Dose Cancer Research Results
Dose, Dosage: Click to Expand ⟱
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Drug dosage vs efficacy, and actual dosage number of research papers.
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Scientific Papers found: Click to Expand⟱
*toxicity↑, A 44-year-old previously well man ingested ten times the recommended dose of 5-HTP powder. After four hours he developed marked antegrade and retrograde amnesia, disorientation and confusion in the absence of loss of consciousness, seizure activity o
*Dose↑, A previously well 44-year-old male was admitted following inadvertent intake of 800 mg of powdered 5-HTP supplement, instead of the intended 80 mg
*Dose↑, A 3-year-old, male neutered Labrador Retriever, weighing 28.2 kg, presented to the emergency department ... after ingesting a human supplement containing 200 mg of 5-HTP. The amount of 5-HTP ingested was estimated between 980 and 1988mg
*toxicity↝, At presentation, the dog demonstrated progressive neurologic abnormalities consistent with serotonin syndrome, including altered mentation and ataxia.
IL6↓, This gold(I) compound has anti-inflammatory properties because it reduces IL-6 expression via inhibition of the NF-κB-IL-6-STAT3 signaling pathway.
NF-kB↓,
ATF2↓,
TrxR↓, by inhibiting redox enzymes such as thioredoxin reductase, auranofin increases cellular oxidative stress and promotes apoptosis.
ROS↑,
Apoptosis↑,
IL6↓, Recently, it was reported that auranofin reduced by 95% SARS-CoV-2 RNA in infected human cells in vitro and decreased SARS-CoV-2-induced cytokine expression, including IL-6.
Dose↑, After 14 days of treatment with 21 mg/day auranofin, plasma gold concentration reached 1.18 µM to 2.21 µM ‘auranofin equivalent’
*Dose?, Subjects received orally 6 mg (p.o.) of auranofin daily, the recommended dose for rheumatoid arthritis, for 7 days and were followed for 126 days.
*Half-Life↝, The mean gold maximum concentration in plasma (Cmax) at day 7 was 0.312 μg/ml and the half-life (t1/2) 35 days, so steady-state blood levels would not be reached in short-term therapy.
*Dose↑, The highest concentration of gold, 13 μM (auranofin equivalent), or more than 25× the 50% inhibitory concentration (IC50) for E. histolytica and 4× that for Giardia, was in feces at 7 days.
*toxicity↝, Long-term (months to years) auranofin therapy was linked to side effects, including diarrhea (40% of subjects), skin rashes (2% to 5%), hematologic abnormalities (rare), and proteinuria (5%)
*Bacteria↓, Higher doses of auranofin will clearly be required for some infections.
*Dose↑, The FDA has approved clinical trials using auranofin at up to 21 mg/day for treatment of relapsed chronic lymphocytic leukemia after daily doses of 9 and 12 mg for at least 28 days were well tolerated
*Half-Life↝, Fecal silver began to decline at 12 h for all the AgNPs and was at baseline levels by 48 h.
*toxicity↓, Acute ingestion of AgNP is well-tolerated at high doses, irrespective of size or coating
*Dose↑, The doses utilized in this study (0.1, 1 and 10 mg/kg bw/d) were equivalent to, respectively, 20×, 200× and 2000× the EPA oral reference dose (RfD, 0.005 mg/kg bw/d) for silver
*other↝, Previous estimates of colloidal silver doses associated with clinically evident argyria range between 40× and 700× the oral RfD, although these typically represent repeated exposures
*eff↝, Acute ingestion of AgNP is well-tolerated with concurrent antibiotic administration
*BioAv↓, Oral bioavailability was previously determined as low (4.2%) for a single 10 mg/kg bw dose of 7.9 nm AgNP-citrate in rats
mt-ROS↑, mitochondria are the primary source of ROS production induced by LA and that these ROS are involved in
the apoptotic process.
Apoptosis↑,
Casp9↑,
Bcl-2↓,
eff↓, that all the tested antioxidants were able to inhibit apoptosis induced by LA or DHLA indicating that multiple ROS are involved in the apoptotic process.
eff↑, The pro-oxidant role of LA is generally observed under nonoxidative stress conditions, which is also supported by this study
H2O2↑, LA also induced peroxide generation in these cells
Dose↑, 100uM was enough to generate mitochondrial ROS in lung cancer cells
*CRP↓, Following Amla supplementation, pooled results showed a significant reduction in CRP (p = 0.002), fasting blood glucose (FBG) (p < 0.001), low-density lipoprotein cholesterol (LDL-c) (p < 0.001),
*glucose↓,
*LDL↓,
Dose↑, More over, the supplement was more effective in doses of 1 g/d
chemoP↑, Our comprehensive data suggests that antioxidant has superior potential of ameliorating chemotherapeutic induced toxicity
ChemoSen↑, Antioxidant supplementation during chemotherapy also promises higher therapeutic efficiency and increased survival times in patients
OS↑,
Dose↑, On the contrary, many integrative practitioner converse uses of antioxidant supplements allowing patients to tolerate possibly higher effective doses of chemotherapy
Risk↓, Among antioxidant users, frequent use of vitamin C and vitamin E was associated with decreased risk of BC recurrence, vitamin E use was associated with decreased risk of all cause mortality
eff↓, but conversely, frequent use of combination carotenoids was associated with increased risk of death from breast cancer and all cause mortality
*Inflam↓, anti-inflammatory, anticarcinogenic, and free radical-scavenging activities.
*ROS↓,
*Aβ↓, Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but the mechanism was unclear. I
*memory↑, involving improvement of the learning and memory capabilities,
*AChE↓, improvement of cholinergic system involving the inhibition of AChE activity and elevation of ACh level, and modification of BNDF, TrkB, and phospho-CREB levels.
*Ach↑,
*Dose↑, Apigenin, at doses of 10 mg/kg and 20 mg/kg, promoted learning and memory
*BDNF↑, apigenin also increased BDNF level and up-regulated its receptor TrkB and pCREB in A25-35 -induced amnesic mice.
*TrkB↑,
*p‑CREB↑,
*BBB↑, Additionally, we found that treatment with apigenin was effective in preserving anatomical and functional integrity of the BBB per-
meability.
*Ca+2?, A relevant effect of apigenin by suppressing the Ca 2+ influx through both voltage- and receptor-operated calcium channels
might be attributed to the changes of rCBF
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology
*p‑PPARγ↓, preventing the phosphorylation of peroxisome proliferator-activated receptors (PPARγ)
*cardioP↑, cardioprotective activity by AMP-activated protein kinase (AMPK) activation and suppressing mitochondrial apoptosis.
*AMPK↑,
*BioAv↝, The oral bioavailability was found to be 32.4 ± 4.8% after 5 mg/kg intravenous and 10 mg/kg oral WA administration.
*Half-Life↝, The stability studies of WA in gastric fluid, liver microsomes, and intestinal microflora solution showed similar results in male rats and humans with a half-life of 5.6 min.
*Half-Life↝, WA reduced quickly, and 27.1% left within 1 h
*Dose↑, WA showed that formulation at dose 4800 mg having equivalent to 216 mg of WA, was tolerated well without showing any dose-limiting toxicity.
*chemoPv↑, Here, we discuss the chemo-preventive effects of WA on multiple organs.
IL6↓, attenuates IL-6 in inducible (MCF-7 and MDA-MB-231)
STAT3↓, WA displayed downregulation of STAT3 transcriptional activity
ROS↓, associated with reactive oxygen species (ROS) generation, resulted in apoptosis of cells. The WA treatment decreases the oxidative phosphorylation
OXPHOS↓,
PCNA↓, uppresses human breast cells’ proliferation by decreasing the proliferating cell nuclear antigen (PCNA) expression
LDH↓, WA treatment decreases the lactate dehydrogenase (LDH) expression, increases AMP protein kinase activation, and reduces adenosine triphosphate
AMPK↑,
TumCCA↑, (SKOV3 andCaOV3), WA arrest the G2/M phase cell cycle
NOTCH3↓, It downregulated the Notch-3/Akt/Bcl-2 signaling mediated cell survival, thereby causing caspase-3 stimulation, which induces apoptosis.
Akt↓,
Bcl-2↓,
Casp3↑,
Apoptosis↑,
eff↑, Withaferin-A, combined with doxorubicin, and cisplatin at suboptimal dose generates ROS and causes cell death
NF-kB↓, reduces the cytosolic and nuclear levels of NF-κB-related phospho-p65 cytokines in xenografted tumors
CSCs↓, WA can be used as a pharmaceutical agent that effectively kills cancer stem cells (CSCs).
HSP90↓, WA inhibit Hsp90 chaperone activity, disrupting Hsp90 client proteins, thus showing antiproliferative effects
PI3K↓, WA inhibited PI3K/AKT pathway.
FOXO3↑, Par-4 and FOXO3A proapoptotic proteins were increased in Pten-KO mice supplemented with WA.
β-catenin/ZEB1↓, decreased pAKT expression and the β-catenin and N-cadherin epithelial-to-mesenchymal transition markers in WA-treated tumors control
N-cadherin↓,
EMT↓,
FASN↓, WA intraperitoneal administration (0.1 mg) resulted in significant suppression of circulatory free fatty acid and fatty acid synthase expression, ATP citrate lyase,
ACLY↓,
ROS↑, WA generates ROS followed by the activation of Nrf2, HO-1, NQO1 pathways, and upregulating the expression of the c-Jun-N-terminal kinase (JNK)
NRF2↑,
HO-1↑,
NQO1↑,
JNK↑,
mTOR↓, suppressing the mTOR/STAT3 pathway
neuroP↑, neuroprotective ability of WA (50 mg/kg b.w)
*TNF-α↓, WA attenuate the levels of neuroinflammatory mediators (TNF-α, IL-1β, and IL-6)
*IL1β↓,
*IL6↓,
*IL8↓, WA decreases the pro-inflammatory cytokines (IL-6, TNFα, IL-8, IL-18)
*IL18↓,
RadioS↑, radiosensitizing combination effect of WA and hyperthermia (HT) or radiotherapy (RT)
eff↑, WA and cisplatin at suboptimal dose generates ROS and causes cell death [41]. The actions of this combination is attributed by eradicating cells, revealing markers of cancer stem cells like CD34, CD44, Oct4, CD24, and CD117
Dose↑, However, most in vitro and in vivo studies have used ASX at concentrations that are not achievable by humans.
*BioAv↝, consuming a single dose of 40 mg ASX, the plasma ASX concentration of 32 male subjects (average body weight: 81.5 kg) increased to ∼190 μg/L
*BioAv↝, 100 mg ASX supplementation in male volunteers (90–100 kg BW) resulted in circulating concentrations of ASX reaching a maximum of 120 μg/L (21). This is equivalent to 0.4 μΜ ASX treatment in the cells with 2 mL media
*antiOx↑, Because the potent antioxidative efficacy of ASX has attracted growing interest and attention in recent years, much evidence has accumulated with regard to ASX treatment in alleviating lung diseases.
*NRF2↑, ASX exerts its antioxidative effects by activating the Nrf2 –antioxidant response element (ARE) signaling pathway
*ERK↓, In mice, ASX showed substantial efficacy in inhibiting ERK1/2 activation in the chronic lung inflammation model (100 mg/kg BW ASX), as well as the ALI model (5 mg/kg BW ASX)
Risk↓, increasing amount of data, from preclinical and epidemiological studies, that support an inverse association between the use of statins, potent inhibitors of MVA biosynthetic pathway, and mortality rate in specific cancers
Dose↑, cancer treatment demands the use of relatively high doses of single statins for a prolonged period, thereby limiting this therapeutic strategy due to adverse effects.
ChemoSen↑, synergistic effects of tolerable doses of statins with conventional chemotherapy might enhance efficacy with lower doses of each drug and, probably, reduce adverse effects and resistance.
chemoP↑,
HMG-CoA↓, potential use of MVA pathway inhibitors to improve therapeutic window in cancer.
EMT↓, statins may suppress epithelial-mesenchymal transition (EMT) program together with the inhibition of cancer stem cell generation, maintenance, and expansion
CSCs↓,
HH↝, inhibitors of MVA pathway (e.g., statins) that modulate Hh pathway activity could represent potential drugs in Hh pathway-related cancers.
YAP/TEAD↝, MVA participates in the regulation of YAP-TAZ expression and transcriptional activity and reveal an original process through which statins have anticancer effects.
Inflam↓, BBR has documented to have anti-diabetic, anti-inflammatory and anti-microbial (both anti-bacterial and anti-fungal) properties.
IL6↓, BBRs can inhibit IL-6, TNF-alpha, monocyte chemo-attractant protein 1 (MCP1) and COX-2 production and expression.
MCP1/CCL2↓,
COX2/PTGS2↓,
PGE2↓, BBRs can also effect prostaglandin E2 (PGE2)
MMP2↓, and decrease the expression of key genes involved in metastasis including: MMP2 and MMP9.
MMP9↓,
DNAdam↑, BBR induces double strand DNA breaks and has similar effects as ionizing radiation
eff↝, In some cell types, this response has been reported to be TP53-dependent
Telomerase↓, This positively-charged nitrogen may result in the strong complex formations between BBR and nucleic acids and induce telomerase inhibition and topoisomerase poisoning
Bcl-2↓, BBR have been shown to suppress BCL-2 and expression of other genes by interacting with the TATA-binding protein and the TATA-box in certain gene promoter regions
AMPK↑, BBR has been shown in some studies to localize to the mitochondria and inhibit the electron transport chain and activate AMPK.
ROS↑, targeting the activity of mTOR/S6 and the generation of ROS
MMP↓, BBR has been shown to decrease mitochondrial membrane potential and intracellular ATP levels.
ATP↓,
p‑mTORC1↓, BBR induces AMPK activation and inhibits mTORC1 phosphorylation by suppressing phosphorylation of S6K at Thr 389 and S6 at Ser 240/244
p‑S6K↓,
ERK↓, BBR also suppresses ERK activation in MIA-PaCa-2 cells in response to fetal bovine serum, insulin or neurotensin stimulation
PI3K↓, Activation of AMPK is associated with inhibition of the PI3K/PTEN/Akt/mTORC1 and Raf/MEK/ERK pathways which are associated with cellular proliferation.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt. In HCT116 cells, PTEN inhibits Akt signaling and proliferation.
Akt↓,
Raf↓,
MEK↓,
Dose↓, The effects of low doses of BBR (300 nM) on MIA-PaCa-2 cells were determined to be dependent on AMPK as knockdown of the alpha1 and alpha2 catalytic subunits of AMPK prevented the inhibitory effects of BBR on mTORC1 and ERK activities and DNA synthes
Dose↑, In contrast, higher doses of BBR inhibited mTORC1 and ERK activities and DNA synthesis by AMPK-independent mechanisms [223,224].
selectivity↑, BBR has been shown to have minimal effects on “normal cells” but has anti-proliferative effects on cancer cells (e.g., breast, liver, CRC cells) [225–227].
TumCCA↑, BBR induces G1 phase arrest in pancreatic cancer cells, while other drugs such as gemcitabine induce S-phase arrest
eff↑, BBR was determined to enhance the effects of epirubicin (EPI) on T24 bladder cancer cells
EGFR↓, In some glioblastoma cells, BBR has been shown to inhibit EGFR signaling by suppression of the Raf/MEK/ERK pathway but not AKT signaling
Glycolysis↓, accompanied by impaired glycolytic capacity.
Dose?, The IC50 for BBR was determined to be 134 micrograms/ml.
p27/CDKN1B↑, Increased p27Kip1 and decreased CDK2, CDK4, Cyclin D and Cyclin E were observed.
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↓,
Bax:Bcl2↑, Increased BAX/BCL2 ratio was observed.
Casp3↑, The mitochondrial membrane potential was disrupted and activated caspase 3 and caspases 9 were observed
Casp9↑,
VEGFR2/KDR/Flk1↓, BBR treatment decreased VEGFR, Akt and ERK1,2 activation and the expression of MMP2 and MMP9 [235].
ChemoSen↑, BBR has been shown to increase the anti-tumor effects of tamoxifen (TAM) in both drug-sensitive MCF-7 and drug-resistant MCF-7/TAM cells.
eff↑, The combination of BBR and CUR has been shown to be effective in suppressing the growth of certain breast cancer cell lines.
eff↑, BBR has been shown to synergize with the HSP-90 inhibitor NVP-AUY922 in inducing death of human CRC.
PGE2↓, BBR inhibits COX2 and PEG2 in CRC.
JAK2↓, BBR prevented the invasion and metastasis of CRC cells via inhibiting the COX2/PGE2 and JAK2/STAT3 signaling pathways.
STAT3↓,
CXCR4↓, BBR has been observed to inhibit the expression of the chemokine receptors (CXCR4 and CCR7) at the mRNA level in esophageal cancer cells.
CCR7↓,
uPA↓, BBR has also been shown to induce plasminogen activator inhibitor-1 (PAI-1) and suppress uPA in HCC cells which suppressed their invasiveness and motility.
CSCs↓, BBR has been shown to inhibit stemness, EMT and induce neuronal differentiation in neuroblastoma cells. BBR inhibited the expression of many genes associated with neuronal differentiation
EMT↓,
Diff↓,
CD133↓, BBR also suppressed the expression of many genes associated with cancer stemness such as beta-catenin, CD133, NESTIN, N-MYC, NOTCH and SOX2
Nestin↓,
n-MYC↓,
NOTCH↓,
SOX2↓,
Hif1a↓, BBR inhibited HIF-1alpha and VEGF expression in prostate cancer cells and increased their radio-sensitivity in in vitro as well as in animal studies [290].
VEGF↓,
RadioS↑,
*BBB↑, A growing body of evidence confirms that the ‘orifice-opening’ effect of borneol is principally derived from opening the BBB. Borneol is therefore believed to be an effective adjuvant that can improve drug delivery to the brain
*other↑, Borneol also protects the structural integrity of the BBB against pathological damage.
*P-gp/ABCB1↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*toxicity⇅, Natural borneol has been extensively used in aromatherapy and in natural and cosmetic products because of its low toxicity compared to synthetic borneol, which toxicity is relatively high as it degrades slowly during storage, and noxious camphor
*BioAv⇅, In mice, a single oral dose of borneol accumulates in organs in the order of liver > brain > kidney > heart > spleen > muscle > lung, which confirms its considerably higher bioavailability in the brain than in most other organs
*Dose↑, Intranasal drug delivery can avoid gastrointestinal destruction and hepatic first-pass metabolism, resulting in rapid onset of effect and high brain bioavailability.
*ABC↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*MRP1/ABCC1↓, including multidrug resistance protein 1 (Mrp1), 1a (Mdr1a) and 1 b (Mdr1b),
*5HT↑, systemic borneol was found to increase the levels of histamine and serotonin in the hypothalamus
*GABA↑, and levels of l-aspartic acid, glutamate, glycine and γ-aminobutyric acid (GABA) in the corpus striatum of rats (Zhang et al., 2012).
*eff↑, Co-incubation with borneol increased the uptake of Huperzine A loaded aprotinin-modified nanoparticles by capillary endothelial cells
*hs-CRP↓, reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor μ (TNF-μ);
*TNF-α↓,
*SOD↑, raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase
*Catalase↑,
*GPx↑,
*cognitive↑, improves the brains electrical activity, cognitive performance, and short-term memory for elders; restricted boron intake adversely affected brain function and cognitive performance.
*memory↑, In humans, boron deprivation (<0.3 mg/d) resulted in poorer performance on tasks of motor speed and dexterity, attention, and short-term memory.
*Risk↓, Boron-rich diets and regions where the soil and water are rich in boron correlate with lower risks of several types of cancer, including prostate, breast, cervical, and lung cancers.
*SAM-e↑,
*NAD↝, Boron strongly binds oxidized NAD+,76 and, thus, might influence reactions in which NAD+ is involved
*ATP↝,
*Ca+2↝, Because of its positive charge, magnesium stabilizes cell membranes, balances the actions of calcium, and functions as a signal transducer
HDAC↓, some boronated compounds are histone deacetylase inhibitors
TumVol↓,
IGF-1↓, expression of IGF-1 in the tumors was significantly reduced by boron treatment
PSA↓, Boronic acid has been shown to inhibit PSA activity.
Cyc↓, boric acid inhibits the growth of prostate-cancer cells both by decreasing expression of A-E cyclin
TumCMig↓,
*serineP↓, Boron exists in the human body mostly in the form of boric acid, a serine protease inhibitor.
HIF-1↓, shown to greatly inhibit hypoxia-inducible factor (HIF) 1
*ChemoSideEff↓, An in vitro study found that boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel
*VitD↑, greater production of 25-hydroxylase, and, thus, greater potential for vitamin-D activation
*Mag↑, Boron significantly improves magnesium absorption and deposition in bone
*eff↑, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Risk↓, risk of prostate cancer was 52% lower in men whose diets supplied more than 1.8 mg/d of boron compared with those whose dietary boron intake was less than or equal to 0.9 mg/d.
*Inflam↓, As research into the chemistry of boron-containing compounds has increased, they have been shown to be potent antiosteoporotic, anti-inflammatory, and antineoplastic agents
*neuroP↑, In addition, boron has anti-inflammatory effects that can help alleviate arthritis and improve brain function and has demonstrated such significant anticancer
*Calcium↑, increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.
*BMD↑, boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency
*chemoP↑, may help ameliorate the adverse effects of traditional chemotherapeutic agents. boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel, an anticancer drug commonly used to treat breast, ovarian
AntiCan↑, demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma
*Dose↑, only an upper intake level (UL) of 20 mg/d for individuals aged ≥ 18 y.
*Dose↝, substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables
*BMPs↑, Boron was also found to increase mRNA expression of alkaline phosphatase and bone morphogenetic proteins (BMPs)
*testos↑, 1 week of boron supplementation of 6 mg/d, a further study by Naghii et al20 of healthy males (n = 8) found (1) a significant increase in free testosterone,
angioG↓, Inhibition of tumor-induced angiogenesis prevents growth of many types of solid tumors and provides a novel approach for cancer treatment; thus, HIF-1 is a target of antineoplastic therapy.
Apoptosis↑, Cancer cells, however, commonly overexpress sugar transporters and/or underexpress borate export, rendering sugar-borate esters as promising chemopreventive agents
*selectivity↑, In normal cells, the 2 latter, cell-destructive effects do not occur because the amount of borate present in a healthy diet, 1 to 10 mg/d, is easily exported from normal cells.
*chemoPv↑, promising chemopreventive agents
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Risk↓, A diet with low B has been found to lead to a number of general health problems and to increase cancer risk.
*memory↑, The most common symptoms of B deficiency include arthritis, memory loss, osteoporosis, degenerative and soft cartilage diseases, hormonal disequilibria and a drop in libido
*Dose↑, The B Tolerable Upper Intake Level (UL) for adults of ~18 years is ~20 mg B per day
Risk↓, Dietary B is inversely correlated with the occurrence of prostate cancer . Diets rich in boron could significantly reduce some cancer types, especially breast, prostate, lung and cervical forms of cancer.
other↝, In Japan, breast cancer is a rare disease compared to the Western countries (Tominaga & Kuroishi, 1999). When Japanese women immigrated to the USA, they acquired the same risk for breast cancer as that in the general population of women in the USA
*testos↑, After one week, supplementation of healthy males with 10 mg B/day resulted in a
significant rise in the plasma free testosterone concentration, which is an observation based
on recent clinical data
other↝, preclinical studies have suggested that testosterone serves as a natural, endogenous protector of the breast.
Risk↓, vitamin D is important as a protective agent against the development of breast cancer
TumCP↓, Boric acid (BA) is one of the most studied B-containing chemicals. BA has been demonstrated to control the proliferation of some cancer cell types
Apoptosis↑, Bortezomib (PS-341) (Teicher et al., 1999) is a boronic acid derivative and a proteasome inhibitor, which is a novel target in cancer therapy. This compound disrupts cell cycle regulation and induces apoptosis.
eff↑, Bortezomib could have a significant anti-tumour activity when it is used in combination with other active conventional agents
*other↝, Men with higher boron intakes (about 6 mg/day) had significantly smaller prostate glands than men who consumed less boron (0.64–0.88 mg/day)
Risk↑, Several observational studies found that boron intakes are inversely associated with prostate cancer risk in men and with lung and cervical cancer risk in women
*Dose↑, Tolerable Upper Intake Levels (ULs) for Boron: 19+ years 20 mg
*memory↑, BA significantly improved learning and memory impairments induced by AlCl3 treatment.
*AChE↓, BA treatment significantly decreased acetylcholinesterase levels and reduced amyloid-beta (Aβ) expression
*Aβ↓,
*TNF-α↓, BA ameliorated the increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), inhibited lipid peroxidation, and increased total antioxidants in the brain.
*IL1β↓,
*lipid-P↓,
*TAC↑,
*BDNF↑, Indeed, BA significantly suppressed AlCl3-induced decrease of brain-derived neurotrophic factor, pGSK-3β (Ser 9), and β-catenin.
*β-catenin/ZEB1↑,
*Dose↑, BA (250 mg/kg) showed a significant protective effect compared to a lower dose.
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1/CCL2↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2/PTGS2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2
pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma
concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer
*glucose↓, OGTT showed that plasma glucose levels in volunteers who received capsicum were significantly lower than those in the placebo group at 30 and 45 minutes
*Insulin↑, Furthermore, plasma insulin levels were significantly higher at 60, 75, 105, and 120 minutes
*Dose↑, 5 grams of capsicum presented capsaicin levels that were associated with a decrease in plasma glucose levels and the maintenance of insulin levels.
*AntiDiabetic↑, The present result might have clinical implications in the management of type 2 diabetes
Dose↑, The maximum-tolerated dose was 4.2 g/m(2) once daily or 1.0 g/m(2) three times daily.
toxicity↝, Oral GTE at the doses studied can be taken safely for at least 6 months.
*Dose↑, In a phase I clinical trial, CHL was well tolerated up to 3000 mg and achieved serum concentrations >5 μM in healthy male volunteers.
*toxicity↓, CHL demonstrates a favorable safety profile, immunomodulatory capacity, and antiviral efficacy, supporting its potential as a broad-spectrum agent for COVID-19 management.
*Imm↑,
*Ach↑, Choline is also the precursor for acetylcholine, a neurotransmitter which activates the alpha7 nicotinic acetylcholine receptor (α7nAchR), and also acts as an agonist for the Sigma‐1 R (σ1R).
*Aβ↓, Lifelong choline supplementation significantly reduced amyloid‐β plaque load and improved spatial memory in APP/PS1 mice.
*memory↑,
*APP↓, Mechanistically, these changes were linked to a decrease of the amyloidogenic processing of APP, reductions in disease‐associated microglial activation, and a downregulation of the α7nAch and σ1 receptors.
*eff↑, Additional dietary choline is a putative treatment option that may prevent AD progression.
*neuroP↑, This suggests that additional choline in diet may be beneficial in preventing neuropathological changes associated with the aging brain.
*Dose↑, The tolerable upper limit (TUL) of choline unlikely to cause side effects for adult females and males (>19 years of age) is 3,500 mg/day, which is 8.24 times higher than the 425 mg/day recommendation for females and 6.36 times higher than the 550 mg/
*Dose↝, The CP recipe includes around fifty (some times more depending on the brand) bioactive herbs (with the major ingredient, Amla or Indian gooseberry) and herbal extracts, which are processed by the traditional Ayurvedic pharmaceutical process, and the
*antiOx↑, Compelling evidences suggest that CP possess rich nutraceutical value along with potential antioxidant, anti-inflammatory, and immunomodulatory properties
*Inflam↓,
*Imm↑, In a clinical study conducted on the 15–75 years age group (with no underlying organic disease), CP was found to reduce the disease symptoms of seasonal influences, improved pulmonary functions, quality of life, and provided 3-times immunity with no
*QoL↑,
*Dose↑, In Ayurvedic Pharmacopoeia of India, the standard dose of CP is mentioned 12 g twice a day
*Dose↝, generally 12–28 g per day, with lukewarm milk or water
TCA↑,
FASN↑, Cytosolic acetyl-CoA sustains fatty acid (FA) synthesis (FAS)
Glycolysis↓,
glucoNG↑, while it enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
PFK1↓, citrate directly inhibits the main regulators of glycolysis, phosphofructokinase-1 (PFK1) and phosphofructokinase-2 (PFK2)
PFK2↓, well-known inhibitor of PFK
FBPase↑, enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
TumCP↓, inhibits the proliferation of various cancer cells of solid tumors (human mesothelioma, gastric and ovarian cancer cells) at high concentrations (10–20 mM),
eff↑, promoting apoptosis and the sensitization of cells to cisplatin
ACLY↓, higher concentrations (10 mM or more) decreased both acetylation and ACLY expression
Dose↑, In various cell lines, a high concentration of citrate—generally above 10 mM—inhibits the proliferation of cancer cells in a dose dependent manner
Casp3↑,
Casp2↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
Mcl-1↓,
IGF-1R↓, citrate at high concentration (10 mM) also inhibits the insulin-like growth factor-1 receptor (IGF-1R)
PI3K↓, pathways
Akt↓, activates PTEN, the key phosphatase inhibiting the PI3K/Akt pathway
mTOR↓,
PTEN↑, high dose of citrate activates PTEN
ChemoSen↑, citrate increases the sensibility of cells to chemotherapy (in particular, cisplatin)
Dose?, oral gavage of citrate sodium (4 g/kg twice a day) for several weeks (4 to 7 weeks) significantly regressed tumors
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*neuroP↑, Curcumin has an outstanding safety profile and a number of pleiotropic actions with potential for neuroprotective efficacy, including anti-inflammatory, antioxidant, and anti-protein-aggregate activities.
*Inflam↓,
*antiOx↑,
*BioAv↓, despite concerns about poor oral bioavailability, curcumin has at least 10 known neuroprotective action
*AP-1↓, Curcumin inhibition of AP-1 and NF-κB-mediated transcription occurs at relatively low (<100 nM) doses and might be due to inhibition of histone acetylase (HAT) or activation of histone deacetylase (HDAC) activity
*NF-kB↓,
*HATs↓,
*HDAC↑,
Dose↑, At high doses (>3 µM) that are relevant to colon cancer but unlikely achievable with oral delivery in plasma and tissues outside of the gut, curcumin can act as an alkylating agent,10 a phase II enzyme inducer,11 and stimulate antioxidant response el
*ROS↓, We also found that curcmin reduced oxidative damage, inflammation, and cognitive deficits in rats receiving CNS infusions of toxic Aβ
*cognitive↑,
*Aβ↓, dose-dependently blocked Aβ aggregation at submicromolar concentrations
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*BioAv↓, limited systemic bioavailability of curcumin has hindered its development as a potential therapeutic agent
*BioAv↑, recent introduction of unique extraction processes and various delivery methods has resulted in the development of new curcumin formulations and significantly improved its bioavailability.
Dose↑, daily consumption of 3.6 g of curcumin resulted in achieving curcumin concentration in the malignant colorectal tissues ranging from 7 to 20 nmol/g.
*Dose↝, pharmacokinetics of curcumin show that only 0.13–1.35 µg/mL concentration of curcumin was present in the blood from 1 to 2 g/kg when gavaged
*BBB↑, Curcumin has been shown to be detectable in the brain after oral administration
*cognitive↑, urcumin treatment in a mouse model of Alzheimer disease resulted in significant improvement in cognitive function
*BioAv↑, piperine, a major component of black and long peppers, has been shown to inhibit enzymatic conjugation of curcumin allowing greater levels of unconjugated curcumin to be absorbed into portal blood circulation14 and increased curcumin tissue retention
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*OS↑, plateaued and has remained stable for the last 5 years
with good quality of life.
QoL↑, may help to improve quality of life,
Dose↑, few months later, she also embarked on a once-weekly course of hyperbaric oxygen therapy (90 min at 2 ATA) which she has maintained ever since.
Dose↑, oral curcumin complexed with bioperine (to aid absorption), as a single dose of 8 g each evening on an empty stomach.
IL6↓, curcumin prevents myeloma cell proliferation through inhibition of IL-6-induced STAT-3 phosphorylation
STAT3↓, curcumin downregulated the expression of NFkB, COX-2 and STAT3
NF-kB↓,
COX2/PTGS2↓,
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AR↓, results indicate that one of the potential mechanisms for the anticancer effect of the curcumin analogues was inhibition of AR pathways in human prostate cancer cells.
PSA↓, F10 and E10 resulted in a marked decrease in the level of PSA while the other compounds (curcumin, A10, B10 and C10) were less active.
Dose↑, However, in these studies, curcumin was used at relatively high concentrations, typically at >20 μM. I
tumCV↓, DHA treatment markedly reduced CRC cell viability in a time- and concentration-dependent manner without inducing apoptosis.
selectivity↑, whereas organoids from normal colon tissue were less affected.
Ferroptosis↑, DHA induced ferroptosis in both CRC cells and PDTOs, as evidenced by lipid peroxide accumulation
lipid-P↑, Lipid peroxidation levels in cells increased significantly following treatment with 50 µM and 100 µM DHA, reaching levels higher than those induced by Erastin, a well-established ferroptosis inducer
mt-ROS↑, DHA localized predominantly to the endoplasmic reticulum and mitochondria, where it promoted oxidative stress.
ChemoSen↑, DHA impaired the regrowth of oxaliplatin-tolerant persister cells and enhanced oxaliplatin efficacy in sequential treatment models.
*toxicity↓, low-toxicity strategy to enhance chemotherapy efficacy and target drug-tolerant persister cells in colorectal cancer.
TumCG↓, DHA treatment inhibits colorectal cancer cells growth inducing non-apoptotic cell death
eff↑, the administration of DHA together with Erastin markedly enhanced cell death, even at concentrations of 10 µM DHA, usually insufficient to induce any cytotoxic effects.
eff↑, Furthermore, the combined treatment with DHA made Erastin effective at inducing cell death at a concentration as low as 2 µM
Dose↝, lowest concentration of 10 µM, DHA already exerted a significant effect on organoid growth, whereas at the higher concentration (100 µM) the response exceeded that achieved with chemotherapy treatment alone,
mtDam↑, DHA accumulation in the endoplasmic reticulum was accompanied by mitochondrial dysfunction and increased ROS production, likely amplifying lipid peroxidation
*Inflam↓, dietary DHA supplementation has been shown to reduce intestinal inflammation induced by chemotherapy
*chemoP↑,
Dose↑, Moreover, they are compatible with tissue accumulation achieved through sustained dietary supplementation
*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants
toxicity↓, D-Limonene is well tolerated in cancer patients at doses which may have clinical activity. The favorable toxicity profile supports further clinical evaluation.
Dose↑, The MTD was 8 g/m2 per day; nausea, vomiting and diarrhea were dose limiting. Peak plasma concentration (Cmax) for D-limonene ranged from 10.8+/-6.7 to 20.5+/-11.2 microM
OS↑, One partial response in a breast cancer patient on 8 g/m2 per day was maintained for 11 months; three patients with colorectal carcinoma had prolonged stable disease.
TumCCA↑, Ellagic acid effectively induced G1-phase cell cycle arrest and suppressed CDK4, thereby reducing S-phase entry and enhancing radiation-induced apoptosis in TNBC cells.
CDK4↓,
RadioS↑,
TumCG↓, In vivo, ellagic acid significantly enhanced tumor growth inhibition when combined with radiotherapy.
*radioP↑, Importantly, ellagic acid also mitigated RIMI by reducing cardiomyocyte apoptosis, preserving myocardial structure, and maintaining left ventricular systolic function.
*cardioP↑, it sensitizes tumors by targeting the CARM1-CDK4 axis while protecting the heart through potent antioxidant activity.
*antiOx↑,
*ROS↓, The results showed that EA treatment significantly reduced the ROS fluorescence signal in H9C2 cardiomyocytes
Dose↑, ellagic acid was administered daily via intraperitoneal injection. (mice)
selectivity↑, In stark contrast, EA operates with tissue selectivity. It does not act as a blanket protector; instead, it exploits the fundamental biological difference between proliferating cancer cells and cardiomyocytes.
BioAv↓, its notoriously poor aqueous solubility and moderate oral bioavailability present significant translational hurdles.
*Dose↑, Oral administration of EGb 761 at 25, 50 and 100 mg/kg/day and bilobalide at 3 and 6 mg/kg/day for 7 days before ischemia
*Stroke↓, These results suggest that oral administration of bilobalide and EGb 761 protect against ischemia-induced neuron death and reductions in mitochondrial gene expression.
TrxR↓, EGCG-induced inactivation of TrxR and decreased cell survival, revealing TrxR as a new target of EGCG.
Trx↓,
ROS↑, EGCG induced inactivation of Trx/TrxR in parallel with increased ROS levels in HeLa cells.
Dose↑, Statistics indicated that ROS levels were significantly higher within a range of 50-200uM EGCG than that at 25 uM EGCG, but there were no significant differences in ROS levels between 50 uM vs 100 uM,
*neuroP↑, Regulation of α-, β-, γ-secretase activity, inhibition of tau phosphorylation, anti-oxidation, anti-inflammation, anti-apoptosis, and inhibition of AchE activity are reported as the main neuroprotective mechanisms.
*tau↓,
*antiOx↑,
*Inflam↓,
*Apoptosis↓,
*AChE↓,
*TNF-α↓, Inhibiting TNF-α/JNK pathway
*JNK↓,
*NGF↑, Increasing the level of NGF. EGCG (2 mg/kg) mouse
*SOD↑, figure 7
*GPx↑, EGCG enhanced the activity of T-SOD and GSH-Px and reduced MDA content in the hippocampus.
*MDA↓,
*NO↓,
*ROS↓,
*iNOS↓,
*COX2/PTGS2↓, anti apoptosis
*BAX↓, EGCG prevented LPS-induced elevation of GFAP, iNOS, and COX-2.
*CHOP/DDIT3↓,
*GRP78/BiP↓,
*Bcl-2↑,
*Dose↑, The highest safe dose for more than a month of treatment allowed by FDA is 800 mg of EGCG daily with food.
*BioAv↑, In preclinical and phase I clinical trials, it has been shown that bioavailability of EGCG is increased when it is consumed on a fasting basis.
*hepatoP↓, However, the rate of hepatotoxicity is also increased
MMP↓, nsPEF bypasses plasma-membrane shielding to porate organelles, collapse mitochondrial potential, perturb ER calcium, and transiently open the nuclear envelope.
Ca+2↑,
eff↑, synergy with checkpoint blockade.
ER Stress↑, capacity to directly target organelles such as mitochondria, endoplasmic reticulum (ER),
selectivity↑, selectively ablate solid tumors, suppress metastatic spread, and prime systemic anti-tumor immunity while sparing adjacent normal tissue [7,9,10,11,12,13,14,15].
CSCs↓, Preclinical investigations have demonstrated that nsPEFs significantly reduce CSC-associated subpopulations, including CD44+/CD24− cells in breast cancer xenografts and CD133+ glioma stem-like cells
CD44↓,
CD133↓,
ROS↑, nsPEFs release Ca2+ from the ER, disrupt mitochondrial membrane potential, induce reactive oxygen species (ROS) generation, and perturb nuclear chromatin structure within nanoseconds
Imm↑, nsPEFs not only eliminate local tumor cells but also convert the tumor into an in situ vaccine, amplifying their therapeutic relevance in the era of immunotherapy
DNAdam↑, figure 2
MOMP↑, induce mitochondrial outer membrane permeabilization (MOMP)
Cyt‑c↑,
Casp9↑, Subsequent release of cytochrome c enables apoptosome assembly, caspase-9 activation, and downstream activation of caspases-3/7, culminating in cell death
Casp3↑,
Casp9↑,
TumCD↑,
Fas↑, In certain cell types, nsEP can also activate the extrinsic pathway, where Fas receptor clustering stimulates caspase-8.
UPR↑, This rapid surge triggers ER stress pathways, activates unfolded protein response (UPR) signaling, and promotes cross-talk with mitochondria through mitochondria-associated membranes (MAMs)
Dose↝, longer ns pulses (100–300 ns) generate sustained plasma membrane charging, resulting in robust Ca2+ influx, osmotic imbalance, and apoptotic priming.
Dose↝, A critical threshold of 10–20 kV/cm is generally required to initiate pore formation in malignant cells, with higher amplitudes (>30–40 kV/cm) producing more extensive permeabilization [100].
Dose↓, Low pulse counts (<100) frequently produce reversible stress responses, such as transient mitochondrial depolarization or ER Ca2+ release, without committing cells to apoptosis. I
Dose↑, In contrast, higher pulse counts (500–1000) lead to irreversible apoptosis, caspase activation, and release of DAMPs that initiate ICD [80,106].
HMGB1↓, ICD after nsPEF is characterized by surface exposure of calreticulin, extracellular ATP release, and HMGB1 emission
eff↑, The integration of nsPEFs with NP-based systems thus represents a synergistic platform where physical membrane poration and molecular targeting cooperate to maximize therapeutic efficacy.
EPR↑, demonstrates that PEF + AuNPs enhanced membrane permeabilization compared with PEF alone,
ChemoSen↑, The superior efficacy of delayed drug administration following nsPEF exposure can be attributed to transient biophysical and biochemical changes that persist after pulsing.
ETC↝, study demonstrated that nsPEFs dynamically alter trans-plasma membrane electron transport (tPMET) and mitochondrial electron transport chain activity, resulting in differential ROS generation in cancer versus non-cancer cells (Figure 9).
*AntiAge↑, Mechanistically, nsPEFs upregulated HIF-1α and SIRT1, mediators of mitochondrial retrograde signaling, thereby reversing hallmarks of aging
*Hif1a↑,
*SIRT1↑,
*toxicity∅, Administration of Clovinol did not result in any toxicologically significant changes in clinical/behavioural observations, ophthalmic examinations, body weights, organ weights, feed consumption, urinalysis, hematology and clinical biochemistry parame
*Dose↑, no observed-adverse-effect level (NOAEL) as 1000 mg/kg b.wt./day
*Bacteria↓, Clove oil and its major component eugenol [70–85% (w/v)], exhibited several therapeutic effects including antibacterial, antifungal, analgesic, antispasmodic, anticarminative, antiseptic, and insecticidal effects
*Inflam↓, Major pharmacological activities of clove oil and eugenol include antioxidant, anti-inflammatory, antidiabetic, hypolipidemic, antinociceptive, hepatoprotective, antiviral and anticancer properties
*antiOx↑,
*AntiDiabetic↑,
*hepatoP↑,
*AntiCan↑,
*AntiThr↑, such as gallic acid, ellagic acid, tannins, flavonoids and their glycosides were reported to possess aphrodisiac, hypoglycemic, gastroprotective, anti-inflammatory and antithrombotic effects
eff↑, Most guidelines for cancer survivors suggest that physical activity and exercise should be an integral and continuous part of care for all cancer survivors
Dose↑, Strong evidence supports the promotion of physical activity and exercise for adult cancer patients before, during, and after cancer treatment, across all cancer types, and including patients with advanced disease
*other↝, 1) Does UMFA affect biological pathways leading to adverse health effects?
*other↝, 2) Does elevated folate status resulting from any form of folate intake affect vitamin B-12 function and its roles in sustaining health?
*Dose↑, For the purposes of this article, excessive folic acid intake constitutes exposure doses that exceed the UL of 1000 µg/d for adults set by the Institute of Medicine in 1998
*Dose↝, The use of dietary supplements is the primary source of excessive folic acid intake: ∼35% of US adults and 28% of children aged 1–13 y regularly use supplements containing folic acid;
*Risk↓, Low consumption of total folate is considered to be an independent risk factor for colorectal cancer and perhaps also for cancers of the breast, lung, pancreas, and others
*cognitive↑, continuing 400 µg/d supplementation into the second and third trimesters has been observed to result in higher cognition scores among offspring at 3 and 7 y of age
*toxicity↝, This effect of vitamin B-12 deficiency on impairing folate metabolism and nucleotide synthesis is known as the “methyl trap,” which results in megaloblastic anemia
*toxicity↑, After discontinuation of the self-administration of fenbendazole, the patient's liver dysfunction spontaneously resolved.
Dose↑, 1 g orally per day for 3 consecutive days, followed by 4 days off. She repeated this weekly schedule for approximately one month, from early July until August 9, 2019
*toxicity↑, confirmed severe drug-induced liver injury, hepatocellular pattern, associated with the self-administration of fenbendazole in a 67-year-old woman who presented with 2 weeks of jaundice.
Dose↑, Fenbendazole 3 g per dose, three times per week—specifically, three 1-g packets each dosing day.
toxicity↑, 47-year-old woman with metastatic colon cancer on nivolumab/relatlimab who developed severe hepatocellular liver injury after increasing her self-administered dose of fenbendazole.
Dose↑, initial dose: 222 mg, three times per week for six weeks Weekly exposure: 666 mg/week
Escalated dose: 222 mg every day Weekly exposure: 1,554 mg/week
toxicity↑, jaundice, and abdominal pain following a 3-month regimen of alternating these agents daily at a dosage of “one squirt”
Dose↑, (estimated to be 0.18 mg/kg of ivermectin and 0.98 mg/kg of fenbendazole)
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Inflam↓, anti-inflammatory, chemopreventive, chemotherapeutic
ChemoSen↑,
chemoPv↑,
eff↑, fisetin significantly impairs carcinoma cell growth in the presence of ascorbic acid, which results in a 61% inhibition of cell growth, in 72 h; the treatment with ascorbic acid alone had no effect on cellular proliferation (Kandaswami et al., 1993)
memory↑, enhancement of the long-term memory, antidepressant effects, inhibition of ischemic reperfusion injury and amelioration of behavioral deficits following a stroke
neuroP↑,
*Dose↑, Mayo Clinic has recently designed and begun a clinical trial aimed at the “Alleviation by Fisetin of Frailty, Inflammation, and Related Measures in Older Adults” (AFFIRM-LITE) with fisetin orally in doses up to 20 mg/kg of patient body weight
BioAv↓, In view of poor solubility (10.45 μg/mL), relatively low oral bioavailability (44%) and rapid metabolism,
BBB↑, fisetin in combination with other epigenetically active molecules which are able to cross the blood-aqueous and blood-retina barriers exhibit synergistic beneficial effects.
*neuroP↑, As a hydrophobic agent, FIS readily penetrates cell membranes and accumulates in cells to exert neuroprotective, neurotrophic and antioxidant effects
*antiOx↑,
*Inflam↓, FIS treatment may include alleviating inflammation, cell apoptosis and oxidative stress
RenoP↑, alleviates cell apoptosis and inflammation in acute kidney injury
COX2/PTGS2↓, FIS induces apoptosis in various tumor cells by, for example, inhibiting cyclooxygenase-2, inhibiting the Wnt/EGFR/NF-κB pathway, activating the caspase-3 cascade
Wnt↓,
EGFR↓,
NF-kB↓,
Casp3↑,
Ca+2↑, activating the caspase-3 and Ca2+ dependent endonuclease, and activating the caspase-8/caspase-3 dependent pathway via ERK1/2.
Casp8↑,
TumCCA↑, FIS controls the cell cycle and inhibits cyclin-dependent kinases (CDKs) in human cancer cell lines,
CDK1↓,
PI3K↓, by inhibition of PI3K/Akt/mTOR signaling [20], mitogen-activated protein kinases (MAPK) [21], and nuclear transcription factor (NF-κB)
Akt↓,
mTOR↓,
MAPK↓,
*P53↓, FIS inhibits aging by reducing p53, p21 and p16 expression in mouse and human tissues
*P21↓,
*p16↓,
mTORC1↓, FIS induces autophagic cell death by inhibiting both the mTORC1 and mTORC2 pathways
mTORC2↓,
P53↑, FIS significantly increases the expression of p53 and p21 proteins and lowers the levels of cyclin D1 [27,28], cyclin A, CDK4 and CDK2, thus contributing to cell-cycle arrest.
P21↑,
cycD1/CCND1↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
BAX↑, FIS also increases Bax [27,28] and Bak [27] protein expression, but reduces the levels of Bcl-2 [27,28], Bcl-xL [27] and PCNA [28], and then starts the mitochondrial apoptotic pathway.
Bcl-2↓,
PCNA↓,
HER2/EBBR2↓, FIS reduces HER2 tyrosine phosphorylation in a dose-dependent manner and aids in proteasomal degradation of HER2 rather than lysosomal degradation
Cyt‑c↑, FIS cells causes destabilization of the mitochondrial membrane and an increase in cytochrome c levels, which is consistent with the loss of mitochondrial membrane integrity.
MMP↓,
cl‑Casp9↑,
MMP2↓, FIS reduces the enzymatic activity of both MMP-2 and MMP-9.
MMP9↓,
cl‑PARP↑, cell membrane, mitochondrial depolarization, activation of caspase-7, -8 and -9, and cleavage of PARP
uPA↓, interestingly, the promoter activity of the uPA gene is suppressed by FIS
DR4↑, induces upregulation of DR4 and DR5 death receptor expression in a dose-dependent manner
DR5↑,
ROS↓, FIS induces an increase in intracellular Ca2+ but reduces the production of ROS in WEHI-3 cells (myelomonocytic leukemia)
AIF↑, It also increases the levels of caspase-3 and AIF mRNA, but also increases necrosis markers including RIP3 and PARP1
CDC25↓, FIS reduces the expression of cdc25a, but increases the expression of p-p53, Chk1, p21 and p27, which may lead to a G0/G1 arrest.
Dose↑, FIS in concentrations from 0 to 10 μM does not affect cell viability; however, its use at concentrations of 20–40 μM significantly reduces the viability of lung cancer cells
CHOP/DDIT3↑, CaKi : FIS induces upregulation of CHOP expression and ROS production
ROS↑, NCI-H460 :FIS increases the ER stress signaling FIS increases the level of mitochondrial ROS FIS induces mitochondrial Ca2+ overloading and ER stress FIS induced ER stress-mediated cell death via activation of the MAPK pathway
cMyc↓, FIS influences proliferation related genes such as cyclin D1, c-myc and cyclooxygenase (COX)-2 by downregulating them.
cardioP↑, cardioprotective activity
UGDH↓, UGDH revealed that gallic acid was a non-competitive inhibitor with respect to UDP-glucose and NAD+. I
UGDH↓, In contrast, quercetin showed a competitive inhibition and a mixed-type inhibition with respect to UDP-glucose and NAD+, respectively.
TumCP↓, gallic acid and quercetin are effective inhibitors of UGDH that exert strong antiproliferative activity in breast cancer cells.
Dose↑, The concentrations of gallic acid and quercetin needed to produce effects on UGDH are at least 10-fold higher than can be predicted to be reached under in vivo dietary conditions
*BioAv↓, oral bioavailability of polyphenols including gallic acid and quercetin is very low, producing plasma concentrations most likely only 1/10th to 1/100th of those necessary to produce an effect
eff?, However, it is still not understood if the polyphenols have to be in the free form to exert their activity, or the conjugated polyphenols can exert similar activity, as it has been reported for quercetin
*Dose↓, The estimated average dietary intake of Ge in humans is 1.5 mg/d. Ge is widely distributed in edible foods, all of which, with few exceptions, contain less than 5 ppm Ge, since higher levels are toxic to most plants
*Dose↑, germanium sesquioxide (Ge-132) and lactate-citrate-germanate (Ge lactate citrate) have been sold as "nutritional supplements" in some countries for their purported immunomodulatory effects or as health-producing elixirs, resulting in intakes of Ge si
*toxicity↑, Since 1982, there have been 18 reported cases of acute renal dysfunction or failure, including two deaths, linked to oral intake of Ge elixirs containing germanium dioxide (GeO2) or Ge-132.
*creat↑, Serum creatinine levels have been well above 400 mumol/L in such patients
*Dose↑, In 17 of 18 cases, accumulated elemental Ge intakes reportedly ranged between 16 to 328 g over a 4-36 mo period, or between 100 to 2000 times the average estimated dietary intake for human.
*other?, It is recommended that patients exposed to long-term (greater than 3 mo) Ge supplementation at levels well above the estimated daily intake be medically supervised and monitored for potential renal-, pulmonary- or neurotoxicity.
Dose↑, it was found that the ginger supplement intake group, which took not more than 1 g of ginger supplementation per day for above four days, had significantly less acute vomiting than the control group
Vomit↓,
Showing Research Papers: 1 to 50 of 91
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 91
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
UGDH↓, 2, Vomit↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, H2O2↑, 1, HO-1↑, 1, lipid-P?, 1, lipid-P↑, 1, NQO1↑, 1, NRF2↑, 1, OXPHOS↓, 1, ROS↓, 2, ROS↑, 6, mt-ROS↑, 2, Trx↓, 1, TrxR↓, 2,
Metal & Cofactor Biology(tgid=2) ⓘ
Tf↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 1, ATP↓, 1, CDC25↓, 1, ETC↝, 1, Insulin↓, 1, MEK↓, 1, MMP↓, 3, mtDam↑, 1, Raf↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACLY↓, 2, AMPK↑, 3, cMyc↓, 2, FASN↓, 1, FASN↑, 1, FBPase↑, 1, glucoNG↑, 1, Glycolysis↓, 2, HMG-CoA↓, 1, LDH↓, 1, PFK1↓, 1, PFK2↓, 1, PPARα↓, 1, p‑S6K↓, 1, TCA↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, Apoptosis↑, 5, ATF2↓, 1, BAX↑, 1, Bax:Bcl2↑, 1, Bcl-2↓, 4, Bcl-xL↓, 1, Casp2↑, 1, Casp3↑, 6, Casp8↑, 3, Casp9↑, 5, cl‑Casp9↑, 1, Cyt‑c↑, 2, DR4↑, 2, DR5↑, 2, Fas↑, 1, Ferroptosis↑, 1, JNK↑, 1, MAPK↓, 1, Mcl-1↓, 1, MOMP↑, 1, p27/CDKN1B↑, 1, Telomerase↓, 1, TumCD↑, 1, YAP/TEAD↝, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1, other↝, 2, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, ER Stress↑, 1, HSP90↓, 1, UPR↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 2, P53↑, 1, cl‑PARP↑, 2, PCNA↓, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 3, CDK4↓, 4, Cyc↓, 1, cycA1/CCNA1↓, 1, cycD1/CCND1↓, 3, cycE/CCNE↓, 2, P21↑, 1, p‑RB1↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD133↓, 2, CD44↓, 1, CSCs↓, 4, Diff↓, 1, EMT↓, 5, ERK↓, 1, p‑ERK↓, 1, FOXO3↑, 1, HDAC↓, 1, HH↝, 1, IGF-1↓, 1, IGF-1↑, 1, IGF-1R↓, 1, Let-7↑, 1, mTOR↓, 3, mTORC1↓, 1, p‑mTORC1↓, 1, mTORC2↓, 1, n-MYC↓, 1, Nestin↓, 1, NOTCH↓, 1, NOTCH3↓, 1, PI3K↓, 4, PTEN↑, 2, SOX2↓, 1, STAT3↓, 4, TOP1↓, 1, TOP2↑, 1, TumCG↓, 3, Wnt↓, 2,
Migration(tgid=13) ⓘ
AntiAg↑, 1, Ca+2↑, 2, E-cadherin↑, 1, miR-200b↑, 1, MMP1↓, 1, MMP2↓, 4, MMP9↓, 4, N-cadherin↓, 1, PDGF↓, 1, Slug↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 3, TumMeta↓, 1, Twist↓, 1, uPA↓, 2, Vim↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, EGFR↓, 2, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 1, p‑PDGFR-BB↓, 1, TXA2↓, 1, VEGF↓, 3, VEGFR2/KDR/Flk1↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CCR7↓, 1, COX1↓, 1, COX2/PTGS2↓, 4, CXCR4↓, 2, HMGB1↓, 1, IKKα↓, 1, IL1α↓, 1, IL6↓, 5, Imm↑, 1, Inflam↓, 2, JAK2↓, 1, MCP1/CCL2↓, 2, MIP2↓, 1, NF-kB↓, 5, PD-L1↓, 1, PGE2↓, 3, PSA↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 2, ChemoSen↑, 8, Dose?, 2, Dose↓, 2, Dose↑, 30, Dose↝, 3, eff?, 1, eff↓, 2, eff↑, 20, eff↝, 2, Half-Life↓, 1, RadioS↑, 5, selectivity↑, 4,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 2, ascitic↓, 1, BG↓, 1, EGFR↓, 2, HER2/EBBR2↓, 1, IL6↓, 5, LDH↓, 1, PD-L1↓, 1, PSA↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, cardioP↑, 1, chemoP↑, 2, chemoPv↑, 2, ChemoSideEff↓, 1, memory↑, 1, neuroP↑, 2, OS↑, 2, QoL↑, 1, QoL∅, 1, RenoP↑, 1, Risk↓, 6, Risk↑, 1, toxicity↓, 2, toxicity↑, 2, toxicity↝, 2, TumVol↓, 1,
Total Targets: 204
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 7, Catalase↑, 1, GPx↑, 2, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, OXPHOS↑, 1, ROS↓, 4, SAM-e↑, 1, SOD↑, 2, TAC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↝, 1, Insulin↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, p‑CREB↑, 1, glucose↓, 2, LDL↓, 1, NAD↝, 1, p‑PPARγ↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, iNOS↓, 1, JNK↓, 1, MAPK↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 2, AntiThr↑, 1, HATs↓, 1, other?, 1, other↑, 1, other↝, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, GRP78/BiP↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
p16↓, 1, P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, HDAC↑, 1,
Migration(tgid=13) ⓘ
AP-1↓, 1, APP↓, 1, Ca+2?, 1, Ca+2↝, 2, serineP↓, 1, β-catenin/ZEB1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↑, 1, NO↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 3, P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, CRP↓, 1, IL18↓, 1, IL1β↓, 2, IL6↓, 1, IL8↓, 1, Imm↑, 2, Inflam↓, 9, NF-kB↓, 2, TNF-α↓, 5, VitD↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 3, BDNF↑, 2, GABA↑, 1, NGF↑, 1, tau↓, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 4,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
testos↑, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
ABC↓, 1, BioAv↓, 4, BioAv↑, 3, BioAv⇅, 1, BioAv↝, 3, Dose?, 1, Dose↓, 1, Dose↑, 23, Dose↝, 5, eff↑, 3, eff↝, 1, Half-Life↝, 4, MRP1/ABCC1↓, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BMD↑, 1, BMPs↑, 1, Calcium↑, 1, creat↑, 1, CRP↓, 1, hs-CRP↓, 1, IL6↓, 1, Mag↑, 1, VitD↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 2, cardioP↑, 2, chemoP↑, 2, chemoPv↑, 2, ChemoSideEff↓, 1, cognitive↑, 4, hepatoP↓, 1, hepatoP↑, 1, memory↑, 5, neuroP↑, 5, OS↑, 1, QoL↑, 1, radioP↑, 1, Risk↓, 2, toxicity↓, 3, toxicity↑, 4, toxicity⇅, 1, toxicity↝, 3, toxicity∅, 2,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 2,
Total Targets: 115
Scientific Paper Hit Count for: Dose, Dosage
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#:1114 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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