Imm Cancer Research Results
Imm, immunostimulatory: Click to Expand ⟱
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Enhance the immune response in patients.
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Scientific Papers found: Click to Expand⟱
TumCP↓, mechanism of action of celastrol in terms of inhibition of cell proliferation and regulation of the cell cycle, regulation of apoptosis and autophagy, inhibition of cell invasion and metastasis, anti-inflammation, regulation of immunotherapy, and an
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumCI↓,
TumMeta↓,
Imm↝,
angioG↓,
Cyt‑c↑, release of cytochrome c (CytC)
ROS↑, increasing ROS levels, and activating the mitochondrial apoptosis pathway
BAX↑, upregulating the expression of CytC and the pro-apoptotic protein Bax, activating caspase-3 and caspase-9, and leading to the cleavage of PARP
Casp3↑,
Casp9↑,
cl‑PARP↑,
PrxII↓, binds to peroxiredoxin-2 (Prdx2) and inhibits its enzyme activity,
ER Stress↑, resulting in ROS-dependent endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells
mtDam↑,
CHOP/DDIT3↑, celastrol upregulates the expression of CHOP, Bip, XBP1s, and IRE1 proteins,
Inflam↓, Anti-inflammatory properties of celastrol
NF-kB↓, Celastrol additionally obstructed NF-κB and its downstream gene products, such as CXCR4 and MMP9, and reduced serum IL-6 and TNF-α levels to inhibit cell invasion and migration in vivo
CXCR4↓,
MMP9↓,
IL6↓,
TNF-α↓,
HSP90↓, accumulation may be due to the inhibition of HSP90 and the stress response
neuroP↑, Our mass spectrometry research also showed that celastrol directly binds to HSP90 and HSP70, exerting antitumor and neuroprotective effects
STAT3↓, Celastrol exerts anti-tumor activity by inhibiting STAT3
Prx↓, celastrol binds directly to Prdx1, Prdx2, Prdx4, and Prdx6 via active cysteine sites, inhibiting their antioxidant activity without affecting protein expression
HO-1↑, Celastrol also targeted heme oxygenase-1 (HO-1), increasing its expression in activated hematopoietic stem cells
eff↑, Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, an
eff↑, celastrol, when combined with EGFR tyrosine kinase inhibitors (EGFR-TKIs), effectively inhibits the growth and invasion of T790M mutant human lung cancer H1975
BioAv↑, nano-delivery systems present a novel pathway for the development and clinical application of celastrol, potentially overcoming existing limitations and maximizing its therapeutic potential.
toxicity↑, several significant challenges, including its pronounced hepatic and renal toxicity and potential for causing immunosuppression
CardioT↑, celastrol, which includes hepatotoxicity, cardiotoxicity, infertility toxicity, hematopoietic system toxicity and nephrotoxicity.
hepatoP↓,
*Inflam↓, Fucoidan, a sulfated polysaccharide derived from brown seaweeds, exhibits notable anti-inflammatory, antioxidant, and anticancer properties.
*antiOx↑,
AntiCan↑,
BioAv↑, Researchers have explored fucoidan-based nanoparticles to improve its solubility, enhance tumor-targeting efficiency, and expand its therapeutic potential.
Apoptosis↑, fucoidan induces cancer cell apoptosis, suppresses angiogenesis, and modulates immune responses.
angioG↓,
Imm↝,
ChemoSen↑, When combined with chemotherapeutics, siRNA, or immunomodulators, fucoidan nanoparticles exhibit synergistic anticancer effects while minimizing systemic toxicity.
chemoP↑,
antiOx↑, anti-oxidant, antiviral, immunoregulatory, anti-coagulant, anti-thrombotic, anti-lipidemic, anti-diabetic, anti-tumor, anti-metastatic, and anti-angiogenic properties
AntiViral↑,
Imm↝,
*AntiThr↑,
*AntiDiabetic↑,
AntiTum↑,
TumMeta↑,
angioG↓,
Hif1a↓, ↓ HIF-1α and VEGF in hypoxic-like conditions
VEGF↓,
MMPs↓, ↓ MMPs
EMT↓, ↓ EMT (↓ N-cadherin; ↑ E-cadherin)
N-cadherin↓,
E-cadherin↑,
TIMP1↑, ↑ TIMP
PI3K↓, ↓ PI3K/Akt/mTOR
Akt↓,
mTOR↓,
MMP2↓, ↓ MMP-2, 9
ChemoSen↑, available findings indicate that oral intake of fucoidan as dietary supplement in combination with conventional adjuvant chemotherapy can prolong survival time, decrease some adverse effects (e.g., fatigue)
OS↑,
fatigue↓,
CD31/PECAM-1↓, fig 2
angioG↓, HNE exerted anti-angiogenetic effects in HUVEC and anti-proliferative effects in five cancer cell lines
TumCP↓,
*Inflam↓, a broad pharmacological spectrum is ascribed to Christmas rose: anti-bacterial, anti-inflammatory, cholesterol- and blood glucose-lowering, neuroprotective, hepatoprotective and immune-modulating effects.
*Bacteria↓,
*glucose↓,
*neuroP↓,
*hepatoP↓,
*Imm↝,
ChemoSen↑, It enhances the efficacy of chemotherapies, such as cisplatin and paclitaxel, RTK inhibitors, such as cabozantinib and erlotinib, and mAbs, such as cetuximab.
Imm↝, honokiol aids in post-transplant cancer prevention by modulating immune responses, reducing tumor progression, and lowering the required dose of immunosuppressants, such as cyclosporine A and rapamycin.
*hepatoP↑, figure1
*cardioP↑,
*neuroP↑,
*AntiCan↑,
*Inflam↓,
*antiOx↑,
eff↑, By lowering systemic glucose levels, metformin limits the energy supply available to cancer cells, thereby inhibiting their growth and proliferation. Studies have shown that combining metformin with honokiol yields promising synergistic effects.
*TNF-α↓, potent anti-inflammatory properties, contributing to its anti-cancer effects. It inhibits the production of key pro-inflammatory cytokines, including tumor necrosis factor-alpha, IL-1 beta, and IL-6,
*IL1?,
*IL6?,
ICD↑, FDA-approved anti-parasitic drug ivermectin induces immunogenic cancer cell death (ICD) and robust T cell infiltration into breast tumors.
Imm↝, ivermectin also selectively targets immunosuppressive populations including myeloid cells and Tregs, resulting in enhanced Teff/Tregs ratio
eff↑, While neither agent alone showed efficacy in vivo, combination therapy with ivermectin and checkpoint inhibitor anti-PD1 antibody achieved synergy in limiting tumor growth (p = 0.03) and promoted complete responses
TumVol↓, Mean tumor volume over time was significantly decreased by the ivermectin and anti-PD1 antibody combination relative to no treatment
*BioAv↓, pharmacokinetic studies indicate that following oral administration, only a small portion of isovitexin is directly absorbed, while the majority is transferred to the intestine and metabolized by gut microbiota.
*Imm↝, Isovitexin demonstrates diverse biological activities, including immunomodulatory, antioxidant properties, anticancer activity, neuroprotection, regulation of bone homeostasis, and hepatoprotective effects.
*antiOx↑,
*AntiCan↑,
*neuroP↑,
*hepatoP↑,
*Inflam↓, These activities are mediated through multiple mechanisms, including anti-inflammatory effects through inhibition of the Nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase pathways,
*NF-kB↓,
*MAPK↓,
*MPO↓, antioxidant effects by suppression of myeloperoxidase activity and the scavenging of reactive oxygen species (ROS), and anticancer activity by promoting autophagy and apoptosis.
*ROS↓,
TumAuto↑,
Apoptosis↑,
DCells↓, inhibiting the activation of dendritic cells and CD4+ T-cells,
CD4+↓,
OS↑, Oral administration of juglone significantly reduced mortality and morbidity associated with GVHD while maintaining graft-versus-leukaemia activity.
Imm↝, Juglone is a potent immunomodulator for GVHD prophylaxis.
antiNeop↑, Kaempferol (KAE), a natural flavonoid, has emerged as a promising multi-target antineoplastic agent characterized by high efficacy and minimal systemic toxicity.
*toxicity↓,
TumCCA↑, KAE orchestrates tumor eradication by enforcing cell cycle arrest across multiple phases and triggering a complex, interconnected network of programmed cell death.
ROS↑, We highlight how reactive oxygen species and endoplasmic reticulum stress serve as central upstream nodes driving the mechanistic crosstalk among apoptosis, lethal autophagy, gasdermin E-mediated pyroptosis, and ferroptosis.
ER Stress↑,
TumAuto↑,
Pyro↑,
Ferroptosis↑,
angioG↓, KAE actively remodels the tumor microenvironment by inhibiting angiogenesis and repolarizing tumor-associated macrophages, thereby converting immunosuppressive "cold" tumors into immune-active "hot" tumors.
Imm↝,
eff↑, this review introduces the emerging prebiotic-like crosstalk between KAE and the gut microbiome, providing a strong mechanistic rationale for its synergistic application with immune checkpoint inhibitors.
ChemoSen↑, As a potent chemosensitizer, KAE also overcomes multidrug resistance and mitigates chemotherapy-induced toxicities.
MPT↑, This leads to the opening of the mitochondrial permeability transition (MPTP) pore and the collapse of the mitochondrial membrane potential (ΔΨm).
MMP↓,
mtDam↑, damaged mitochondria release pro-apoptotic factors, including cytochrome c, into the cytoplasm, inducing the formation of the apoptosome.
Cyt‑c↑,
Bax:Bcl2↑, upregulation of the Bax/Bcl-2 ratio.
Fas↑, demonstrated that in colorectal cancer models, KAE treatment significantly upregulates the expression of membrane-bound FAS ligand.
DR4↑, KAE directly upregulates the expression of death receptor 4 and death receptor 5 in human ovarian cancer cells (OVCAR-3 and SKOV-3) by activating the JNK/ERK-CHOP signaling pathway.
DR5↑,
JNK↑,
ERK↑,
CHOP/DDIT3↑,
ER Stress↑, Studies have shown that KAE possesses significant ERS-inducing activity, leading to the pathological accumulation of unfolded or misfolded proteins within the endoplasmic reticulum (ER) lumen, which in turn triggers a persistent unfolded protein resp
UPR↑,
Ca+2↑, accumulated cytosolic Ca²+ acts as a central apoptotic signal
PI3K↓, The inhibition of the PI3K/Akt/mTOR pathway is a primary mechanism for this effect.
Akt↓,
mTOR↓,
AMPK↑, Conversely, KAE reactivates the AMPK pathway.
*Ferroptosis↓, KAE acts as a potent antioxidant in normal tissues to prevent ferroptosis-induced injury.
*antiOx↑,
*NRF2↑, KAE effectively suppresses ferroptosis by strongly activating the Nrf2/glutathione peroxidase 4 (GPX4) antioxidant axis.
*GPx4↑,
*ROS↓, It actively reduces intracellular ROS, malondialdehyde, and iron (Fe²+) accumulation while upregulating the protective SLC7A11 transporter
*MDA↓,
*i-Iron↓,
*xCT/SLC7A11↑,
VEGF↓, KAE not only inhibits VEGF expression driven by hypoxia-inducible factor-1α (HIF-1α) but also simultaneously blocks the Wnt/β-catenin signaling pathway and the epithelial-mesenchymal transition (EMT) process
Wnt↓,
β-catenin/ZEB1↓,
EMT↓,
STAT3↓, KAE blocks the persistent activation of the STAT3 signaling pathway, leading to the downregulation of M2 phenotypic markers and the inhibition of the inflammatory chemokine CCL2 release.
M2 MC↓,
MCP1/CCL2↓,
MMP9↓, thereby downregulating the protein expression and enzymatic activity of MMP-9.
MMP2↓, in tongue squamous cell carcinoma models, KAE inhibits the expression of MMP-2 and its tissue inhibitor, TIMP-2, at the transcriptional level
TIMP2↓,
ChemoSen↑, When combined with classical chemotherapeutics, KAE functions as a potent sensitizer, amplifying the lethal effects of the drugs through complementary signaling networks.
PKM2↑, In colorectal cancer cells, KAE promotes the expression of microRNA-326 (miR-326), which directly targets the 3′-UTR of the pyruvate kinase M2 (PKM2) isoform to inhibit glycolysis.
Glycolysis↓,
CSCs↓, profound chemosensitizing effect by downregulating core stemness transcription factors (such as SOX2 and OCT4) and disrupting the CD44-NANOG-MDR1 resistance complex
SOX4↓,
OCT4↓,
CD44↓,
Nanog↓,
MDR1↓,
*GutMicro↑, KAE exerts a remarkable prebiotic-like effect by remodeling the architectural composition of the gut microbiota
GutMicro↑, A key feature of gut dysbiosis in CRC is the enrichment of pathogenic bacteria alongside the depletion of beneficial commensals. Probiotic supplementation has been shown to counteract this imbalance and suppress tumor progression
IBI↑, probiotics suppress CRC development through multifaceted actions, including directly inhibiting tumor cell growth, reducing inflammation, reinforcing the intestinal barrier, and reprogramming host immunity.
TumCG↓,
Inflam↓,
Imm↝,
eff↑, enhance immunotherapy and chemotherapy, thereby offering a complementary paradigm for CRC prevention and treatment.
*other↝, Licorice always functions as an adjuvant drug in traditional Chinese medicine to reduce the toxicity of other medicinal herbs or enhance their pharmacological effects.
*Inflam↓, LA demonstrates various pharmacological properties, including anti-inflammation, antibacterial, antioxidant, anti-parasitic, bone protection, neuroprotection, skin protection, and blood glucose and lipid regulation.
*Bacteria↓,
*antiOx↑,
*AntiP↑,
*neuroP↑,
*glucose↝,
*lipid-P↓,
PKCδ↓, Downregulation of PKCε, p70S6K, and Akt is also described
P70S6K↓,
Akt↓,
ER Stress↑, LA induced ER stress in HepG2 cells to induce apoptosis
Apoptosis↑,
Ca+2↑, enhancing cytosolic Ca2+ release from the ER
PI3K↓, apoptosis of MCF-7 by inhibiting PI3K-Akt-mTOR signaling, thereby increasing caspase-3 activity, decreasing expression of B-cell lymphoma-2, and triggering the release of cytochrome from mitochondria into the cytoplasm
mTOR↓,
Casp3↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑, upregulation of Bax expression and PARP cleavage, downregulation of Bcl-2 and Cyclin D1, and accumulation of reactive oxygen species (ROS)
cl‑PARP↑,
cycD1/CCND1↑,
ROS↑,
CHOP/DDIT3↑, CHOP expression was elevated in parallel
ERK↑, LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner.
p38↑,
JNK↓, LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy
IAP1↓,
XIAP↓,
survivin↓,
cFLIP↓,
RIP1↓,
EGFR↓, promoted the degradation of EGFR, Met, Her2
MET↓,
HER2/EBBR2↓,
p‑4E-BP1↓, LA may inhibit the phosphorylation of 4EBP1 (Ser 65) and activate the PERK-eIF2α pathway to inhibit PD-L1 translation
PERK↑,
eIF2α↑,
PD-L1↓,
HK2↓, Hexokinase 2Â (HK2) expression was downregulated at a lower dose, attenuating glycolysis elevation and inducing apoptosis in MKN-45 and SGC7901 cells
Glycolysis↓,
Sp1/3/4↓, LA induced apoptosis via downregulating the expression of specificity protein 1 (Sp1), upregulating Bax, Bid, Bcl-xl, caspase-3, and PARP cleavage with doses of 10–40 μM
FasL↑, LA induced apoptosis in KB cells, relying on activation of caspase-dependent factor associated suicide ligand (FasL) mediated death receptor pathway.
MMP↓, reducing mitochondrial membrane potential and inhibiting ATP production in vitro
ATP↓,
TumAuto↑, The literature also showed that LA induced apoptosis and autophagy in SiHa
WEE1↑, LA blocked the cell cycle in HepG2 cells by increasing the expression of Weel, P21, Cyclin D1, and JNK1 and decreasing the expression of Survivin, Cyclin B1, and CDK1 using doses of 30–70 μM
P21↑,
CDK1↓,
TumCCA↑,
TumCMig↓, LA exhibited the ability to inhibit migration and invasion of A549 and H460 cells at relatively lower doses (2–20 μM)
TumCI↓,
ABCG2↓, downregulating the expression of breast cancer resistance protein (BCRP)
HSP90↓, LA also reduced Hsp90 activity in gefitinib-resistant NSCLC cells (H1975) via binding to the N-terminal ATP binding site of Hsp90 to reduce drug resistance
T-Cell↑, LA (40 mg/kg) to C3H/HeN mice bearing UM-UC-3 cells enhanced the activity of cytotoxic T lymphocytes and counts of CD4+ CD25+ Foxp3+ T regulatory T cells. Thus, LA might treat bladder cancer by modulating the tumor immune microenvironment
CD4+↑,
CD25+↑,
FOXP3↑,
Imm↝,
*Inflam↓, LA demonstrates anti-inflammatory activity via interaction with MAPK, NF-κB, NLRP3, and Nrf2 signaling in the acute lung, kidney, and liver injury (acute inflammation) and arthritis and asthma
*NF-kB↓,
*NRF2↑,
*AntiArt↑,
Apoptosis↑, 20 Hz; 3 mT, 60mins/day PEMFs increased apoptosis in MCF7 cells but had no effect on MCF10 cells
selectivity↑,
ROS↑, 50 Hz, 0.1–1.0 mT) for 30 min, and long‐term PEMF: undifferentiated PC12 cells increased ROS levels and decreased catalase activity
Catalase↓,
TumVol↓, 1 Hz, 100 mT, Mice exposed for 60 and 180 min daily showed a 30% and 70% tumor reduction
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies
Ca+2↝, During immediate PEMF exposure in undifferentiated PC12 cells, no change in intracellular Ca2+ concentration was observed, while it increased after long‐term exposure.
eff↝, undifferentiated PC12 cells were more sensitive to PEMFs exposure, while the differentiated PC12 cells were more stable and resistant to stress, probably due to the action of the cell surface NGF receptors such as p75NR
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies 95, 96, 97, 98, 99, 104.
Imm↝, PEMFs have also an immunomodulatory effect, as supported by in vivo evidence showing an increase in tumor necrosis factor alpha levels that induce an anti‐tumoral response
TNF-α↑,
Casp8↑, leading to the activation of a proapoptotic pathway induced by caspase‐8 interaction with Fas‐associated death domain,
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
WEE1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↓, 1, Ferroptosis↑, 1, HO-1↑, 1, ICD↑, 1, Prx↓, 1, PrxII↓, 1, ROS↑, 4,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, MMP↓, 2, MPT↑, 1, mtDam↑, 2, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, Glycolysis↓, 2, HK2↓, 1, PKM2↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Apoptosis↑, 5, BAX↑, 2, Bax:Bcl2↑, 1, Bcl-2↓, 1, Casp3↑, 2, Casp8↑, 1, Casp9↑, 1, cFLIP↓, 1, Cyt‑c↑, 3, DR4↑, 1, DR5↑, 1, Fas↑, 1, FasL↑, 1, Ferroptosis↑, 1, IAP1↓, 1, JNK↓, 1, JNK↑, 1, p38↑, 1, Pyro↑, 1, RIP1↓, 1, survivin↓, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1, Sp1/3/4↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 3, eIF2α↑, 1, ER Stress↑, 4, HSP90↓, 2, PERK↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 4,
DNA Damage & Repair(tgid=10) ⓘ
cl‑PARP↑, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, cycD1/CCND1↑, 1, P21↑, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
p‑4E-BP1↓, 1, CD44↓, 1, CSCs↓, 1, EMT↓, 2, ERK↑, 2, mTOR↓, 3, Nanog↓, 1, OCT4↓, 1, P70S6K↓, 1, PI3K↓, 3, STAT3↓, 2, TumCG↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 2, Ca+2↝, 1, CD31/PECAM-1↓, 1, E-cadherin↑, 1, MET↓, 1, MMP2↓, 2, MMP9↓, 2, MMPs↓, 1, N-cadherin↓, 1, PKCδ↓, 1, SOX4↓, 1, TIMP1↑, 1, TIMP2↓, 1, TumCI↓, 2, TumCMig↓, 1, TumCP↓, 2, TumMeta↓, 1, TumMeta↑, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 7, EGFR↓, 1, Hif1a↓, 1, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↓, 1, CD4+↑, 1, CXCR4↓, 1, DCells↓, 1, FOXP3↑, 1, IL6↓, 1, Imm↝, 10, Inflam↓, 2, M2 MC↓, 1, MCP1/CCL2↓, 1, NF-kB↓, 1, PD-L1↓, 1, T-Cell↑, 1, TNF-α↓, 1, TNF-α↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ABCG2↓, 1, BioAv↑, 2, ChemoSen↑, 5, eff↑, 6, eff↝, 1, MDR1↓, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, GutMicro↑, 1, HER2/EBBR2↓, 1, IL6↓, 1, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, antiNeop↑, 1, AntiTum↑, 1, CardioT↑, 1, chemoP↑, 1, fatigue↓, 1, hepatoP↓, 1, neuroP↑, 1, OS↑, 2, toxicity↑, 1, TumVol↓, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1,
Total Targets: 131
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiP↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 5, Ferroptosis↓, 1, GPx4↑, 1, i-Iron↓, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NRF2↑, 2, ROS↓, 2, xCT/SLC7A11↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↓, 1, glucose↝, 1,
Cell Death(tgid=5) ⓘ
Ferroptosis↓, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, other↝, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1?, 1, IL6?, 1, Imm↝, 2, Inflam↓, 6, NF-kB↓, 2, TNF-α↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
GutMicro↑, 1, IL6?, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, AntiDiabetic↑, 1, cardioP↑, 1, hepatoP↓, 1, hepatoP↑, 2, neuroP↓, 1, neuroP↑, 3, toxicity↓, 1,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 2,
Total Targets: 36
Scientific Paper Hit Count for: Imm, immunostimulatory
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
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