antiNeop Cancer Research Results
antiNeop, antineoplastic: Click to Expand ⟱
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Antineoplastic is a medical term that literally means “against new growth” and is used to describe agents or therapies that prevent, inhibit, or kill cancer cells.
-In oncology, antineoplastic usually implies anticancer activity
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Scientific Papers found: Click to Expand⟱
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Ovarian, |
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antiNeop↑, We have recently demonstrated the anti-neoplastic effect of Amla extract (Emblica officinalis, AE) on OC cells in vitro and in vivo.
TumCP↓, The inhibitory effect of AE on proliferation, migration and invasiveness (P≤0.001) of SKOV3 cells and >90% attenuation of tumor growth in a xenograft mouse model suggested multiple targets.
TumCMig↓,
TumCI↓,
TumCG↓,
miR-375↑, >2,000-fold increase in the expression of miR-375 in AE-treated SKOV3 cells
IGFR↓, AE also decreased the gene and protein expression of IGF1R, a target of miR-375 (P≤0.001), and SNAIL1 (P≤0.002), an EMT-associated transcription factor that represses E-cadherin expression (P≤0.003).
Snail↓,
E-cadherin↑, AE increased E-cadherin expression (P≤0.001).
Apoptosis↑, Disulfiram (DSF), as an anti-alcoholic drug, kills the cancer cells by inducing apoptosis
tumCV↑, DSF was associated with enhanced apoptosis and tumor inhibition rates,
eff↑, The greatest anti-tumor activity was observed when DSF was used as combination therapy or as a nanoparticle-encapsulated molecule
toxicity↓, noticeable body weight loss after DSF treatment, which indicated that there was no major toxicity of DSF.
antiNeop↑, antineoplastic activity of DSF was first recorded in 1977
ChemoSen↑, The synergistic effect of Cis, DOX, TMZ, PTX, Gy, and DSF in induced apoptosis was significantly higher than that of DSF or Cis or DOX or TMZ or Gy alone
RadioS↑, Tumor cell growth was significantly inhibited when DSF, chemotherapy, and radiation therapy were used simultaneously, as shown in the examined in vivo studies
OS↑, All three studies show that DSF is safe and seems to prolong survival of cancer patients
ROS↑, Metabolites of DSF chelate with metal ions, leading to alterations in the intracellular levels of metal ions, enhancement of oxidative stress, inhibition of the activities of superoxide dismutase or matrix metalloproteinases,
SOD↓,
MMP1↓,
eff↑, observation that the combination of DSF with metal ions (Cu, Ag) leads to enhanced anticancer effectiveness is in accordance with the observations of in vitro and animal experiments
Half-Life↓, At the pH of 7.4, the half-life of DSF is 1–1.5 min
Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2/PTGS2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3
protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells
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GC, |
SGC-7901 |
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in-vitro, |
BC, |
MGC803 |
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antiNeop↑, Formononetin exhibits anti‐neoplastic activities in specific types of cancers, such as colon carcinoma and breast cancer.
tumCV↓, formononetin decreased the viability of GC cell line SGC‐7901 and MGC‐803.
TumCMig↓, formononetin suppressed the migration and invasion abilities of GC cells.
TumCI↓,
Dose↝, mice were treated with either 100 μL formononetin (30 mg/kg) or saline (vehicle) using the method of intragastric administration three times a week.
miR-542↓, miR‐542‐5p rather than miR‐1976 and miR‐450b was significantly reduced by formononetin in SGC‐7901 and MGC‐803 cells compared to the untreated control
TumCG↓, miR‐542‐5p inhibitor suppresses GC cells growth and invasion
*toxicity↓, Fucoidan is a versatile, nontoxic marine-origin heteropolysaccharide that has received much attention due to its beneficial biological properties and safety.
*AntiViral↑, ucoidan has been demonstrated to exhibit a variety of conventional bioactivities, such as antiviral, antioxidant, and immune-modulatory characteristics, and anticancer activity against a wide range of malignancies has also recently been discovered.
*antiOx↑,
*Imm⇅,
AntiCan↑,
TumCCA↑, Fucoidan inhibits tumorigenesis by prompting cell cycle arrest and apoptosis, blocking metastasis and angiogenesis, and modulating physiological signaling molecules.
Apoptosis↑,
TumMeta↓,
angioG↓,
antiNeop↑, Fucoidans’ capacity to bind to Toll-like receptors and intervene with the action of vascular endothelial growth factors (VEGF) and matrix metalloproteinases (MMPs) could explain their anti-neoplastic properties
VEGF↓,
MMPs↓,
BioAv↑, Low molecular weight fractions (LMWF), in particular, are thought to be more biocompatible [47]
BioAv↑, in rats, following topical administration of fucoidan (MW 750 kDa) from Fucus vesiculosus demonstrated fine skin-penetrating characteristics.
ROS⇅, Induction/inhibition of reactive oxygen species (ROS), mitochondrial instability, and caspase and poly (ADP-ribose) polymerase (PARP) cleavage are all aspects of it
cl‑PARP↑, fucoidan treatment causes PARP cleavage and caspase-3/7 activation in MCF-7 cells, which are hallmarks of apoptosis [
Casp3↑,
Casp7↑,
ROS↑, human hepatoma SMMC-7721 cells, fucoidan therapy caused noteworthy growth inhibition and ROS-mediated apoptosi
GSH↓, lower glutathione consumption (GSH), mitochondrial swelling, and depolarization of the mitochondrial membrane potential
MMP↓,
PI3K↓, Fucoidan inhibits PI3K, suppressing ERK and activates MAPK, limiting cancer cell proliferation and decreasing Bcl-2 to Bax ratio, inducing caspase-dependent apoptosis in BEL-7402 and LM3 cell lines
ERK↓,
MAPK↑,
TumCP↓,
Bax:Bcl2↑,
TJ↑, Meanwhile, dietary fucoidan progressively restores intestinal villi by upregulating the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1, and Claudin-8 via p38 MAPK and ERK1/2 activation.
ZO-1↑,
OCLN↑,
CLDN1↑,
IBI↑, fucoidan supplementation improves intestinal barrier function by enhancing intestinal microbiota diversity
GutMicro↑,
NK cell↑, ↑NK cell-mediated anticancer immunity
STAT3↓, Inhibits STAT3 Signaling
eff↑, Astragalus polysaccharide as a topical mucosal adjuvant to boost the anticancer efficacy of immune checkpoint inhibitors
*antiOx↑, Several beneficial effects are reported for gallic acid, including antioxidant, anti-inflammatory, and antineoplastic properties.
*Inflam↓,
*antiNeop↑,
*cardioP↑, reported to have therapeutic activities in gastrointestinal, neuropsychological, metabolic, and cardiovascular disorders
*Bacteria↓, Antimicrobial activity
*AST↓, Beryllium-induced hepatorenal toxicity ↓AST, ALT, ALP, LPO, AMND, ↑GSH, CAT, SOD, GPx & GST, ↓Cr & urea
*ALAT↓,
*ALP↓,
*lipid-P↓,
*GSH↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*Urea↓,
*creat↓,
tumCV↓, human NCSLC NCI-H460 cells In vivo: mouse NCI-H460 xenograft model In vitro: ↓viability, induction of G2/M phase cell cycle arrest, ↑intracellular Ca2+, CDK1 activity, caspase-3, caspase-8 & caspase-9 activation, ↓ΔΨ
TumCCA↑,
i-Ca+2↑,
CDK1↑,
Casp3↑,
Casp8↑,
Casp9↑,
MMP↓,
ROS↑, In vitro: induction of S phase cell cycle arrest ↑ROS
MMPs↓, it can inhibit the invasion and metastasis by decreasing the matrix metalloproteinase expression and activity
*GastroP↑, Beside the gastroprotective activity, gallic acid ameliorates the hepatotoxic effects of xenobiotic agents by acting as an antioxidant compound that scavenges free radicals, such as ROS
*hepatoP↑,
*ROS↓,
*AChE↑, Gallic acid is also able to reverse the scopolamine-induced amnesia in mice, probably through inhibiting oxidative stress and decreasing acetylcholinesterase (AChE) enzyme activity in the brain
*BioAv↝, Furthermore, a pharmacokinetics study of garcinol in Sprague Dawley rats showed 26.64 ± 0.23% and 35.72 ± 0.97% oral bioavailability at two doses, that is 22.5 and 45 mg/kg, respectively.
*Dose↝, The Cmax values at these two oral doses were 2317.69 ± 180.44 and 3446.14 ± 190.12 ng/mL.
*Inflam↓, The anti-inflammatory and antioxidant properties of garcinol make it suitable as a cancer chemopreventive agent
*antiOx↑,
*chemoPv↑,
Wnt↓, Garcinol stands out as a possible anticancer molecule that inhibits the important signalling pathways (Wnt/-catenin, ERK1/2 and PI3K/Akt) involved in malignant development in colon cancer, breast cancer, hepatocellular carcinoma, leukaemia, prostate
β-catenin/ZEB1↓,
ERK↓,
PI3K↓,
Akt↓,
NF-kB↓, inhibits cancer cell proliferation by effectively inhibiting several significant regulatory pathways like NF-kB, STAT3, etc
STAT3↓,
TumCP↓,
antiNeop↑, Even though it is a potent antineoplastic modulator, garcinol is still in its preclinical development stage
ChemoSen↑, it was believed that the administration of chemotherapeutic agents in combination with garcinol shows a synergistic therapeutic effect with protective action.
chemoP↑,
antiOx↑, demonstrated to be anti-oxidant, anti-inflammatory and anti-cancer in nature.
Inflam↓,
AntiCan↑,
NF-kB↓, Garcinia indica has been found to be an effective inhibitor of several key regulatory pathways (e.g., NF-kB, STAT3 etc.) in cancer cells, thereby being able to control malignant growth of solid tumours in vivo.
STAT3↓,
antiNeop↑, Despite its high potential as an anti-neoplastic modulator of several cancer types such as head and neck cancer, breast cancer, hepatocellular carcinoma, prostate cancer, colon cancer etc.
5LO↓, ability of garcinol to bind and inhibit 5-lipoxygenase (5-Lox),
eff↑, . The addition of 10 % FBS (fetal bovine serum) to medium leads to approximately 10-fold decrease in IC 50 value of garcinol for HCT116 cell growth.
HATs↓, Garcinol has been demonstrated to inhibit HATs such as p300 and PCAF both in vitro and in vivo
p300↓,
PCAF↓,
miR-200c↑, Garcinol treatment has been shown to cause upregulation of several tumor suppressor miRNAs, of which miR-200c was found to target and downregulate Notch1 in pancreatic CSCs
NOTCH1↓,
CSCs↓,
COX2/PTGS2↓, garcinol has been shown to cause significant reduction in expression level of cyclooxygenase-2 (COX-2), cyclin D1, and vascular endothelial growth factor
cycD1/CCND1↓,
VEGF↓,
PI3K↓, via inhibition of the extracellular signal-regulated protein kinase 1/2, PI3K/Akt and Wnt/b-catenin
Akt↓,
Wnt↑,
β-catenin/ZEB1↓,
ROS↑, It could lead to accumulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress modulator GADD153
CHOP/DDIT3↑,
Bax:Bcl2↑, increased Bax2/Bcl-2 ratio, elevated tBid (truncated Bid), and caspase 8 in cancer cell.
Casp8↑,
FAK↓, garcinol can lead to inhibition of tyrosine phosphorylation of focal adhesion kinase (FAK),
*neuroP↑, garcinol being considered in development of therapeutics for neurodegenerative diseases such as Alzheimers’s, Parkinson’s to attenuate oxidative stress-induced neurotoxicity.
PCNA↓, Significant reduction in proliferating cell nuclear antigen (PCNA) index in ACF was also observed with gar-
cinol treatment
*GSTs↑, Garcinol administration in such cases was also seen to enhance activities of liver glutathione S-transferase (GST) and quinone reductase (QR), which play an important role in detoxification process of body
ERK↓, ERK1/2
PI3K/Akt↓,
Wnt/(β-catenin)↓,
STAT3↓,
NF-kB↓,
ChemoSen↑, cisplatin or paclitaxel, in the presence of garcinol can lead to a significant increase in the treatment outcome
COX2/PTGS2↓,
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
VEGF↓,
TGF-β↓,
HATs↓,
E-cadherin↑,
Vim↓,
Zeb1↓,
ZEB2↓,
Let-7↑,
MMP9↓,
TumCCA↑, cycle arrest at G0/G1 phase
ROS↑,
MMP↓,
IL6↓,
NOTCH1↓,
antiNeop↑,
AntiTum↑, As inhibitors of SUMOylation, GAs demonstrate significant antitumor activity, and can exert antineoplastic effects through multiple pathways, which positions them as potentially promising therapeutic agents for cancer treatment.
SUMO↓,
antiNeop↑,
*Inflam↓, GAs exhibit notable anti-inflammatory, antibacterial, and antiviral properties, highlighting their multifaceted medicinal potential.
*Bacteria↓,
*AntiViral↑,
*toxicity↑, the associated risks of liver and kidney damage must not be overlooked. GAs can induce significant hepatic damage by promoting cellular apoptosis, oxidative stress, and the disruption of various metabolic processes.
*ROS↑,
*toxicity↝, Due to their recognized toxicity, the concentration of GAs is typically regulated to within 5ppm in the standardized G. biloba leaf extract EGb 761.
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Lung, |
H520 |
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antiNeop↑, Grape seed procyanidin extract (GSE) has been shown to exert antineoplastic properties in preclinical studies.
Ki-67↓, Three months of LP treatment significantly decreased bronchial Ki-67 labeling index (LI), a marker of cell proliferation on the bronchial epithelium.
other↑, One month of LP treatment significantly increases eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the omega-3 polyunsaturated fatty acids (n-3 PUFA)s with well-established anti-cancer properties.
PGE3↑, Furthermore, 3 month of LP treatment significantly increases serum prostaglanding (PG) E3, a metabolite of EPA with anti-inflammatory and antineoplastic properties.
TumCP↓, IBC could inhibit Panc 02 cell proliferation and induce apoptosis via increasing the production of reactive oxygen species.
Apoptosis↑,
ROS↑,
TumW↓, IBC could attenuate the weight of solid tumors, increase CD8+ T cells, and reduce M2 macrophages in the tumor tissue and spleen
CD8+↑,
M2 MC↓,
CSCs↓, IBC alleviated the proportion of myeloid-derived suppressor cells (MDSCs) in the tumor tissue but had no change in the spleen.
antiNeop↑, IBC as an antineoplastic agent, which could attenuate the growth of pancreatic cancer via activating the immune activity
Imm↑,
eff↓, NAC pretreatment abrogated apoptosis produced by IBC in Panc 02 cells.
Bcl-2↓, IBC could decrease the expression of Bcl-2 and increase expression of Bax
BAX↑,
TumCP↓, Studies in mammary cancer demonstrated that moderately high concentrations of molecular iodine (I2) have a antiproliferative and apoptotic effect either in vivo as in vitro
Apoptosis↑,
Dose↝, Virgin Sprague-Dawley rats were treated with methyl-nitrosourea (MNU: single dose ip, 50 mg/Kg bw)
other↑, tumoral but not normal mammary tissue contained an elevated basal concentration of AA and significantly more AA-iodinated called 6-iodolactone (6-IL) after chronic I2 treatment.
BloodF↓, Tumors from I2-treated rats showed fewer cells positive to proliferating cell nuclear antigen, lower blood vessel density, as well as decreases in vascular endothelial growth factor, urokinase-type plasminogen activator, and PPAR type alpha (PPARα).
VEGF↓,
UroPA↓,
PPARα↓,
DR4↑, These same tumors showed increases in the cell death markers, TUNEL-positive cells (p < 0.05) and the enzyme caspase-3 (trend), as well as significant induction of PPAR type gamma (PPARγ).
Casp3↑,
PPARγ↑,
antiNeop↑, Together, these data demonstrate that the antineoplasic effect of iodine involves 6-IL formation and PPARγ induction.
Risk↓, Cancer incidence was 37.5% lower in I2-treated than in control rats, whereas the number of tumors per rat and latency were similar for all groups
6IL↑,
antiNeop↑, we have shown that supplementation with molecular iodine (I2) has a powerful antineoplastic effect in methylnitrosourea (MNU)-induced experimental models of MC.
antiOx↑, showed a consistent antioxidant effect of I2 in normal and tumoral tissues.
Dose↝, DOX dose (16 mg/kg) or with lower doses (8 and 4 mg/Kg), in each case with and without 0.05% I2 in drinking water.
TumVol↓, short I2 treatment induced adjuvant antineoplastic effects (decreased tumor size and proliferating cell nuclear antigen level) with significant protection against body weight loss and cardiotoxicity
PCNA↓,
Weight↑,
cardioP↑,
ChemoSen↑, DOX-I2 combination exerts antineoplastic, chemosensitivity, and cardioprotective effects and could be a promising strategy against breast cancer progression.
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Pca, |
LNCaP |
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Pca, |
DU145 |
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in-vitro, |
Pca, |
PC3 |
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PPARγ↑, Molecular iodine (I2) induces cytotoxic effects in prostate cancer cell lines and antineoplastic effects in neuroblastoma and breast cancer through the indirect activation of PPARG.
antiNeop↑,
TumCD↑, I2 promoted cytotoxic effects, whereas in surviving cells, it stimulated the outgrowth of neurite-like projections, regulated lipid content, and reduced invasive capacity.
TumCI↓,
AntiCan⇅, I2 showed anti-cancer (cytotoxic, anti-invasive) and pro-cancer (pro-neurite, lipid accumulation, desmoplasia) effects through a PPARG-independent mechanism.
antiOx↑, Prostate and prostate cancer cells capture I2, which exerts antioxidant, anti-inflammatory, and apoptotic actions depending on the cellular context
Inflam↓,
Apoptosis↑,
tumCV↓, I2 Decreases Cell Viability and Invasive Capacity in Prostate Cancer Cell Lines
Dose↝, advanced group, 16 patients received I2 or placebo, along with Neo treatment (30-90 days) (3 luminal A; 6 luminal B; 7 triple negative). After surgery, all patients received I2 (3 mg/day) for 3 years.
OS↑, After 3 years, three placebo patients (1 luminal B; 2 triple negative) presented recurrence, and one died (triple negative). In contrast, only one patient in the I2 treatment group presented with recurrence (luminal B), yet no patients died.
antiNeop↑, I2 supplementation enhances the antineoplastic response of Neo
eff↑, supporting the notion that I2 is an effective adjuvant in the treatment of chemoresistant breast cancer.
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BC, |
MDA-MB-231 |
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antiNeop↑, moderate (SW35/21.7) and low (SW35/9.9) doses of shock waves had significant antineoplastic effects and, in combination with iodine supplement, attenuated the aggressiveness of these cells by decreasing expression of the markers of stem cells (CD44 a
CSCsMark↓,
CD44↓, decreasing expression of the markers of stem cells (CD44 and Sox2) and invasion (HIF and VEGF).
SOX2↓,
HIF-1↓,
VEGF↓,
Dose↝, All animals received de-ionized water to drink, and the iodine groups were supplemented with a solution of 0.0025% I 2 (»150-180 ug/d per animal).
Dose↝, sudden and simultaneous expansion of 3000 piezoelectric elements mounted on a hemispherical aluminum backing excited by a high-voltage pulse.
EPR↝, To determine if shock waves increase the uptake of I 2 , the intratumor content of this halogen was quantified in tumor samples.
PPARγ↑, PPARg protein exhibited a significant increase only in tumors of mice treated with the I 2 supplement
Showing Research Papers: 1 to 17 of 17
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
6IL↑, 1, miR-375↑, 1, miR-542↓, 1, PGE3↑, 1, SUMO↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, GSH↓, 1, ROS↑, 7, ROS⇅, 1, SOD↓, 1, Thiols↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 4,
Core Metabolism/Glycolysis(tgid=4) ⓘ
PDK1↓, 1, PI3K/Akt↓, 1, PPARα↓, 1, PPARγ↑, 3,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Apoptosis↑, 6, BAD↓, 1, BAX↑, 3, Bax:Bcl2↑, 2, Bcl-2↓, 3, Casp3↑, 5, Casp7↑, 1, Casp8↑, 2, Casp9↑, 2, DR4↑, 1, MAPK↑, 1, survivin↓, 1, TumCD↑, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
HATs↓, 2, other↑, 2, PCAF↓, 1, tumCV↓, 3, tumCV↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, P53↑, 1, PARP↑, 1, cl‑PARP↑, 1, PCNA↓, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↑, 1, cycD1/CCND1↓, 2, E2Fs↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD44↓, 2, CSCs↓, 3, CSCsMark↓, 1, EpCAM↓, 1, ERK↓, 3, FOXO3↝, 1, IGFR↓, 1, Let-7↑, 1, mTOR↓, 1, NOTCH1↓, 3, OCT4↓, 1, p300↓, 1, PI3K↓, 4, SOX2↓, 1, STAT3↓, 4, TumCG↓, 3, Wnt↓, 1, Wnt↑, 1, Wnt/(β-catenin)↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, i-Ca+2↑, 1, CLDN1↑, 1, E-cadherin↑, 2, FAK↓, 1, Ki-67↓, 1, miR-200c↑, 1, MMP1↓, 1, MMP2↓, 1, MMP9↓, 2, MMPs↓, 2, RECK↑, 1, Snail↓, 1, TGF-β↓, 1, TIMP1↑, 1, TIMP2↑, 1, TJ↑, 1, TumCI↓, 3, TumCMig↓, 2, TumCP↓, 5, TumMeta↓, 2, UroPA↓, 1, VEGFR1↓, 1, Vim↓, 1, Zeb1↓, 1, ZEB2↓, 1, ZO-1↑, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, EPR↝, 1, HIF-1↓, 1, VEGF↓, 6,
Barriers & Transport(tgid=15) ⓘ
IBI↑, 1, OCLN↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, IL6↓, 1, Imm↑, 1, Inflam↓, 2, M2 MC↓, 1, NF-kB↓, 4, NK cell↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, ChemoSen↑, 4, Dose↝, 7, eff↓, 1, eff↑, 5, Half-Life↓, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↓, 1, GutMicro↑, 1, HER2/EBBR2↓, 1, IL6↓, 1, Ki-67↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, AntiCan⇅, 1, antiNeop↑, 16, AntiTum↑, 1, cardioP↑, 1, chemoP↑, 1, OS↑, 2, Risk↓, 1, toxicity↓, 1, TumVol↓, 1, TumW↓, 1, Weight↑, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 1,
Total Targets: 133
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 4, Catalase↑, 2, GPx↑, 2, GSH↑, 1, GSTs↑, 3, lipid-P↓, 2, ROS↓, 2, ROS↑, 1, SOD↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1,
Cell Death(tgid=5) ⓘ
iNOS↓, 1,
Barriers & Transport(tgid=15) ⓘ
GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, IL6↓, 1, Imm⇅, 1, Inflam↓, 4, TNF-α↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, BioAv↝, 1, Dose↝, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, creat↓, 1, IL6↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
antiNeop↑, 1, cardioP↑, 2, chemoPv↑, 1, hepatoP↑, 1, neuroP↑, 2, Pain↓, 1, toxicity↓, 1, toxicity↑, 1, toxicity↝, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 2, Bacteria↓, 3,
Total Targets: 40
Scientific Paper Hit Count for: antiNeop, antineoplastic
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#:1403 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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