NA Cancer Research Results

NA, NA: Click to Expand ⟱
Source: NA
Type: NA
NA
Scientific Papers found: Click to Expand⟱
6323- Eug,    Eugenol: An Insight Into the Anticancer Perspective and Pharmacological Aspects
- Review, Var, NA - Review, Arthritis, NA
*AntiCan↑, (Eug), a volatile phenolic bioactive compound with a formula of C10H12O2, has been reported to have anticancer, antidiabetic, cardio‐ and pulmonary protective roles.
*AntiDiabetic↑,
*cardioP↑, Eugenol has been proven effective in modulating gut microbiota and attenuating adiposity in high‐fat diet‐fed C57BL/6J mice.
*toxicity↝, According to WHO, the safe dose of eugenol is 2.5 mg/kg for consumption
*GutMicro↑,
*neuroP↑, Moreover, it has the ability to improve gut health and prevent neurodegenerative disorders.
*BioAv⇅, Furthermore, multiple carriers like liposomes, glycodendritic polyamine dextran, solid lipid nanoparticles, and corn protein nanoparticles have been reported to deliver eugenol.
*BioAv↝, Eugenol (150 mg) in gelatin capsules was orally administered in healthy adults and absorbed very quickly, and ~55% is eliminated in urine after being transformed to glucuronic acid or eugenol sulfate conjugate in the liver
*antiOx↑, The studies on eugenol have proved its antioxidant and anti‐inflammatory properties.
*Inflam↑,
*AntiArt↑, aMateen et al. (2019) reported that eugenol alleviated arthritis via attenuating pro‐inflammatory cytokines (TNF‐α, IL‐6, IL‐10).
*TNF-α↓,
*IL6↓,
*IL10↓,
*GSH↑, Eugenol (2.5, 5, 10 mg/kg) improved GSH, GPx, and CAT levels while reducing carrageenan‐induced OS in arthritic rats (Adefegha et al. 2019).
*GPx↑,
*Catalase↑,
*MDA↓, reported reduced MDA and improved SOD, CAT, and TAC levels.
*TAC↑,
TumCMig↓, eugenol subdued cell migration and invasion by suppressing angiogenesis‐related protein expression and modulating JAK2/STAT3 pathways.
TumCI↓,
Akt↑, MDA‐MB‐231, SK‐BR‐3 ↑AKT, FOXO3a, Caspase‐3/9, p21
FOXO3↑,
Casp3↑,
Casp9↑,
P21↑,
angioG↓, Eugenol has been reported to reduce angiogenesis, inhibit invasion, and trigger apoptosis
TumCI↓,
Apoptosis↑,
NF-kB↓, GC via apoptosis induction, metastasis inhibition, downregulation of NF‐κB, and angiogenesis reduction is shown in Figure 3
eff↑, eugenol (153 μM) combined with 5‐fluorouracil proved effective in inhibiting cell growth and division in HeLa cells.
eff↑, eugenol (200–350 μM) with sulforaphane (6.5–8 μM) lowered the expressions of COX‐2, IL‐β, and Bcl‐2 and inhibited cell proliferation
ChemoSen↑, co‐treatment of eugenol and cisplatin reduced cell proliferation and induced apoptosis in G361 melanoma cells via inhibited MMP and proteasome activity,
NA↑, Eugenol proved effective in HL‐60 cell lines by inducing ROS‐mediated apoptosis with a 23.7 IC50 value
Casp3↑, eugenol‐induced apoptosis via ROS production and caspase‐9/3 activation.
Casp9↑,
*AntiDiabetic↑, Chilukoti et al. (2024) verified the antidiabetic activity of eugenol in rats.
*glucose↓, eugenol (400 mg/kg) significantly lowered glucose levels, reduced OS and inflammation, inhibited MDA levels, and improved GSH.
*ROS↓,
*Inflam↓,
*MDA↓,
*GSH↑,
*BioAv↑, Multiple delivery systems, such as liposomes, nanoparticles, nanoemulsions, and hydrogels, enhance its bioavailability, controlled release, and targeted delivery, making eugenol more effective for pharmaceutical and biomedical applications.

7599- HPT,  Rad,    Recent development on hyperthermia: An effective cotreatment improving radiotherapy outcome
- Review, Var, NA
NA↑, As an adjunct to radiotherapy and chemotherapy, hyperthermia enhances the therapeutic efficacy against both primary and recurrent tumors.
RadioS↑, The present review explores the mechanisms underlying the synergy between radiotherapy and hyperthermia, while reviewing the outcomes of relevant clinical trials.
DNArepair↓, Key mechanisms of action include inhibition of DNA repair, reduction of hypoxic tumor cell populations, enhancement of drug uptake and improved perfusion and oxygenation.
Hypoxia↓,
EPR↑,
LC↑, Its application has improved both local control and overall survival (OS),
OS↑,
*toxicity↓, Randomized clinical trials (4–6) have demonstrated that combined therapy effectively prolongs disease-free survival and ensures local tumor control without added toxicity.
Dose↝, fever-range temperatures (39–40°C), moderate heating to induce cellular stress (41–43°C) and high-intensity thermal ablation >43°C for cell destruction.
BloodF↑, Hyperthermia is particularly toxic to cells in acidic environments (29), and increased blood flow helps clear acidic metabolites, restore normal extracellular pH
pH↝,
Imm↑, Under heat stress, tumor cells release heat shock protein 70 (HSP70), triggering antitumor immune responses
HSP70/HSPA5↑,

7618- HPT,    ESHO 2-85. Hyperthermia as an adjuvant to radiation therapy in the treatment of advanced neck nodes: A randomized multicenter study by the European Society for Hyperthermic Oncology
ORR↑, complete response rate was 53% in the RT versus 80% in the RT+HT group, and 3-year persistent local control rate was 32% for RT alone versus 53% for RT+HT; HR: 0.48 [0.23–0.98].
NA↑, The ESHO 2–85 study demonstrated that addition of a weekly HT treatment to RT of advanced neck nodes significantly enhanced the persistent tumor control.
NA↑, HT was associated with moderate to severe pain and discomfort in 38% of the treatments.
BioAv↝, The clinical application of heat was (and still is) hampered by the difficulties to provide a homogeneous heating to a given target.
Dose↝, Each heat session should aim for a minimal tumor temperature 60 min at 43.0°C or equivalen
Dose↝, HT was applied with electromagnetic heating.

7770- IBC,    Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction
- in-vitro, Lung, NA - vitro+vivo, BC, 4T1
necrosis↑, Here, we found that IBC induced regulated necrosis in cancer cells.
ROS↑, IBC triggered non-apoptotic cell death in lung and breast cancer cells mediated by reactive oxygen species (ROS).
mtDam↑, IBC caused mitochondrial injury and dysfunction as evidenced by mitochondrial Ca2+ overload, the opening of MPT pore, mitochondrial membrane potential collapse, and structural damages.
Ca+2↑,
NA↑,
MMP↓,
TumCG↓, IBC showed an anticancer effect in a 4T1 breast cancer cell-derived allograft mouse model,

7818- IBC,    Isobavachalcone, a chalcone constituent of Angelica keiskei, induces apoptosis in neuroblastoma
- in-vitro, neuroblastoma, NA
TumCD↑, All chalcones exhibited cytotoxicity against neuroblastoma cells, and two of them (isobavachalcone and xanthoangelol H) had no effect on normal cells even at high concentration (10(-4) M) exposure.
selectivity↑, apoptosis, including cell shrinkage, chromatin condensation, nuclear fragmentation and formation of apoptotic bodies, were observed in isobavachalcone-treated cells
Apoptosis↑,
DNAdam↑,
pro‑Casp3↑, isobavachalcone significantly reduced pro-caspase-3 and pro-caspase-9, and subsequently increased the level of cleaved caspase-3 and cleaved caspase-9 in both neuroblastoma cell lines.
pro‑Casp9↑,
cl‑Casp3↑,
cl‑Casp9↑,
NA↑, Bax was markedly induced by isobavachalcone application.
BAX?,

7768- IBC,    Isobavachalcone Induces ROS-Mediated Apoptosis via Targeting Thioredoxin Reductase 1 in Human Prostate Cancer PC-3 Cells
- in-vitro, NA, PC3
NA↑, In our study, we found that IBC may induce reactive oxygen species- (ROS-) mediated apoptosis via interaction with a selenocysteine (Sec) containing the antioxidant enzyme thioredoxin reductase 1 (TrxR1),
TrxR1↓, and induce lethal endoplasmic reticulum (ER) stress by inhibiting TrxR1 activity and increasing ROS levels in human prostate cancer PC-3 cells.
ER Stress↑,
TumCP↓, IBC Inhibits Proliferation of PC-3 Cells
Apoptosis↑, IBC Induces Apoptosis of PC-3 Cells
GRP78/BiP↑, IBC led to the upregulation of GRP78, ATF4, XBP-1, and Chop mRNA levels in PC-3 cells in a dose-dependent manner
ATF4↑,
XBP-1↑,
CHOP/DDIT3↑,
p‑eIF2α↑, eIF2α levels peaked when treated with 15 μM IBC
eff↓, ROS levels decreased in cells cotreated with NAC and IBC
cl‑Casp3↑, IBC was found to significantly reduce pro-caspase-3 levels with a concurrent increase in cleaved caspase-3 levels in PC-3 cells.

7636- Ins,    Myo-Inositol: Pharmacokinetics, Biological Functions, and Therapeutic Potential in Liver Protection: Insights from Preclinical Models
*glucose↝, Myo-inositol, the most common stereoisomer of inositol, plays an important role in many physiological processes, such as cell signaling, regulation of glucose and lipid metabolism, and protection of cells against oxidative stress.
*lipid-P↓,
*ROS↓,
*BioAv↑, characterized by high oral bioavailability and is primarily eliminated via the kidneys.
*hepatoP↑, Preclinical studies have shown that myo-inositol has hepatoprotective potential, reducing oxidative stress, inflammation, and lipid accumulation in hepatocytes,
*Inflam↓,
*MMP↑, Recent findings suggest that it contributes to the stabilization of mitochondrial membranes and enhances ATP production efficiency,
*ATP↑,
*GutMicro↑, Evidence indicates that myo-inositol may influence intestinal microbiota composition, enhancing populations of beneficial bacterial strains while reducing endotoxemia linked to non-alcoholic fatty liver disease
*Dose↝, a significant portion of the body’s requirement is also supplied by the diet-rich sources, including fruits, whole grains, legumes, and nuts.
*Half-Life↝, Studies on rats has revealed that the highest plasma concentrations were observed within 1–2 h after oral intake, while the half-life ranged from 4 to 8 h.
*BioAv↑, In the case of intravenous administration, higher bioavailability and faster tissue distribution were achieved. intravenous administration of myo-inositol is rare
*eff↑, myo-inositol supplementation may potentially synergize with antioxidants (e.g., vitamin E, curcumin), enhancing their protective effects on the liver and other organs exposed to oxidative stress
*hepatoP↑, Myo-inositol may exert hepatoprotective effects through several biological mechanisms. A key role is played by its involvement in lipid metabolism regulation, modulation of oxidative stress, and influence on insulin signaling.
*SOD↑, Moreover, myo-inositol and its derivatives (including D-chiro-inositol) affect the activation of antioxidant enzymes such as superoxide dismutase (SOD) and catalase, thereby limiting oxidative damage to hepatocytes
*Catalase↑,
*Casp3↓, inhibit the expression of apoptosis markers such as caspase-3,
*ALAT↓, decreased activity of transaminases (ALT, AST).
*AST↓,
*AMPK↑, regulation of lipid metabolism through the activation of AMP-activated protein kinase (AMPK) and downregulation of sterol regulatory element-binding proteins (SREBPs).
*SREBP1/SREBF1↑,
*NA↑,

7856- isoO,    Isoorientin induces the apoptosis and cell cycle arrest of A549 human lung cancer cells via the ROS‑regulated MAPK, STAT3 and NF‑κB signaling pathways
- in-vitro, Lung, A549
Bacteria↓, Isoorientin (ISO) is a naturally occurring C‑glycosyl flavone that has various pharmacological properties, such as anti‑bacterial and anti‑inflammatory effects
Inflam↓,
TumCD↑, ISO exerted significant cytotoxic effects on 3 lung cancer cell lines, but had no obvious side‑effects on normal cells.
selectivity↑,
Apoptosis↑, ISO induced mitochondrial‑dependent apoptosis by reducing mitochondrial membrane potential
MMP↓,
BAX↑, ISO also increased the expression levels of Bax, cleaved‑caspase‑3 (cle‑cas‑3) and poly(ADP‑ribose) polymerase (PARP; cle‑PARP), and decreased the expression levels of Bcl‑2 in A549 cells.
cl‑Casp3↑,
PARP↓,
Bcl-2↓,
TumCCA↑, ISO induced G2/M cell cycle arrest by decreasing the expression levels of cyclin B1 and CDK1/2, and increasing the expression levels of p21 and p27 in A549 cells.
CycB/CCNB1↓,
CDK1↓,
CDK2↓,
NA↑,
p27/CDKN1B↑,
ROS↑, As the duration of ISO treatment increased, intracellular reactive oxygen species (ROS) levels in A549 cells also increased.
eff↓, pre‑treatment of the cells with the ROS scavenger, N‑acetylcysteine (NAC), inhibited ISO‑induced apoptosis.
p‑p38↑, ISO increased the expression levels of p‑p38, p‑JNK and IκB‑α; and decreased the expression levels of p‑extracellular signal‑regulated kinase (ERK), p‑signal transducer and activator of transcription (STAT)3, (NF)‑κB
p‑JNK↑,
ERK↓,
STAT3↓,
NF-kB↓,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

LC↑, 1,   NA↑, 8,   ORR↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,   TrxR1↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   mtDam↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↑, 4,   BAX?, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 2,   cl‑Casp3↑, 3,   pro‑Casp3↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   pro‑Casp9↑, 1,   p‑JNK↑, 1,   necrosis↑, 1,   p27/CDKN1B↑, 1,   p‑p38↑, 1,   TumCD↑, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↑, 1,   XBP-1↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   DNArepair↓, 1,   PARP↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   FOXO3↑, 1,   STAT3↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   ATF4↑, 1,   EPR↑, 1,   Hypoxia↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   Dose↝, 3,   eff↓, 2,   eff↑, 2,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,  

Functional Outcomes(tgid=23) ⓘ

OS↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx↑, 1,   GSH↑, 2,   lipid-P↓, 1,   MDA↓, 2,   ROS↓, 2,   SOD↑, 1,   TAC↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,   glucose↓, 1,   glucose↝, 1,   SREBP1/SREBF1↑, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL10↓, 1,   IL6↓, 1,   Inflam↓, 2,   Inflam↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 3,   BioAv⇅, 1,   BioAv↝, 1,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   GutMicro↑, 2,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 2,   cardioP↑, 1,   hepatoP↑, 2,   neuroP↑, 1,   toxicity↓, 1,   toxicity↝, 1,  
Total Targets: 41

Scientific Paper Hit Count for: NA, NA
3 Isobavachalcone
2 Hyperthermia
1 Eugenol
1 Radiotherapy/Radiation
1 Inositol
1 isoorientin
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#:0  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page