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.
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Scientific Papers found: Click to Expand⟱
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in-vivo, |
Melanoma, |
SK-MEL-28 |
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in-vivo, |
Melanoma, |
WM35 |
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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
CD4+↑,
CXCc↑, CXCR3+
PD-1↝, restored the efficacy of PD-1 blockade
CK2↓, Apigenin: Selective CK2 inhibitor
CD4+↑,
CD8+↑,
Ikaros↑, (API) stabilized Ikaros expression and prevented Ikaros downregulation
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Review, |
Var, |
NA |
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Review, |
Park, |
NA |
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Review, |
AD, |
NA |
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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↓,
*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↓, 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↓,
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↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,
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in-vivo, |
Melanoma, |
B16-F10 |
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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
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vitro+vivo, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
MDA-MB-453 |
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in-vitro, |
Nor, |
MCF10 |
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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
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
*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
*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.
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in-vitro, |
Ovarian, |
NA |
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in-vivo, |
NA, |
NA |
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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+↑,
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in-vitro, |
BC, |
4T1 |
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in-vitro, |
Nor, |
3T3 |
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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
PD-L1↓, in cells with high PD-L1 expression
T-Cell↑, facilitates T cell killing of tumor cells
CD4+↑,
CD8+↑,
TumCG↓, mice
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↑,
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↓,
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
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α↓,
*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.
OS↑,
TumCG↓, inhibit
IL6↓,
GM-CSF↓,
CXCc↓, keratinocyte-derived chemokine (KC)
Macrophages↑,
DCells↑,
CD4+↑,
CD8+↑,
IL12↑,
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in-vitro, |
Melanoma, |
B16-F10 |
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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+↑,
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 signicant 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 signicantly 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↓,
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 18 of 18
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
ROS?, 1, ROS↓, 1, ROS↑, 3,
Metal & Cofactor Biology(tgid=2) ⓘ
Ikaros↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ETC↓, 1, MMP↓, 2, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, CAIX↑, 1, Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, PKM2↓, 1, Warburg↓, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Apoptosis↑, 4, Bak↓, 1, BAX↑, 3, Bcl-2↓, 3, BID↑, 1, Casp3↑, 4, cl‑Casp3↑, 1, Casp8↑, 2, Casp9↑, 3, CK2↓, 1, Cyt‑c↑, 2, Fas↑, 1, GSDME-N↑, 1, JNK↑, 1, MAPK↑, 1, p27↑, 1, Pyro↑, 1, TumCD↑, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
BowelM↑, 1, ChrMod↑, 2, tumCV?, 1, tumCV↓, 3,
DNA Damage & Repair(tgid=10) ⓘ
DNArepair↑, 1, P53↑, 2, p‑P53↑, 1, PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 2, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, FGF↓, 1, IGF-1R↓, 1, PI3K↓, 1, PTEN↑, 1, STAT3↓, 1, TumCG↓, 7, TumCG↑, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 1, Ca+2↝, 1, CEA↓, 1, CXCL12↓, 1, E-cadherin↑, 1, MMP13↓, 1, MMP2↓, 1, MMP9↓, 1, TIMP2↑, 1, Treg lymp↓, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 3, TumMeta↓, 3, TumMeta↑, 1, Vim↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
EGFR↑, 1, Hif1a↓, 1, NO↓, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
CellMemb↓, 1, GLUT1↓, 1, GLUT1↑, 1, GLUT3↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 14, COX2↓, 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↑, 2, Macrophages↑, 1, NF-kB↓, 3, NF-kB↑, 1, NK cell↑, 1, PD-1↝, 1, PD-L1↓, 3, RANTES↓, 1, T-Cell↑, 3, Th1 response↑, 1, TNF-α↑, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
RANKL↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, ChemoSen↑, 1, Dose∅, 1, eff↓, 2, eff↑, 2, RadioS↑, 2, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
CEA↓, 1, EGFR↑, 1, HER2/EBBR2↓, 1, IL6↓, 3, PD-L1↓, 3,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 5, AntiTum↑, 2, Appetite↑, 1, breath↑, 1, chemoP↑, 1, ChemoSideEff↓, 1, hepatoP↑, 1, OS↑, 5, OS⇅, 1, Pain↓, 2, QoL↑, 1, radioP↑, 2, Sleep↑, 1, Strength↑, 2, toxicity↓, 1, Weight↑, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 11,
Total Targets: 136
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 3,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, Catalase↑, 3, GPx↑, 1, GSH↑, 3, HDL↑, 1, Keap1↑, 1, lipid-P↓, 2, MDA↓, 1, ROS↓, 3, SOD↑, 3, TBARS↓, 1, uricA↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, AMPK↑, 1, LDL↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Cyt‑c↓, 1, iNOS↓, 2,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTOR↓, 1,
Migration(tgid=13) ⓘ
MMP13↓, 1, Treg lymp↓, 1, β-Endo↑, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, GastroP↑, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 4, COX2↓, 2, CXCc↓, 1, IFN-γ↓, 2, IL17↓, 2, IL1β↓, 1, IL6↓, 1, IL6↑, 1, Imm↑, 3, Inflam↓, 3, MCP1↓, 1, MIP‑1α↓, 1, NK cell↑, 1, Th1 response↑, 1, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↓, 1, AChE↓, 1, BChE↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, BACE↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, Dose↝, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BMD↑, 1, creat↓, 1, GutMicro↑, 1, IL6↓, 1, IL6↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, cardioP↑, 2, hepatoP↑, 1, motorD↑, 1, neuroP↑, 1, OS↑, 1, Pain↓, 1, RenoP↑, 1, toxicity↓, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, CD8+↑, 1,
Total Targets: 73
Scientific Paper Hit Count for: CD4+, CD4+ T Cells
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
wNotes=on sortOrder:rid,rpid
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