MB 231 cells with 25 µM Q increased the expression of Nrf2, while 50 and 75 µM Q decreased the mRNA levels of Nrf2.

3107- VitC,    Repurposing Vitamin C for Cancer Treatment: Focus on Targeting the Tumor Microenvironment
- Review, Var, NA
Risk↓, VitC supplementation resulted in dose-dependent reductions in all-cause mortality and the risk of various cancers
*ROS↓, Vitamin C (VitC) at the physiological dose (μM) is known to exhibit antioxidant properties.
ROS↑, However, it functions as a prooxidant at the pharmacological dose (mM) achieved by intravenous administration.
VEGF↓, VitC suppressed tumor angiogenesis in colon cancer-bearing mice by downregulating the expression and secretion of VEGF-A and VEGF-D
COX2↓, VitC impairs COX-2 activity and inhibits VEGF mRNA expression in melanoma cells in a time-dependent manner
ER Stress↑, VitC increases the ER stress-mediated breast cancer apoptosis via activation of the IRE-JNK-CHOP signaling pathway, an effect independent of ROS
IRE1↑,
JNK↑,
CHOP↑,
Hif1a↓, On the one hand, VitC directly inhibits HIF-1α-mediated glycolysis-related genes expression and the downstream acidic metabolites
eff↑, ROS generated by VitC treatment exerts a synergistic effect with other glycolysis inhibitors, providing a combined therapeutic strategy
Glycolysis↓,
MMPs↓, VitC inhibits a variety of metalloproteinases (MMPs) mRNA, which degrade ECM and release growth factors that drive tumor metastasis
TumMeta↓,
YAP/TEAD↓, VitC treatment reduces YAP1 expression while upregulating SYNPO-2; therefore, inhibiting metastasis of TNBC
eff↑, VitC enhances the killing efficiency of Hep G2 cells by low-dose sorafenib in vitro.
TET1↑, VitC stimulation of TET2 activity in the renal cell carcinoma

3106- VitC,    Protective effect of vitamin C on oxidative stress: a randomized controlled trial
- Trial, Nor, NA
*ROS↓, Vitamin C was suggested to reduce oxidative stress among subjects with atrophic gastritis.

3105- VitC,    ROS-lowering doses of vitamins C and A accelerate malignant melanoma metastasis
- Review, Var, NA
TumMeta↑, Our current finding that also VitC and the two Vitamin A-related compounds β-carotene and retinyl palmitate can accelerate melanoma metastasis suggest that several antioxidant compounds relevant to the human diet have the capacity to spread tumors.

2485- VitC,  TACE,    High-Dose Vitamin C Promotes Regression of Multiple Pulmonary Metastases Originating from Hepatocellular Carcinoma
- Case Report, HCC, NA
ROS↑, high-dose vitamin C can act as a prooxidant, conferring selective toxic effects on cancer cells.
Dose↝, Twenty grams of vitamin C in 250 mL normal saline was initially administered via an ante-cubital vein twice a week in September 2011. To neutralize acidic pH (3.5-5.0) of vitamin C, it was mixed with NaHCO3, resulting in pH 6.2
Dose↝, high-dose vitamin C administration was continued for more than a year. In July 2013, she finally decided to undergo TACE
TumCG↓, Hepatocellular carcinoma regressed completely after the fourth TACE treatment (
Remission↑, describe a case of regression of multiple pulmonary metastases after treatment with high-dose vitamin C, which enabled a subsequent trial of TACE, eventually leading to complete remission

3104- VitC,    Pro- and Antioxidant Effects of Vitamin C in Cancer in correspondence to Its Dietary and Pharmacological Concentrations
*antiOx↑, Vitamin C is an antioxidant that may scavenge reactive oxygen species preventing DNA damage and other effects important in cancer transformation
*ROS↓,
*DNAdam↓,
ROS↑, High pharmacological doses of vitamin C may induce prooxidant effects, detrimental for cancer cells.
TET1↑, Vitamin C may change the metabolomic and epigenetic profiles of cancer cells, and activation of ten-eleven translocation (TET) proteins and downregulation of pluripotency factors by the vitamin may eradicate cancer stem cells.
CSCs↓,
HIF-1↓, Vitamin C induces degradation of hypoxia-inducible factor, HIF-1, essential for the survival of tumor cells in hypoxic conditions
BioAv↑, Flavonoids may modulate bioavailability of vitamin C. Animal studies with flavonoid-rich extracts or purified plant flavonoids showed an enhanced uptake of vitamin C when it was administered together with flavonoids
selectivity↑, Chen et al. demonstrated that intravenous administration of ascorbic acid at high concentrations was toxic for many types of cancer cells in xenografts in mice with no effect on normal cells

3103- VitC,    Effect of Vitamin C on Reactive Oxygen Species Formation in Erythrocytes of Sickle Cell Anemia Patients
- Human, Nor, NA
*ROS↓, Vitamin C reduced ROS formation in HbSS cells. Future studies should focus on a role for Vitamin C as a safe, cheap addition to maintenance therapy of sickle cell patients.

3102- VitC,    Two Faces of Vitamin C—Antioxidative and Pro-Oxidative Agent
- Review, Var, NA - Review, Stroke, NA
*radioP↑, evidence that vitamin C has radioprotective properties.
*Dose↝, recommended daily dose of vitamin C is on average 75 mg for women and 90 mg for men
ROS↑, Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals. elevated iron levels recognized in cancer cells
*neuroP↑, Ascorbate appears to be a significant neuroprotector
other↓, It is believed that high-dose vitamin C supplementation may be protective and reduce the size of ischemia
*ROS↓, Vitamin C appears to quench ROS, which contributes to the stabilization of the mitochondrial membrane
*MMP↑,

3101- VitC,    Vitamin C stimulates or attenuates reactive oxygen and nitrogen species (ROS, RNS) production depending on cell state: Quantitative amperometric measurements of oxidative bursts at PLB-985 and RAW 264.7 cells at the single cell level
- in-vitro, Nor, RAW264.7 - in-vitro, AML, PLB-985
*antiOx↑, widely publicized as a universal anti-oxidant
*ROS↓, H-atom donors or radical scavengers (AA, vitamins E, Q, glutathione, etc.) present in aerobic cells regulate reactive oxygen and nitrogen species (ROS and RNS) by quenching them to avoid RNS and ROS-induced profound damages to surrounding cells and t
*RNS↓,
ROS↑, PLB‑985(cancer) cells that exhibited enhanced ROS production following AA treatment

2592- VitC,    Ascorbic acid restores sensitivity to imatinib via suppression of Nrf2-dependent gene expression in the imatinib-resistant cell line
- in-vitro, CLL, NA
NRF2↓, addition of ascorbic acid to KCL22/SR cells resulted in a decrease in Nrf2-DNA binding and decreases in levels of gamma-GCSl mRNA and GSH.
GSH↓,

3153- VitC,    Vitamin C Status and Cognitive Function: A Systematic Review
- Review, AD, NA
cognitive↑, studies demonstrated higher mean vitamin C concentrations in the cognitively intact groups of participants compared to cognitively impaired groups
eff↑, Moreover, it can be speculated that a consistently high Vitamin C status acts in a preventive manner, while vitamin C supplementation per se is not a treatment for clinical AD

3137- VitC,    Vitamin C inhibits the growth of colorectal cancer cell HCT116 and reverses the glucose-induced oncogenic effect by downregulating the Warburg effect
- in-vitro, CRC, HCT116
Warburg↓, Notably, as a potential Warburg effect inhibitor, VC suppressed cancer growth in a concentration-dependent manner
TumCG↓,

114- VitC,  QC,    Chemoprevention of prostate cancer cells by vitamin C plus quercetin: role of Nrf2 in inducing oxidative stress
- in-vitro, Pca, PC3 - in-vitro, NA, DU145
GPx↓,
GSR↓,
NQO1↓,
NRF2↓,
ROS↑,

3151- VitC,    Role of Vitamin C in the Function of the Vascular Endothelium
- Review, Nor, NA
angioG↓, It is likely, however, that such effects are related to the use of very high ascorbate concentrations, which have been shown to inhibit angiogenesis in excised aortic rings and in subcutaneous Matrigel plugs in vivo

3150- VitC,    Vitamin C: A Review on its Role in the Management of Metabolic Syndrome
- Review, Obesity, NA
*glucose↓, Vitamin C supplementation resulted in significant decreases in blood glucose 16, BP 17, TG and LDL-C 1
*BG↓,
*antiOx↑, vitamin C is a powerful antioxidant because it acts as a reducing agent preventing other compounds from being oxidised.
*ROS↓,

3149- VitC,    Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice through suppressing inflammatory reaction and ER stress
- in-vivo, Nor, NA
*hepatoP↑, Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice
*ALAT↓, showed in reductions of serological levels of transaminases (ALT and AST), lipids (TG and TC), fasting glucose and insulin, inflammatory cytokines (TNF-α and IL6)
*AST↓,
*TNF-α↓,
*IL6↓,
*ER Stress↓, Further, intrahepatic expressions of endoplasmic reticulum (ER) stress-based ATF6, eIF2α, GRP78, XBP1 proteins were down-regulated by treatments of VC.
*ATF6↓,
*eIF2α↓,
*GRP78/BiP↓,
*XBP-1↓,
*Inflam↓, suppressing hepatocellular inflammatory reaction and ER stress.

3148- VitC,    Antioxidants in brain tumors: current therapeutic significance and future prospects
- Review, Var, NA
*antiOx↑, At dietary concentrations, vitamin C exhibits an antioxidant mechanism and prevent tumorigenesis [74]. Vitamin C prevents DNA damage by reducing OS, thereby preventing carcinogenesis
*ROS↓,
chemoP↑, Vitamin C exhibits both chemopreventive and chemotherapeutic roles via antioxidant and prooxidant mechanisms, respectively
ChemoSen↑,
TET2↑, activating ten-eleven translocation proteins (TETs)
eff↑, A regular supplement of vitamin C during pregnancy was found to reduce the risk of the fetus in developing pediatric brain tumors
OS↑, ascorbate demonstrated safety and chemotherapeutic efficacy in prolonging life span and improving quality of life
QoL↑,
eff↑, Vitamin C has been found to enhance the chemotherapeutic effects of methotrexate on glioblastoma cells

3147- VitC,    Vitamin C modulates the metabolic and cytokine profiles, alleviates hepatic endoplasmic reticulum stress, and increases the life span of Gulo−/− mice
- in-vivo, Nor, NA
*OS↑, life span suggesting that vitamin C modulates endoplasmic reticulum stress response and longevity in Gulo−/− mice.
*ER Stress↓,
*GRP78/BiP↓, There was a decrease in GRP78 in Gulo−/− mice treated with 0.4% ascorbate

3146- VitC,    Vitamin C protects against hypoxia, inflammation, and ER stress in primary human preadipocytes and adipocytes
- in-vivo, Nor, NA
*Obesity↓, These findings indicate that Vitamin C can reduce obesity-associated cellular stress and thus provide a rationale for future investigations.
*ER Stress↓, Vitamin C prevented the increase in hypoxia (Fig. 1A–B), significantly reduced the induction of ER stress
*Inflam↓, nd ameliorated the increased expression of inflammatory genes
Hif1a↓, Vitamin C treatment for 24 and 48 h significantly reducing induction of HIF1α protein by 30–40% and VEGFA and GLUT1 mRNA by 40–80%
VEGF↓,
GLUT1↓,
GRP78/BiP↓, significantly reversing the effects of TNFα+PA pre-treatment only on GRP78 induction, by 30–40%

3145- VitC,    Vitamin C inhibits the growth of colorectal cancer cell HCT116 and reverses the glucose‐induced oncogenic effect by downregulating the Warburg effect
- in-vitro, CRC, HCT116
Warburg↓, Notably, as a potential Warburg effect inhibitor, VC suppressed cancer growth in a concentration-dependent manner and further reversed the glucose-induced oncogenic effect.
TumCG↓,
Glycolysis↓,
GlucoseCon↓, 1 h-exposure to 5 mM VC led to an almost 50% reduction in glucose consumption, ATP and lactate contents in cancer cells, with mild impact on normal cells
ATP↓,
lactateProd↓,
selectivity↑, Meanwhile, normal cell had little apparent change
GLUT1↓, (GLUT1, PKM2, and LDHA) were significantly decreased, with p-AMPK/AMPK increased and p-mTOR/mTOR decreased, consistent with the cytotoxicity on 3 kinds of cancer cells
PKM2↓,
LDHA↓,
mTOR↓,

3144- VitC,    Some characteristics of Rabbit muscle phosphofructokinase-1 inhibition by ascorbate
- in-vitro, Nor, NA
PFK1↓, We found that inhibition by ascorbate was PFK-1 concentration dependent
LDH↓, vitamin C specifically inhibits muscle isozymes of AK (adenylate kinase), LDH, and PFK-1

3143- VitC,  ATO,    Vitamin C enhances the sensitivity of osteosarcoma to arsenic trioxide via inhibiting aerobic glycolysis
- in-vitro, OS, NA
TumCP↓, synthetic application of vitamin C (VitC, 800 μM) and ATO (1 μM) significantly further inhibited the proliferation, migration, and invasion of OS cells and promoted cell apoptosis in vitro.
TumCMig↓,
TumCI↓,
eff↑, synthetic application of vitamin C (VitC, 800 μM) and ATO (1 μM) significantly further inhibited the proliferation,
Glycolysis↓, VitC and ATO directly suppresses the aerobic glycolysis of OS cells with the decreased production of pyruvate, lactate, and ATP via inhibiting the expression of the critical glycolytic genes (PGK1, PGM1, and LDHA).
lactateProd↓,
ATP↓,
PGK1↓,
PGM1↓,
LDHA↓,

3142- VitC,    Vitamin C promotes apoptosis in breast cancer cells by increasing TRAIL expression
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF12A
TET2↑, Vitamin C serves as a cofactor for TET methylcytosine dioxygenases to increase 5hmC generation.
Apoptosis↑, vitamin C treatment induced apoptosis in MDA-MB-231 cells, which was verified in two additional breast cancer cell lines.
TRAIL↑, Vitamin C upregulated TRAIL transcripts (2.3-fold increase) and increased TRAIL protein levels.
BAX↑, apoptosis promoted by vitamin C was associated with Bax and caspases activation, Bcl-xL sequestration, and cytochrome c release
Casp↑,
Cyt‑c↑,
HK2↓, downregulated genes (TFRC, PGK1, BNIP3, NDRG1, BNIP3L, ADM, PDK1, HK2)
PDK1↓,
BNIP3↓,

3141- VitC,    High-dose Vitamin C inhibits PD-L1 expression by activating AMPK in colorectal cancer
- in-vitro, CRC, HCT116
Glycolysis↓, Vitamin C inhibits immune evasion by regulating glycolysis
eff↑, VitC suppresses tumor growth and enhances immunotherapy in combination with anti-PD-L1
PD-L1↓, We found that VitC inhibits aerobic glycolysis in HCT116 cells while also downregulating PD-L1 expression.
AMPK↑, VitC's activation of AMPK, which downregulates HK2 and NF-κB, ultimately resulting in reduced PD-L1 expression and increased T cell infiltration.
HK2↓,
NF-kB↓,
Warburg↓, Our research shows that high-dose VitC downregulating the Warburg effect, suppressing CRC growth
tumCV↓, After treatment with VitC, the cell viability of HCT116 cells significantly decreased
GLUT1↓, marked reduction in the mRNA level of glycolysis-related proteins GLUT1, PKM2, and LDHA
PKM2↓,
LDHA↓,
CD4+↑, Our research shows that high-dose VitC increases CD4+ and CD8+ T cell infiltration in tumor tissues by inhibiting PD-L1
CD8+↑,

3140- VitC,    Vitamin-C-dependent downregulation of the citrate metabolism pathway potentiates pancreatic ductal adenocarcinoma growth arrest
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HEK293
citrate↓, pharmacological doses of vitamin C are capable of exerting an inhibitory action on the activity of CS, reducing glucose-derived citrate levels
FASN↓, Moreover, ascorbate targets citrate metabolism towards the de novo lipogenesis pathway, impairing fatty acid synthase (FASN) and ATP citrate lyase (ACLY) expression.
ACLY↓,
LDH↓, correlated with a remarkable decrease in extracellular pH through inhibition of lactate dehydrogenase (LDH) and overall reduced glycolytic metabolism.
Glycolysis↓,
Warburg↓, Dismissed citrate metabolism correlated with reduced Warburg effectors such as the pyruvate dehydrogenase kinase 1 (PDK1) and the glucose transporter 1 (GLUT1),
PDK1↓,
GLUT1↓,
LDHA↓, Reduced LDHA expression was also observed after vitamin C exposure, leading to a vast extracellular acidification rate (ECAR) reduction.
ECAR↓,
PDH↑, enhancing PDH activity
eff↑, Surprisingly, an impressive 85% of tumor growth inhibition is described in the combinatory treatment of vitamin C and gemcitabine in our preclinical PDAC PDX model

3139- VitC,    Vitamin C and sodium bicarbonate enhance the antioxidant ability of H9C2 cells and induce HSPs to relieve heat stress
- in-vitro, Nor, H9c2
*Apoptosis∅, Supplementation with vitamin C and vitamin C-Na for 16 h had no significant influence on apoptosis, LDH or MDA, but SOD activity was significantly reduced about 8.6% for VC
*LDH∅,
*MDA∅,
*SOD↓, SOD activity was significantly reduced about 8.6% for VC. further heat stress at 5 h, SOD activity recovered slightly but was still lower than that at 1 h.
eff↝, Thus, under heat stress conditions, the concentration of vitamin C entering the cell could be much higher than in normal conditions.

3138- VitC,    The Hypoxia-inducible Factor Renders Cancer Cells More Sensitive to Vitamin C-induced Toxicity
- in-vitro, RCC, RCC4 - in-vitro, CRC, HCT116 - in-vitro, BC, MDA-MB-435 - in-vitro, Ovarian, SKOV3 - in-vitro, Colon, SW48 - in-vitro, GBM, U251
eff↑, Here, we show that a Warburg effect triggered by activation of the hypoxia-inducible factor (HIF) pathway greatly enhances Vc-induced toxicity in multiple cancer cell lines
Warburg↓,
BioAv↑, HIF increases the intracellular uptake of oxidized Vc through its transcriptional target glucose transporter 1 (GLUT1),
ROS↑, resulting high levels of intracellular Vc induce oxidative stress and massive DNA damage, which then causes metabolic exhaustion by depleting cellular ATP reserves.
DNAdam↑,
ATP↓,
eff↑, Activation of HIF increases the susceptibility to Vc-induced cell toxicity
necrosis↑, High intracellular levels of Vc increase ROS and trigger necrosis in VHL-defective renal cancer cells.
PARP↑, Activation of the PARP Pathway by Vc Depletes Intracellular ATP Reserves in VHL-defective Renal Cancer Cells

3122- VitC,    Ascorbic Acid Promotes Plasma Cell Differentiation through Enhancing TET2/3-Mediated DNA Demethylation
TET2↑, ascorbic acid (vitamin C), an essential nutrient, is able to promote plasma cell differentiation and humoral immune response by enhancing TET2/3-mediated DNA demethylation
TET3↑,

3136- VitC,    Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer
- in-vitro, Colon, SW48 - in-vitro, Colon, LoVo
ERK↓, Vitamin C induces RAS detachment from the cell membrane inhibiting ERK 1/2 and PKM2 phosphorylation.
p‑PKM2↓,
GLUT1↓, As a consequence of this activity, strong downregulation of the glucose transporter (GLUT-1) and pyruvate kinase M2 (PKM2)
Warburg↓, causing a major blockage of the Warburg effect and therefore energetic stress.
TumCD↑, Vitamin C selectively kills KRAS mutant colon cancer cells alone or in combination with cetuximab
eff↑, Remarkably, treatment of HT29, SW480 and LoVo cells with cetuximab (0,4 μM) and vitamin C (5mM) abolished cell growth in the three lines tested.
ROS↓, Interestingly, we detected that vitamin C treatment dramatically reduced intracellular ROS levels in SW480 and LoVo cells (Figure 2D),
cMyc↓, strong inhibition of c-Myc oncogene in colonospheres treated at concentrations of vitamin C as low as 100 μM

3135- VitC,    The interplay between vitamin C and thyroid
- Review, Thyroid, NA
AntiCan↑, found anti‐cancer effects for intravenous (IV) administration of vitamin C
ChemoSen↑, vitamin C could enhance the efficacy of monotherapies agents like cisplatin, 23 gemcitabine, 44 , 45 , 46 sorafenib, 47 PLX4032 21 and 5‐fluorouracil 44 in different types of cancers
radioP↑, vitamins like vitamin E and vitamin C as antioxidant agents are game changers and can reduce the toxicity level of radiopharmaceuticals with a higher efficacy of vitamin C.
MAPK↓, Mechanistic studies have also revealed that vitamin C inhibits the MAPK/ERK and PI3K/AKT signalling pathways in BRAF wild‐type or mutant thyroid cancer cells.
ERK↓,
PI3K↓,
Akt↓,
QoL↑, Cancers can influence patients' quality of life, and vitamin C is shown to positively affect pain relief and well‐being.
OS↑, Altogether, high‐dose vitamin C was shown to prolong the survival duration of patients

3134- VitC,    Vitamin C promotes human endothelial cell growth via the ERK-signaling pathway
- in-vitro, Nor, HUVECs
*ERK↑, Physiological vitamin C-concentrations promote proliferation of subconfluent ECs by activating an ERK1/2 controlled pathway

3133- VitC,    Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells
- in-vitro, Ovarian, NA
*SVCT-2↑, In non-cancer cells, Vit C, at a pharmacological concentration, increased SVCT2 and decreased GLUT1, while the opposite effect was noted in cancer cells.
*GLUT1↓,
SVCT-2↓,
GLUT1↑,
TumCP↓, cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p < 0.01), mainly due to the stimulatory effect on the expression of CDK inhibitors, p21 and P53
CDK2↓,
PARP↓, At a pharmacological dose of 1 mM, Vit C decreased PARP expression (1.5-fold; p < 0.05).
selectivity↑, it's nontoxic effects on non-cancer cells

3132- VitC,    Vitamin C affects G0/G1 cell cycle and autophagy by downregulating of cyclin D1 in gastric carcinoma cells
- in-vitro, GC, MKN45
TumCCA↑, Vitamin C significantly elevated the percentage of cells at G0/G1 phase, whereas the percentage of S phase cells was decreased.
cycD1↓, vitamin C treatment resulted in downregulation of cell cycle-related protein Cyclin D1

3131- VitC,    Antioxidant Vitamin C attenuates experimental abdominal aortic aneurysm development in an elastase-induced rat model
- in-vivo, Nor, NA
*MMP2↓, The proteins of matrix metalloproteinase (MMP)-2, MMP-9, and interleukin 6 were markedly downregulated (P < 0.05, respectively)
*MMP9↓,
*TNF-α↓, accompanied with notably reduced messenger RNA expression of tumor necrosis factor-α, MMP-2/9, and interleukin 1β
*IL1β↓,
*TIMP2↑, messenger RNA of tissue inhibitors of metalloproteinase-1 and tissue inhibitors of metalloproteinase-2 were both significantly upregulated in Vitamin C group.
*TIMP1↓,
*antiOx↑, increased level of antioxidant in cooperation with preserving elastin lamellae, inhibiting matrix-degrading proteinases and suppressing inflammatory responses.
*Inflam↓,

3130- VitC,    Effect of high-dose vitamin C on MMP2 expression and invasive ability in human pancreatic cancer cell line PANC-1
- in-vitro, PC, PANC1
MMP2↓, High-dose vitamin C can decrease the expression of MMP2 in PANC-1 cells, and weaken its invasive ability
TumCI↓,

3129- VitC,    Therapeutic treatment with vitamin C reduces focal cerebral ischemia-induced brain infarction in rats by attenuating disruptions of blood brain barrier and cerebral neuronal apoptosis
- in-vivo, Stroke, NA
*BBB↑, Vitamin C alone or combined with rt-PA significantly reduced blood brain barrier permeability, levels of MMP-9,
*MMP9↓,
*MMPs↓, Vitamin C attenuates disruptions of blood brain barrier, inhibits MMPs expressions, and protects tight junction proteins
*MMP2↓, Evan Blue dye extravasation and up-regulation of MMP2 and MMP9, both of which were attenuated by vitamin C treatment
*CLDN1↝, tight junction proteins Claudin-1,Claudin-5, and ZO-1, which helps to maintain the integration of BBB, were also protected by vitamin C treatment
*ZO-1↝,
eff↑, a supra-physiological dose of intravenous vitamin C, with its excellent safety profile and low cost, warrants further evaluation as an adjuvant agent with intravenous thrombolysis or endovascular thrombectomy in the early treatment of acute ischemic

3128- VitC,    Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Community-Acquired Pneumonia and LPS-Induced Macrophages
- in-vitro, Nor, NA
*ROS↓, Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells.
*DNAdam↓,
*TNF-α↓,
*IL6↓,
*p38↓,

3127- VitC,    Vitamin C inhibits the activation of the NLRP3 inflammasome by scavenging mitochondrial ROS
- in-vitro, Nor, NA - in-vivo, Nor, NA
*NLRP3↓, Here we report that vitamin C has an inhibitory effect on the activation of the NLRP3 inflammasome in vitro and in vivo.
*AIM2↓, Vitamin C also inhibits AIM2 and NLRC4 inflammasomes
*mt-ROS↓, Vitamin C inhibits mitochondrial ROS production
*IL1β↓, Vitamin C inhibits LPS -induced IL-1β production in vivo

3126- VitC,    Safety of High-Dose Vitamin C in Non-Intensive Care Hospitalized Patients with COVID-19: An Open-Label Clinical Study
- Study, NA, NA
*NLRP3↓, ascorbic acid may directly inhibit the NLRP3 inflammasome.
*ROS↓, Ascorbic acid, with its potent antioxidant properties, can scavenge R.O.S., thereby reducing oxidative stress
*antiOx↑,

3125- VitC,    Vitamin C inhibits NLRP3 inflammasome activation and delays the development of age-related hearing loss in male C57BL/6 mice
- in-vivo, Nor, NA
*Hear↑, The results showed that vitamin C treatment improved hearing, reduced the production of inflammatory factors, inhibited NLRP3 inflammasome activation
*Inflam↓,
*NLRP3↓,

3124- VitC,    Ascorbic acid improves parthenogenetic embryo development through TET proteins in mice
- in-vivo, Nor, NA
TET2↑, Our results revealed that Vc stimulated the expression of TET proteins in PA embryos.
TET1↑,
TET3↑, present study suggest that up-regulated expression of TET proteins improves PA embryo development by increasing 5hmC levels.

3123- VitC,    Ascorbic Acid Enhances Tet-Mediated 5-Methylcytosine Oxidation and Promotes DNA Demethylation in Mammals
- in-vitro, Nor, mESC
*TET2↑, Here, we demonstrate that a vital nutrient ascorbic acid (AA), or vitamin C (Vc), can directly enhance the catalytic activity of Tet dioxygenases for the oxidation of 5-methylcytosine (5mC)
other↝, In mouse embryonic stem cells, AA significantly increases the levels of all 5mC oxidation products, particularly 5-formylcytosine and 5-carboxylcytosine (by more than an order of magnitude), leading to a global loss of 5mC (∼40%).

608- VitC,    The Levels of Ascorbic Acid in Blood and Mononuclear Blood Cells After Oral Liposome-Encapsulated and Oral Non-Encapsulated Vitamin C Supplementation, Taken Without and with IV Hydrocortisone
other↑, IV hydrocortisone when administered at the time of supplementation by the oral form of vitamin C can increase the transport of ascorbate into white blood cells
other↑, a difference was found in the retention time of the ascorbate in blood with liposomal formulation retention longer

621- VitC,    Sixteen-Year History with High Dose Intravenous Vitamin C Treatment for Various Types of Cancer and Other Diseases
ChemoSideEff∅, no kidney stones

620- VitC,    Case Study: High-Dose Intravenous Vitamin C in the Treatment of a Patient with Adenocarcinoma of the Kidney
- Case Report, NA, NA
OS↑,

619- VitC,    Natural resistance to ascorbic acid induced oxidative stress is mainly mediated by catalase activity in human cancer cells and catalase-silencing sensitizes to oxidative stress
Catalase↝, correlation between catalase activity and the susceptibility to ascorbic acid was observed. Silenced catalase expression increased the susceptibility of the formerly resistant cancer cell line BT-20 to oxidative stress.

618- VitC,    Low levels of catalase enzyme make cancer cells vulnerable to high-dose ascorbate
Catalase↓, results suggest that cancers with low levels of catalase are likely to be the most responsive to high-dose vitamin C therapy, whereas cancers with relatively high levels of catalase may be the least responsive

617- VitC,  Chemo,    The Use of Vitamin C with Chemotherapy in Cancer Treatment: An Annotated Bibliography
- Review, NA, NA
TumCG↓,
ChemoSideEff↓,

616- VitC,    Suppression of alkaline phosphatase in prostate cancer patients by high dose intravenous Vitamin C Treatment: Three cases
- Case Report, NA, NA
PSA↓,
ALP↓,

615- VitC,    High Dose IV Vitamin C and Metastatic Breast Cancer: A Case Report
- Case Report, NA, NA
OS↑, patient showed improvement after receiving high dose IV vitamin C infusions for three months by decreasing tumor marker levels Alkaline Phosphatase (ALP)
Remission↑, remission acheived, still alive

614- VitC,    Vitamin C Pharmacokinetics: Implications for Oral and Intravenous Use
other↑, intravenous administration were 140-fold higher than those from maximum oral doses

613- VitC,    High-dose Vitamin C (Ascorbic Acid) Therapy in the Treatment of Patients with Advanced Cancer
- Review, NA, NA
H2O2↑,

612- VitC,  VitK3,    Effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) treatment on human tumor cell growth in vitro. I. Synergism of combined vitamin C and K3 action
H2O2↑,

611- VitC,    Characterization of a new malignant human T-cell line (PFI-285) sensitive to ascorbic acid
- in-vitro, NA, NA
TumCD↑, Concentrations down to 50 mumol/l killed the cells within hours.

610- VitC,    Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a pro-drug to deliver hydrogen peroxide to tissues
- in-vitro, lymphoma, JPL119 - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, HS587T - in-vitro, Nor, NA
Apoptosis↑, ascorbic acid selectively killed cancer but not normal cells, using concentrations that could only be achieved by i.v. administration
necrosis↑,
H2O2↑,
*toxicity↓, pharmacologic concentrations of ascorbate killed cancer but not normal cells All tested normal cells were insensitive to 20 mM ascorbate.

609- VitC,  ALA,  VitK3,  Se,    Vitamin C and Cancer: Is There A Use For Oral Vitamin C?
OS↑,

622- VitC,    Treatment of Pancreatic Cancer with Pharmacological Ascorbate
- vitro+vivo, PC, NA
H2O2↑,

607- VitC,    Intravenously administered vitamin C as cancer therapy: three cases
- Case Report, NA, NA
necrosis↑,
OS↑, long clinical remissions

606- VitC,    Understanding the Therapeutic Potential of Ascorbic Acid in the Battle to Overcome Cancer
- Review, NA, NA
ROS↑, millimolar (mM) concentrations, also functions as a pro-oxidant
H2O2↑,
Fenton↑, elevated copper concentrations ... made cancer cells vulnerable to the ROS-generated selective cytotoxicity of copper and ascorbic acid

605- VitC,    Therapeutic Use of Vitamin C in Cancer: Physiological Considerations
- Review, NA, NA
ROS↑,
ChemoSideEff↓,

600- VitC,  VitK3,    Serum markers variation consistent with autoschizis induced by ascorbic acid-menadione in patients with prostate cancer
- in-vitro, NA, NA
autoS↑,
TumCD↑,

599- VitC,    Generation of Hydrogen Peroxide in Cancer Cells: Advancing Therapeutic Approaches for Cancer Treatment
- Review, NA, NA
H2O2↑,
DNAdam↑,
ROS↑,
Fenton↑,
Apoptosis↑, Moderate concentrations of H2O2 typically induce apoptosis
necrosis↑, higher H2O2 concentrations induce necrosis

598- VitC,    Ascorbic Acid in Cancer Treatment: Let the Phoenix Fly
- Review, NA, NA
H2O2↑,
ROS↑,
TET1↑, DNA demethylation mediated by ten-eleven translocation enzyme activation
DNAdam↑,
G6PD∅, **** patients who receive intravenous ascorbate must be prescreened for glucose 6 phosphate dehydrogenase deficiency

597- VitC,  STF,  GlucDep,    The Result of Vitamin C Treatment of Patients with Cancer: Conditions Influencing the Effectiveness
other↝, action as an electron donor
H2O2↑, ascorbate readily undergoes pH-dependent autoxidation creating hydrogen peroxide (H2O2).
ROS↑, high concentration is pro-oxidant (IV 25–30 mmol/L are safely achieved)

596- VitC,    High-Dose Vitamin C in Advanced-Stage Cancer Patients
- Review, NA, NA
ChemoSideEff↓, reducing cancer-related symptoms, such as fatigue and bone pain
ROS↑, is able to reduce catalytic metals such as Fe3+ to Fe2+ and Cu2+ to Cu+, increasing the pro-oxidant chemistry of these metals and facilitating the generation of reactive oxygen species
H2O2↑, Reactions of ascorbate with oxygen or with free transition metal ions lead to the generation of superoxide, H2O2 and highly reactive oxidants, such as the hydroxyl radical by promoting the Fenton chemistry
Fenton↑,
Hif1a↝, Ascorbate regulates the transcription of hypoxia inducible factor-1α (HIF-1α)
Dose↑, Results obtained from in vitro studies revealed that millimolar ascorbate plasma concentrations, achievable only after intravenous vitamin C administration, are cytotoxic to fast-growing malignant cells.
BioAv↓, For this reason, ascorbate concentration in plasma does not exceed 100 μmol/L when it is supplied orally with food; even with oral supplementation approaching maximum tolerated doses, it is always <250 μmol/L
Dose↝, 100 mg, the concentration of ascorbate in daily fasting plasma reaches a plateau between 50–60 µmol/L [24]. Whereas increasing the daily dose ten times to 1000 mg gives only a slight increase in plasma concentration to 70–85 μmol/L
Half-Life↝, high concentrations are relatively transient due to the rapid clearance by the kidneys resulting in a half-life of about 2 h in circulation
IL1β↓, IVC (15–50 g up to three times a week) resulted in reduced CRP levels (in 76 ± 13% of study participants) and reduced concentration of pro-inflammatory cytokines (IL-1α, IL-1β, IL-2, IL-8, tumor necrosis factor TNF-α)
IL2↓,
IL8↓,
TNF-α↓,

593- VitC,  MF,    Protective Effect of Ascorbic Acid on Molecular Behavior Changes of Hemoglobin Induced by Magnetic Field Induced by Magnetic Field
RPM↓, Ascorbic acid adds protective effect from magnetic fields

588- VitC,  MF,    Preparation of magnetic nanoparticle integrated nanostructured lipid carriers for controlled delivery of ascorbyl palmitate
other↑, AA, as an antitumor agent

580- VitC,  MF,    Extremely low frequency magnetic field induces oxidative stress in mouse cerebellum
- in-vivo, Nor, NA
*other↓, ascorbic acid levels were significantly decreased by ELF-MF exposure
*MDA↓, significant increase in malondialdehyde level
*GPx∅, increase in superoxide dismutase without alteration in glutathione peroxidase activity
*SOD↑, SOD activity was significantly increased in mouse cerebellum
*GSH∅, GSH contents were not significantly different from sham controls,

579- VitC,  MF,    Effect of Magnetic Field on Ascorbic Acid Oxidase Activity, I
- in-vitro, NA, NA
other↝, significant influence on the activity of the enzyme ascorbic acid oxidase

300- VitC,  ALA,    Combination of High-Dose Parenteral Ascorbate (Vitamin C) and Alpha-Lipoic Acid Failed to Enhance Tumor-Inhibitory Effect But Increased Toxicity in Preclinical Cancer Models
- in-vitro, BC, MDA-MB-231 - in-vitro, Colon, HCT116 - in-vitro, Ovarian, PANC1 - in-vitro, Pca, PC3
TumCG∅,

623- VitC,    The Involvement of Ascorbic Acid in Cancer Treatment
- Review, NA, NA
ROS↑,
GLUT1↓, VC may impede glucose transport and adenosine triphosphate (ATP) production
ATP↓,

1836- VitC,  VitK3,  Chemo,    Vitamins C and K3: A Powerful Redox System for Sensitizing Leukemia Lymphocytes to Everolimus and Barasertib
- in-vitro, AML, NA
tumCV↓, Combined administration of 300 μM vitamin C plus 3 μM pro-vitamin K3 reduced the viability of leukemia lymphocytes by ~20%,
selectivity↑, but did not influence the viability of normal lymphocytes
Apoptosis↑, strong induction of apoptosis
eff↑, Leukemia lymphocytes were more sensitive to combined administration of anticancer drug (everolimus or barasertib) plus vitamins C and K3, compared to normal lymphocytes.
ChemoSen↑, combination of vitamin C plus K3 seems to be a powerful redox system that could specifically influence redox homeostasis of leukemia cells and sensitize them to conventional chemotherapy.

1819- VitC,  VitK3,    The association of vitamins C and K3 kills cancer cells mainly by autoschizis, a novel form of cell death. Basis for their potential use as coadjuvants in anticancer therapy
- Review, Var, NA
Dose?, coadministration of these vitamins (in a ratio of 100:1, for C and K(3), respectively) produced selective cancer cell death.
TumCD↑,
selectivity↑,
H2O2↑, formation of H(2)O(2) during vitamins redox cycling, oxidative stress, DNA fragmentation
ROS↑,
DNAdam↑,

1220- VitC,  VitB1/Thiamine,    The Effect of Thiamine, Ascorbic Acid, and the Combination of Them on the Levels of Matrix Metalloproteinase-9 (MMP-9) and Tissue Inhibitor of Matrix Metalloproteinase-1 (TIMP-1) in Sepsis Patients
- Trial, Sepsis, NA
MMP9:TIMP1↑, highest MMP-9/TIMP-1 ratio was in septic patients receiving thiamine
Sepsis↓, The benefits of ascorbic acid and thiamine in sepsis management have been widely studied.

1219- VitC,    Ascorbic acid and ascorbate-2-phosphate decrease HIF activity and malignant properties of human melanoma cells
- in-vitro, Melanoma, NA
Hif1a↓,

1218- VitC,  ASA,    Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production
- in-vitro, GBM, SK-N-SH
PGE2↓,
COX2↓, owing to its antioxidant properties

1217- VitC,    High-dose vitamin C suppresses the invasion and metastasis of breast cancer cells via inhibiting epithelial-mesenchymal transition
- in-vitro, BC, Bcap37 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
TumCMig↓, only for 2mM otherwise it promoted migration
E-cadherin↑, high dose
Vim↓, high dose
EMT↓, high dose

1216- VitC,    Ascorbic acid induces ferroptosis via STAT3/GPX4 signaling in oropharyngeal cancer
- in-vitro, Laryn, FaDu - in-vitro, SCC, SCC-154
Iron↝, impairing iron metabolism
ROS↑,
tumCV↓,
Ki-67↓,
TumCCA↑, accumulation in the G0/G1 phase
Ferroptosis↑,
GSH↓,
ROS↑,
MDA↑,
STAT3↓,
GPx4↓,
p‑STAT3↓,

1215- VitC,  immuno,    Metabolomics reveals ascorbic acid inhibits ferroptosis in hepatocytes and boosts the effectiveness of anti-PD1 immunotherapy in hepatocellular carcinoma
- ex-vivo, HCC, NA - in-vivo, HCC, NA
other↓, AA in vivo experiments demonstrated a reduction in liver injury in mice
*GPx4↑,
*GSH↑,
GPx4↓,
GSH↓,
selectivity↑, Based on different the and gpx4 response for normal vs cancer cells

1067- VitC,    Vitamin C activates pyruvate dehydrogenase (PDH) targeting the mitochondrial tricarboxylic acid (TCA) cycle in hypoxic KRAS mutant colon cancer
- in-vivo, CRC, NA
PDK1↓,
Hif1a↓,
GLUT1↓,
ATP↓, Vitamin C induced remarkable ATP depletion
MMP↓,

636- VitC,    Acute Effects of Vitamin C Exposure On Colonic Crypts: Direct Modulation of pH Regulation
- in-vivo, NA, NA
pH↓, Acute addition of Vitamin C to the basolateral membrane maintains low intracellular pH for a longer period which could halt and/or prevent tumor formation.
SVCT-2∅, Vitamin C could potentially be transported via SVCT2

635- VitC,  VitK3,    The combination of ascorbate and menadione causes cancer cell death by oxidative stress and replicative stress
- in-vitro, NA, NA
RNR↓, VC/VK3 inhibited RNR mainly by targeting its R2 subunit
GSH↓,
Trx1↓, increased highly oxidized Trx1 (oxidized (and generally less active) means effectively less)
GPx↓, VC/VK3 inhibited glutathione peroxidase activity and led to an elevated level of lipid peroxidation, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway.
lipid-P↑,
AIF↑, which triggered apoptosis-inducing factor (AIF) mediated cell death pathway
ROS↑,

634- VitC,    Intravenous ascorbic acid to prevent and treat cancer-associated sepsis?
- Analysis, NA, NA
other↓, AA may be highly beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRS) and multi organ failure (MOF), has been largely overlooked
iNOS↓,
eNOS↑, AA administration decreases iNOS in the context of inflammation [101,102], but appears to increase eNOS

633- VitC,    Diverse antitumor effects of ascorbic acid on cancer cells and the tumor microenvironment
- Analysis, NA, NA
Fenton↑,
ROS↑,
EMT↓, Ascorbic acid is also known to inhibit EMT of tumor cells
DNAdam↑,
PARP↑, DNA damage increases PARP activity, thereby decreasing NAD+ levels
NAD↓, NAD+
ATP↓,
Apoptosis↑,

632- VitC,    High-Dose Vitamin C: Preclinical Evidence for Tailoring Treatment in Cancer Patients
- Review, NA, NA
SVCT-2∅, vitamin C entry into cells is tightly regulated by SVCT
ROS↑, well-recognized pro-oxidant effects
Hif1a↓, HIF-1α proteasomal degradation
PARP∅, Moreover, vitamin C action at DNA levels may provide the rationale basis for combination therapies with PARP inhibitors and hypomethylating agents.
TET2↑, However, the ability of vitamin C to restore TET2 activity seems to depend on N- and C-terminal lysine acetylation and type of TET2 mutations

631- VitC,    Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2
- vitro+vivo, Liver, NA
SVCT-2∅, response to VC was correlated with sodium-dependent vitamin C transporter 2 (SVCT-2) expressions. Most importantly, SVCT-2 was highly expressed in liver CSCs
ROS↑,
DNAdam↑,
ATP↓,
TumCCA↑,
Apoptosis↑,
OS↑, VC use was linked to improved disease-free survival (DFS) in HCC patients
CD133↓, CD133+
EpCAM↓, EpCAM+
OV6↓, OV6+
γH2AX↑, p-H2AX induced by VC

630- VitC,    Metabolomic alterations in human cancer cells by vitamin C-induced oxidative stress
- in-vitro, BC, MCF-7 - in-vitro, BC, HT-29
TCA↑,
ATP↓,
NAD↓, vitamin C caused cell death through NAD depletion in MCF7 and HT29 cells
H2O2↑,
GSH/GSSG↓,

629- VitC,  Cu,  Fe,    The antioxidant ascorbic acid mobilizes nuclear copper leading to a prooxidant breakage of cellular DNA: implications for chemotherapeutic action against cancer
- in-vitro, NA, NA
ROS↑,
DNAdam↑,
NAD↓,

628- VitC,  Mg,    Enhanced Anticancer Effect of Adding Magnesium to Vitamin C Therapy: Inhibition of Hormetic Response by SVCT-2 Activation
- in-vivo, Colon, CT26 - in-vitro, NA, MCF-7 - in-vitro, NA, SkBr3
AntiCan↑, combined vit c and Mg
SVCT-2↝, Cancer cells that showed high SVCT-2 expression levels were more sensitive to AA treatment (SVCT-2 expression was not changed)
TumCD↑, MgSO4 and MgCl2 significantly increased the cell deaths caused by vitamin C treatment
ROS↑,
P21↑,
proCasp3↑,
TumVol↓, cotreating with vitamin C and magnesium ions inhibited tumor growth more effectively than treating with only vitamin C (mouse)
DNAdam↑,
NAD↓,

627- VitC,    High-Dose Vitamin C for Cancer Therapy
- Review, NA, NA
ROS↑,
PARP↑, ROS activates poly (ADP-ribose) polymerase (PARP), which depletes NAD+
GAPDH↓, Hindering GAPDH can result in an “energy crisis”, due to the decrease in ATP production
DNAdam↑,
ATP↓,

626- VitC,    Systematic Review of Intravenous Ascorbate in Cancer Clinical Trials
- Review, NA, NA
OS↑, 8.75 month increase in progression-free survival (PFS) and an improved trend in overall survival (OS) in the vitamin C treated arm
H2O2↑,

625- VitC,    The Effect of Vitamin C (Ascorbic Acid) in the Treatment of Patients with Cancer: A Systematic Review
OS↑, In 7 studies, the researchers found a positive effect of vitamin C on survival time
Pain↓, 15 patients with bone metastasis IVC had a positive effect on relief of pain
NA↓,

624- VitC,    Ascorbic Acid in Colon Cancer: From the Basic to the Clinical Applications
- Review, NA, NA
OS↑,

2278- VitK2,  VitK3,  VitC,    Vitamin K: Redox-modulation, prevention of mitochondrial dysfunction and anticancer effect
- Review, Var, NA
ChemoSen↑, The analyzed data suggest that vitamin C&K can sensitize cancer cells to conventional chemotherapy, which allows achievement of a lower effective dose of the drug and minimizing the harmful side-effects.
ROS↑, modulation of redox-balance and induction of oxidative stress in cancer cells due to quinone structure of vitamin K.
eff↑, Vitamin C plus K3: A powerful redox-system to sensitize cancer cells towards chemotherapeutics

1828- VitK3,  VitC,    Pankiller effect of prolonged exposure to menadione on glioma cells: potentiation by vitamin C
- in-vivo, GBM, NA
eff↑, menadione:vitamin C at a ratio 1:100 showed higher anti-proliferative activity when compared to each drug alone and allowed to reduce each drug concentration between 2.5 to 5-fold.
ROS↑, cytotoxic effect of menadione is related to the generation of reactive oxygen species
Dose∅, When used in combination at relatively low doses (M:VC at 10 μM:1 mM) for one week M:VC was able to prevent regrowth

1832- VitK3,  VitC,    Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism
- in-vitro, AML, K562
ROS↑, vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress
H2O2↑, hydrogen peroxide generation,
NF-kB↑, activation of NF-κB,
P53↑, p53, c-Jun, protease caspase-3 activation
cJun↑,
Casp3↑,
MMP↓, mitochondria depolarization leading to nuclei fragmentation
DNAdam↑,
Dose?, Jurkat and K562 cells are exposed to VC and VK3 in a ratio 1000:1 (10 mM: 10 μM) or 100:1 (300 μM: 3 μM), respectively

1835- VitK3,  VitC,    Potential therapeutic application of the association of vitamins C and K3 in cancer treatment
- Review, Var, NA
ROS↑, A large body of evidence supports the idea that oxidative stress induced by redox cycling of vitamins C and K(3) in association surpasses cancer cellular defense systems and results in cell death
TumCD↑,
TumCG↓, Combined vitamin C and K(3) administration in vitro and in vivo produced tumor growth inhibition and increased the life-span of tumor-bearing mice.
OS↑,

1837- VitK3,  VitC,    Alpha-Tocopheryl Succinate Inhibits Autophagic Survival of Prostate Cancer Cells Induced by Vitamin K3 and Ascorbate to Trigger Cell Death
- in-vivo, Pca, NA
eff↑, the combination of α-TOS, VK3 and AA was more efficient in tumor suppression than when the drugs were given separately, without deleterious side effects.
ROS↑, The generation of ROS, cellular response to oxidative stress, and autophagy were investigated in PC3 prostate cancer cells by using drugs at sub-toxic doses.
TumAuto↑, ROS can induce autophagy


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 128

Results for Effect on Cancer/Diseased Cells:
ACLY↓,1,   AIF↑,1,   Akt↓,1,   ALP↓,1,   AMPK↑,1,   angioG↓,1,   AntiCan↑,2,   AntiTum↑,1,   Apoptosis↑,8,   ATP↓,9,   autoS↑,1,   BAX↑,1,   BioAv↓,1,   BioAv↑,2,   BNIP3↓,1,   Casp↑,1,   Casp3↑,1,   cl‑Casp3↑,1,   proCasp3↑,1,   cl‑Casp9↑,1,   Catalase↓,1,   Catalase↝,1,   CD133↓,1,   CD4+↑,1,   CD8+↑,1,   CDK2↓,1,   chemoP↑,1,   ChemoSen↑,7,   ChemoSideEff↓,4,   ChemoSideEff∅,1,   CHOP↑,1,   citrate↓,1,   cJun↑,1,   cMyc↓,1,   cognitive↑,1,   COX2↓,2,   CRP↓,1,   CSCs↓,1,   cycD1↓,1,   Cyt‑c↑,1,   DNAdam↑,12,   Dose?,2,   Dose↑,2,   Dose↝,4,   Dose∅,1,   E-cadherin↑,1,   ECAR↓,1,   eff↓,5,   eff↑,27,   eff↝,2,   EMT↓,2,   eNOS↑,1,   EpCAM↓,1,   ER Stress↑,1,   ERK↓,2,   FASN↓,1,   Fenton↑,7,   Ferritin↓,1,   Ferroptosis↑,2,   G6PD∅,1,   GAPDH↓,1,   GlucoseCon↓,1,   GLUT1↓,7,   GLUT1↑,1,   Glycolysis↓,5,   GPx↓,2,   GPx4↓,3,   GRP78/BiP↓,1,   GSH↓,4,   GSH/GSSG↓,1,   GSR↓,1,   H2O2↑,14,   Half-Life↝,1,   HIF-1↓,1,   Hif1a↓,7,   Hif1a↝,1,   HK2↓,2,   HO-1↓,3,   HO-1↑,1,   IFN-γ↓,1,   IGF-1↓,1,   IL1β↓,1,   IL2↓,1,   IL6↓,1,   IL8↓,1,   Inflam↓,1,   iNOS↓,1,   IRE1↑,1,   Iron↑,2,   Iron↝,1,   JNK↑,1,   Ki-67↓,1,   lactateProd↓,2,   LDH↓,2,   LDHA↓,4,   lipid-P↑,1,   MAPK↓,1,   MDA↑,1,   MMP↓,2,   MMP2↓,1,   MMP9:TIMP1↑,1,   MMPs↓,1,   mTOR↓,1,   NA↓,1,   NAD↓,4,   necrosis↑,4,   NF-kB↓,2,   NF-kB↑,2,   NQO1↓,1,   NRF2↓,3,   NRF2↑,1,   NRF2⇅,1,   OS↑,13,   other↓,5,   other↑,5,   other↝,5,   OV6↓,1,   P21↑,1,   P53↑,2,   Pain↓,1,   PARP↓,1,   PARP↑,3,   PARP∅,1,   PD-L1↓,1,   PDH↑,1,   PDK1↓,3,   PFK1↓,1,   PGE2↓,1,   PGK1↓,1,   PGM1↓,1,   pH↓,1,   PI3K↓,1,   PKM2↓,2,   p‑PKM2↓,1,   PSA↓,1,   QoL↑,3,   radioP↑,2,   Remission↑,2,   Risk↓,2,   RNR↓,1,   ROS↓,1,   ROS↑,40,   RPM↓,1,   RPM↑,3,   selectivity↑,7,   Sepsis↓,1,   Smad1↑,1,   SOD↓,1,   STAT3↓,1,   STAT3⇅,1,   p‑STAT3↓,1,   SVCT-2↓,1,   SVCT-2↝,1,   SVCT-2∅,3,   TCA↑,1,   TET1↑,5,   TET2↑,11,   TET3↑,2,   TNF-α↓,1,   TRAIL↑,1,   Trx1↓,1,   TumAuto↑,1,   TumCCA↑,3,   TumCD↑,8,   TumCG↓,10,   TumCG∅,1,   TumCI↓,2,   TumCMig↓,2,   TumCP↓,2,   tumCV↓,4,   TumMeta↓,2,   TumMeta↑,1,   TumVol↓,3,   VEGF↓,2,   Vim↓,1,   Warburg↓,6,   Weight↑,1,   YAP/TEAD↓,1,   γH2AX↑,1,  
Total Targets: 179

Results for Effect on Normal Cells:
AIM2↓,1,   ALAT↓,1,   antiOx↑,7,   AP-1↑,1,   Apoptosis∅,1,   AST↓,1,   ATF6↓,1,   BBB↑,1,   BG↓,1,   Catalase↑,2,   CLDN1↝,1,   CRP↓,1,   DNAdam↓,2,   Dose↝,1,   eIF2α↓,1,   ER Stress↓,4,   ERK↑,1,   glucose↓,1,   GLUT1↓,1,   GPx↑,2,   GPx∅,1,   GPx4↑,1,   GRP78/BiP↓,3,   GSH↑,1,   GSH∅,1,   Hear↑,1,   hepatoP↑,1,   IL12↑,1,   IL1β↓,2,   IL2↑,1,   IL6↓,2,   IL6↑,1,   Inflam↓,5,   LDH∅,1,   MAPK↑,1,   MDA↓,1,   MDA∅,1,   MMP↑,1,   MMP2↓,2,   MMP9↓,2,   MMPs↓,1,   neuroP↑,1,   NF-kB↓,1,   NLRP3↓,3,   NRF2↑,2,   Obesity↓,1,   OS↑,1,   other↓,1,   p38↓,1,   p38↑,1,   pH↝,1,   radioP↑,1,   RNS↓,1,   ROS↓,12,   mt-ROS↓,1,   SOD↓,1,   SOD↑,3,   SVCT-2↑,1,   TET2↑,1,   TIMP1↓,1,   TIMP2↑,1,   TNF-α↓,3,   toxicity↓,1,   TumCG∅,1,   VitD↑,1,   XBP-1↓,1,   ZO-1↝,1,  
Total Targets: 67

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:166  Target#:%  State#:%  Dir#:%
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