CD4+ Cancer Research Results

CD4+, CD4+ T Cells: Click to Expand ⟱
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CD4+ T cells are T lymphocytes that express T cell receptors (TCRs).
Majority of cancer immunotherapies focus on harnessing the anti-tumour CD8+ cytotoxic T cell response, the potential role of CD4+ ‘helper’ T cells has largely remained in the background. multifaceted role of CD4+ T cells in the anti-tumour immune response.
CD4+ T cells play a critical role in developing and sustaining effective anti-tumour immunity, even in cancer immunotherapies specifically designed to activate a CD8+ CTL response.
Scientific Papers found: Click to Expand⟱
346- AgNPs,  RSQ,    Investigating Silver Nanoparticles and Resiquimod as a Local Melanoma Treatment
- in-vivo, Melanoma, SK-MEL-28 - in-vivo, Melanoma, WM35
ROS↑,
Ca+2↝, disrupt mitochondrial homeostasis of Ca2+
Casp3↑, x2-4
Casp8↑, x2-4
Casp9↑, x4-14
CD4+↑,
CD8+↑,
tumCV↓,
eff↓, NAC, an ROS scavenger, could efficiently protect B16.F10 cells from the cytotoxic effects of Ag+ even when exposed to high concentrations of Ag+ (250 μg/ml)
*toxicity↓, non-toxic in mice as evidenced by: 1) no significant change in weights during the study period and 2) no significant increases in the levels of liver enzymes, (ALP), (AST), and ALT

542- Akk,  immuno,    Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors
CD4+↑,
CXCc↑, CXCR3+
PD-1↝, restored the efficacy of PD-1 blockade

7399- Amla,    Molecular Mechanisms of Cancer Prevention by Gooseberry (Phyllanthus emblica)
- Review, Var, NA
*Dose↝, P. emblica fruit is the second richest known source of vitamin C (4), as well as having high levels of tannins, alkaloids, polyphenols, vitamins, and minerals. P. emblica contains several biologically-active antioxidant polyphenols, including gallic
*Inflam↓, gooseberry constituents possess anti-inflammatory, anticancer, anti-microbial, and anti-oxidant effects which protect against neurological disorders, have hepatoprotective and cardioprotective activities, and are cancer-preventive
*AntiCan↑,
*antiOx↑,
*neuroP↑,
*hepatoP↑,
*cardioP↑,
*P450↓, via inhibition of cytochrome P450 (CYP450) isozymes
*SOD↑, figure 3
*GPx↑,
*Catalase↑,
*ROS↓,
*CD4+↑,
*CD19↑,
*NK cell↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
Fas↑,
BAX↑,
Bcl-2↓,
*IL10↑,
*TNF-α↓,
*IL6↓,
*iNOS↓,
*COX2/PTGS2↓,
*GSTs↑,
*NF-kB↓,
*AP-1↓,
*cJun↓,
*lipid-P↓, P. emblica extracts scavenge free radicals, protect against lipid peroxidation, and thus may play a role in preventing diseases associated with oxidative stress, including cancer.
TumCG↓, P. emblica extract (50–100 μg/ml) significantly inhibits the cell growth of human colorectal (SW620), lung (A549), breast (MDA-MB-231), cervical (HeLa), ovarian (SK-OV3), and liver (HepG2) cancer cell lines
DNAdam↑, apoptosis was induced by triggering of DNA fragmentation, caspase-3, −7, and −8 activity, and Fas protein expression
TumCCA↑, inducing G2/M phase cell cycle arrest and promoting apoptosis via increasing expression of Fas, FasL, and cleaved caspase-8
MMP2↓, P. emblica extract (1–3 µg/ml) decreases the expression of both MMP2 and MMP9 in human fibrosarcoma (HT1080) cells,
MMP9↓,

315- Api,    Apigenin: Selective CK2 inhibitor increases Ikaros expression and improves T cell homeostasis and function in murine pancreatic cancer
- vitro+vivo, PC, Panc02
CK2↓, Apigenin: Selective CK2 inhibitor
CD4+↑,
CD8+↑,
Ikaros↑, (API) stabilized Ikaros expression and prevented Ikaros downregulation

6542- BSB,    Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol
- Review, Var, NA - Review, Park, NA - Review, AD, NA
AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2/PTGS2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE/β-secretase↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2/PTGS2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2/PTGS2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

1205- Caff,  immuno,    Caffeine-enhanced anti-tumor activity of anti-PD1 monoclonal antibody
- in-vivo, Melanoma, B16-F10
OS↑,
CD4+↑, increase in infiltration of CD4+ and CD8+ T lymphocytes into the B16F10 melanoma tumors.
CD8+↑,
AntiTum↑,
TNF-α↑, increased intra-tumoral TNF-α and IFN-γ levels
IFN-γ↑, increased intra-tumoral TNF-α and IFN-γ levels

6030- CGA,    Chlorogenic acid induces apoptosis, inhibits metastasis and improves antitumor immunity in breast cancer via the NF‑κB signaling pathway
- vitro+vivo, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-453 - in-vitro, Nor, MCF10
NF-kB↓, reported that chlorogenic acid (CGA), a potent NF‑κB inhibitor derived from coffee, exerted antitumor activity in breast cancer.
AntiTum↑,
tumCV↓, CGA inhibited viability and proliferation in breast cancer cells.
TumCP↓,
Apoptosis↑, CGA significantly induced apoptosis and suppressed migration and invasion in breast cancer cells.
TumCMig↓,
TumCI↓,
EMT↓, CGA markedly impaired the NF‑κB and EMT signaling pathways.
TumCG↓, results revealed that CGA markedly retarded tumor growth and prolonged the survival rate of tumor‑bearing mice.
OS↑,
TumMeta↓, GA inhibited pulmonary metastasis of 4T1 cells by enhancing the proportion of CD4+ and CD8+ T cells in spleens of mice, which indicated an improvement of antitumor immunity.
CD4+↑,
CD8+↑,
Imm↑, CGA suppresses the pulmonary metastasis of breast cancer by enhancing antitumor immunity

1033- CHr,    Chrysin inhibits hepatocellular carcinoma progression through suppressing programmed death ligand 1 expression
- vitro+vivo, HCC, NA
TumCG↓,
CD4+↑, enhanced CD4/CD8-
CD8+↑, enhanced CD4/CD8-
PD-L1↓, chrysin significantly down-regulated the expression of PD-L1 in vivo and in vitro

6715- dietF,    Are Fermented Foods Effective against Inflammatory Diseases?
- Review, Nor, NA
*Imm↑, Fermented foods containing probiotic bacteria and fungi can enhance the immune system, improve gastrointestinal health, and lower the risk of developing various inflammatory diseases.
*GastroP↑,
*Inflam↓,
AntiCan↑, Kombucha tea possesses anticancer, antimicrobial, and hepatoprotective properties
*AntiBio↑,
*hepatoP↑,
*CD4+↑, Kombucha consumption also reduced inflammation by increasing polarization of CD4+ T cells (by induction of IL-4 and TGF-β) and by inhibiting IFN-γ and IL-17
*IFN-γ↓,
*IL17↓,
*GutMicro↑, Kombucha intake also promoted the growth of butyrate-producing bacteria in the gut that exert anti-inflammatory effects
*antiOx↑, fermented turmeric demonstrated stronger antioxidative activity than raw turmeric.
*AST↓, After 5 days of fermentation with Bacillus natto, fermented turmeric dramatically decreased the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in contrast to unfermented turmeric.
*ALAT↓,
*HDL↑, After fermentation, there was a considerable rise in HDL cholesterol and a significant decrease in LDL cholesterol [45].
*LDL↓,
*ROS↓, Kimchi has also demonstrated potent radical scavenging and antioxidant activity in vitro, enhancing LLC-PK1 cell viability by protection against lipid peroxidation.
*lipid-P↓,
*Inflam↓, The anti-inflammatory properties of sauerkraut LAB were emphasized in a randomized, double-blinded pilot study on 34 Norwegian inflammatory bowel syndrome (IBS) patients.
*Aβ↓, Mice fed with doenjang-infused high-fat feed had reduced β-amyloid peptide (Aβ) and neuroinflammatory gene levels, further reinforcing the protective effect of fermented soy on the aging brain

6609- Ech,  Cic,    Echinacea purpurea Extract Enhances Natural Killer Cell Activity In Vivo by Upregulating MHC II and Th1-type CD4+ T Cell Responses
- in-vivo, Nor, NA
*Dose↝, We detected chicoric acid, the active substance of E, through high-performance liquid chromatography
*CD4+↑, Oral E intake increased levels of MHC II, CD4+ T cells, Th1 cytokines, and NK cell activity.
*Th1 response↑,
*NK cell↑,
*Imm↑, E treatment increased B cell proliferation, leukocyte counts, and immunoglobulin levels.

1959- GamB,    Gambogic acid induces GSDME dependent pyroptotic signaling pathway via ROS/P53/Mitochondria/Caspase-3 in ovarian cancer cells
- in-vitro, Ovarian, NA - in-vivo, NA, NA
AntiCan↑, Gambogic acid (GA) is a naturally active compound extracted from the Garcinia hanburyi with various anticancer activities.
Pyro↑, This study revealed that GA treatment reduced cell viability by inducing pyroptosis in OC cell lines
tumCV?,
CellMemb↓, loss of cell membrane integrity
cl‑Casp3↑, Cleaved caspase-3 and GSDME-N levels increased after GA treatment
GSDME-N↑,
ROS?, GA significantly increased reactive oxygen species (ROS) and p53 phosphorylation.
p‑P53↑,
eff↓, OC cells pretreated with ROS inhibitor N-Acetylcysteine (NAC) and the specific p53 inhibitor pifithrin-μ could completely reverse the pyroptosis post-treatment.
MMP↓, Elevated p53 and phosphorylated p53 reduced mitochondrial membrane potential (MMP) and Bcl-2
Bcl-2↓,
BAX↑,
mtDam↑, damage mitochondria by releasing cytochrome c to activate the downstream pyroptosis pathway
Cyt‑c↑,
TumCG↓, inhibited tumor growth in ID8 tumor-bearing mice
CD4+↑, high-dose GA increased in tumor-infiltrating lymphocytes CD3, CD4, and CD8 were detected in tumor tissues
CD8+↑,

7482- H2,    Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA - Review, Sepsis, NA - Review, AD, NA
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.

7489- H2,    Molecular Hydrogen in the Treatment of Respiratory Diseases
- Review, Asthma, NA
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

2518- H2,    Hydrogen Therapy Reverses Cancer-Associated Fibroblasts Phenotypes and Remodels Stromal Microenvironment to Stimulate Systematic Anti-Tumor Immunity
- in-vitro, BC, 4T1 - in-vitro, Nor, 3T3
TumCD↑, CaCO3 can not only directly kill tumor cells
CD4+↑, augment immune activities of CD4+ T cells
ROS↓, results indicated that hydrogen therapy by Mg-CaCO3 could decrease MMP and alleviate ROS within CAFs

1021- HNK,    Honokiol suppress the PD-L1 expression to improve anti-tumor immunity in lung cancer
- in-vivo, Lung, NA
PD-L1↓, in cells with high PD-L1 expression
T-Cell↑, facilitates T cell killing of tumor cells
CD4+↑,
CD8+↑,
TumCG↓, mice

7652- IP,    Inulin prebiotic reinforces host cancer immunosurveillance via ɣδ T cell activation
- in-vivo, Melanoma, B16-F10
GutMicro↑, Inulin-enriched diet alters the gut microbiota and promotes Bifidobacterium growth
Imm↑, Here, we show that an inulin-enriched diet, a prebiotic known to promote immunostimulatory bacteria, triggers an enhanced Th1-polarized CD4+ and CD8+ αβ T cell-mediated anti-tumor response and attenuates tumor growth in three preclinical tumor-bear
CD4+↑,
CD8+↑,
TumCG↓,

7667- IP,  H2,    Molecular hydrogen as a potential mediator of the antitumor effect of inulin consumption
*AntiTum↑, Inulin consumption and dihydrogen (H2) administration both exert antitumor effects on preclinical models as well as in clinical trials
*other↑, As H2 is one of the major byproducts of inulin fermentation by bacterial species of the gut microbiota (GM), we hypothesized that H2 could mediate the antitumor effects of inulin.
*NA↝, compared the effects on circulating immunity of a two-week daily inulin gavage with those of the corresponding H2T.
*CD4+↑, Inulin and H2T induced a similar increase in circulating CD4+ and CD8+ T cells.
*CD8+↑,
TumCG↓, both treatments similarly inhibited melanoma tumor growth
Imm↑, results support a mechanism by which the H2 resulting from inulin fermentation by the GM diffuses across the intestinal barrier and stimulates the immunosurveillance responsible for the antitumor effect.

1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27/CDKN1B↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2/PTGS2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated

228- MFrot,  MF,    Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
- NA, MS, NA
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1/CCL2↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α/CCL3↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.

221- MFrot,  MF,    Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular Carcinoma
- in-vivo, Liver, NA
OS↑,
TumCG↓, inhibit
IL6↓,
GM-CSF↓,
CXCc↓, keratinocyte-derived chemokine (KC)
Macrophages↑,
DCells↑,
CD4+↑,
CD8+↑,
IL12↑,

220- MFrot,  MF,    Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation
- in-vitro, Melanoma, B16-F10
OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,

198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

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


Showing Research Papers: 1 to 23 of 23

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 23

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CD47↓, 1,   miR-124-3p↓, 1,   PFS↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS?, 1,   ROS↓, 1,   ROS↑, 4,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ikaros↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ETC↓, 1,   MMP↓, 2,   mtDam↑, 1,   PGC-1α↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   CAIX↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PKM2↓, 1,   SCD1↓, 1,   Warburg↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   Apoptosis↑, 5,   Bak↓, 1,   BAX↑, 4,   Bcl-2↓, 4,   BID↑, 1,   Casp3↑, 6,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 3,   Casp9↑, 4,   CK2↓, 1,   Cyt‑c↑, 2,   Fas↑, 2,   GSDME-N↑, 1,   IAP2/BIRC3↓, 1,   JNK↑, 1,   MAPK↑, 1,   p27/CDKN1B↑, 1,   Pyro↑, 1,   TumCD↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

BowelM↑, 1,   ChrMod↑, 2,   EZH2↓, 1,   tumCV?, 1,   tumCV↓, 3,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   DNArepair↑, 1,   P53↑, 2,   p‑P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 5,  

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

EMT↓, 1,   FGF↓, 1,   IGF-1R↓, 1,   PI3K↓, 2,   PTEN↑, 1,   STAT3↓, 1,   TumCG↓, 10,   TumCG↑, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   Ca+2↝, 1,   CEA↓, 1,   CXCL12↓, 1,   E-cadherin↑, 1,   MALAT1↓, 1,   MMP13↓, 1,   MMP2↓, 2,   MMP9↓, 2,   TIMP2↑, 1,   Treg lymp↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 3,   TumMeta↑, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↑, 1,   Hif1a↓, 2,   NO↓, 1,   VEGF↓, 2,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↓, 1,   GLUT1↓, 1,   GLUT1↑, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 15,   COX2/PTGS2↓, 2,   CXCc↓, 1,   CXCc↑, 1,   CXCL9↓, 1,   DCells↑, 3,   FOXP3↓, 1,   GM-CSF↓, 1,   IFN-γ↓, 1,   IFN-γ↑, 1,   IL1↑, 1,   IL10↑, 1,   IL12↑, 1,   IL6↓, 3,   IL8↓, 1,   Imm↑, 4,   Macrophages↑, 1,   NF-kB↓, 3,   NF-kB↑, 1,   NK cell↑, 2,   PD-1↝, 1,   PD-L1↓, 3,   RANTES↓, 1,   T-Cell↑, 3,   Th1 response↑, 1,   TNF-α↑, 2,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,   RANKL↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 3,   Dose↝, 2,   Dose∅, 1,   eff↓, 2,   eff↑, 4,   RadioS↑, 2,   selectivity↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

CEA↓, 1,   EGFR↑, 1,   EZH2↓, 1,   GutMicro↑, 1,   HER2/EBBR2↓, 1,   IL6↓, 3,   PD-L1↓, 3,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 5,   AntiTum↑, 2,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 3,   ChemoSideEff↓, 1,   hepatoP↑, 1,   NP/CIPN↓, 1,   OS↑, 5,   OS⇅, 1,   Pain↓, 2,   QoL↑, 3,   radioP↑, 4,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   TumVol↓, 2,   TumW↓, 1,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 14,  
Total Targets: 156

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 3,   CD19↑, 1,   compII↑, 1,   NA↝, 1,   SpO2↑, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 5,   Catalase↑, 6,   Fenton↓, 1,   GPx↑, 3,   GSH↑, 3,   GSTs↑, 1,   HDL↑, 1,   HO-1↑, 2,   Keap1↑, 1,   lipid-P↓, 4,   MDA↓, 3,   MPO↓, 2,   NOX4↓, 1,   NRF2↑, 2,   RNS↓, 1,   ROS↓, 6,   SOD↑, 6,   TBARS↓, 2,   uricA↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2,   compIII↑, 1,   MMP↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   AMPK↑, 1,   LDL↓, 2,   NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   Apoptosis↓, 2,   BAX↓, 1,   Bcl-2↑, 2,   Bcl-xL↑, 1,   Casp12↓, 1,   Casp3↓, 2,   Casp9↓, 1,   Cyt‑c↓, 1,   GranB/GZMB↓, 1,   iNOS↓, 3,   p‑JNK↓, 1,   p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   other↑, 2,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

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

mTOR↓, 2,   PI3K↑, 2,   STAT3↑, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   APP↓, 1,   MMP13↓, 1,   TGF-β↑, 1,   Treg lymp↓, 1,   Treg lymp↝, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   β-Endo↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GastroP↑, 2,   IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 8,   COX2/PTGS2↓, 3,   CXCc↓, 1,   FOXP3↑, 1,   HMGB1↓, 1,   IFN-γ↓, 3,   IL10↑, 3,   IL17↓, 2,   IL1β↓, 3,   IL4↓, 1,   IL4↑, 1,   IL6↓, 4,   IL6↑, 1,   Imm↑, 4,   Inflam↓, 6,   JAK2↑, 1,   LPS↓, 1,   M2 MC↑, 1,   MCP1/CCL2↓, 2,   MIP‑1α/CCL3↓, 1,   NF-kB↓, 2,   NK cell↑, 2,   PGE2↓, 1,   Th1 response↑, 1,   TNF-α↓, 5,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   AChE↓, 1,   BChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 3,   BACE/β-secretase↓, 2,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   BioAv↝, 1,   Dose↓, 1,   Dose↑, 1,   Dose↝, 5,   eff↑, 3,   P450↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 2,   BMD↑, 1,   creat↓, 2,   GutMicro↑, 2,   IL6↓, 4,   IL6↑, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   antiPs↑, 1,   AntiTum↑, 1,   cardioP↑, 4,   cognitive↑, 1,   hepatoP↑, 4,   motorD↑, 1,   neuroP↑, 4,   Obesity↓, 1,   OS↑, 2,   Pain↓, 1,   RenoP↑, 2,   toxicity↓, 2,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   CD8+↑, 2,   Sepsis↓, 1,  
Total Targets: 141

Scientific Paper Hit Count for: CD4+, CD4+ T Cells
4 Hydrogen Gas
4 Magnetic Field Rotating
4 Magnetic Fields
2 immunotherapy
2 Inulin Prebiotic
1 Silver-NanoParticles
1 Resiquimod
1 Akkermansia
1 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
1 Apigenin (mainly Parsley)
1 α-Bisabolol / Chamomile oil
1 Caffeine
1 Chlorogenic acid
1 Chrysin
1 diet Fermented Foods
1 Echinacea
1 Cichoric acid / Chicoric acid
1 Gambogic Acid
1 Honokiol
1 Melatonin
1 Vitamin C (Ascorbic Acid)
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#:544  State#:%  Dir#:2
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