T-Cell Cancer Research Results

T-Cell, T lymphocytes: Click to Expand ⟱

Source:

Type: white blood cell

T cells are white blood cells that play a central role in the adaptive immune response.
Subsets and Function:
Cytotoxic T Cells (CD8+): Recognize and kill infected or malignant cells.
Helper T Cells (CD4+): Assist in orchestrating the immune response by secreting cytokines and supporting the functions of other immune cells.
T cells, particularly CD8+ cytotoxic T cells, can recognize tumor antigens presented on major histocompatibility complex (MHC) molecules and directly kill malignant cells.
Regulatory T Cells (Tregs): Maintain immune tolerance and prevent autoimmunity but may also suppress anti-tumor responses in the tumor microenvironment.
Tumor-Infiltrating Lymphocytes (TILs):
Tumor Microenvironment:
The presence of T cells within tumors, often referred to as tumor-infiltrating lymphocytes, is a key indicator of an ongoing anti-tumor immune response.
Regulatory T Cells (Tregs):
Tregs within the tumor environment may inhibit the activity of cytotoxic T cells through the secretion of immunosuppressive cytokines (e.g., IL-10, TGF-β), thus allowing tumors to evade the immune response.

In many cancers, a robust T cell infiltrate is correlated with a better overall survival, lower rates of relapse, and improved responses to therapy.
Assessing the type, density, and activation state of T cells in the tumor microenvironment can provide valuable prognostic information. High levels of active, cytotoxic T cells generally indicate a better prognosis.

Scientific Papers found: Click to Expand⟱

1024-

Api,

CUR,

Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects

vitro+vivo,

Melanoma,

A375

 (30 μM) for 24 h

in-vitro,

Melanoma,

A2058

in-vitro,

Melanoma,

RPMI-7951

TumCG↓,
Apoptosis↑,
PD-L1↓, IFN-γ-induced PD-L1 upregulation was significantly inhibited by flavonoids, especially apigenin
STAT1↓,
tumCV↓,
T-Cell↑, Curcumin and apigenin enhance T cell-mediated melanoma cell killing

1029-

Ba,

BA,

Baicalein and baicalin promote antitumor immunity by suppressing PD-L1 expression in hepatocellular carcinoma cells

vitro+vivo,

HCC,

PD-L1↓, PD-L1 upregulation induced by interferon-γ (IFN-γ) was significantly inhibited by these two flavonoids in vitro
T-Cell↑, Both baicalein and baicalin enhanced the cytotoxicity of T cells to eliminate tumor cells
STAT3↓,

1244-

CGA,

immuno,

Cancer Differentiation Inducer Chlorogenic Acid Suppresses PD-L1 Expression and Boosts Antitumor Immunity of PD-1 Antibody

in-vivo,

NA,

murine tumor xenografts

PD-L1↓,
T-Cell↑,
eff↑, boosting the antitumor effect of the anti-PD-1 antibody.

1574-

Citrate,

Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway

in-vitro,

Lung,

A549

5,10,15mM

in-vitro,

Melanoma,

WM983B

in-vivo,

NA,

4 g/kg citrate twice a day for 4 week

mice. Plasma levels in chronically treated animals were approximately 3 mM

TumCG↓,
eff↑, additional benefit accrued in combination with cisplatin
T-Cell↑, significantly higher infiltrating T-cells
p‑IGF-1R↓, citrate inhibited IGF-1R phosphorylation
p‑Akt↓, inhibited AKT phosphorylation
PTEN↑, activated PTEN
p‑eIF2α↑, increased expression of p-eIF2a p-eIF2a was decreased when PTEN was depleted
OCR↓, citrate treatment of A549 cells dramatically reduced oxygen consumption
ROS↓, observed a decrease in ROS in A549
ECAR∅, acidification rate (ECAR) and found it to be unchanged
IL1↑, s (e.g. interleukin-1, tumor necrosis factor-alpha, etc) and anti-inflammatory cytokines (e.g. interleukin-10 and interleukin 1 receptor antagonist) are activated
TNF-α↑,
IL10↑,
IGF-1R↓, Citrate Inhibits IGF-1R Activation And Its Downstream Pathway
eIF2α↑, eIF2α activity was increased in A549 cells after citrate treatment
PTEN↑, PTEN was activated
TCA↓,
Glycolysis↓, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
selectivity↑, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
*toxicity∅, Chronic citrate treatment was non-toxic as evidenced by gross pathology in numerous organs (liver, lung, spleen and kidney)
Dose∅, corresponding to approximately 56 g of citrate in a 70 kg person

1034-

CUR,

immuno,

Enhanced anti‐tumor effects of the PD‐1 blockade combined with a highly absorptive form of curcumin targeting STAT3

in-vivo,

NA,

mice

DCells↑,
T-Cell↑,

451-

CUR,

The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer

vitro+vivo,

HNSCC,

SCC15

1, 2, 5, 10, 20, 40 and 80 µM, 1, 3, 6, 12 and 24 h; 50 mg/kg, 6 weeks

vitro+vivo,

HNSCC,

SNU1076

vitro+vivo,

HNSCC,

SNU1041

TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

1038-

Fuc,

immuno,

Fucoidan enhances the anti-tumor effect of anti-PD-1 immunotherapy by regulating gut microbiota.

in-vivo,

BC,

GutMicro↑, ucoidan significantly improved the composition of the gut microbiota by increasing the number of potentially beneficial bacteria, such as Bifidobacterium, Faecalibaculum and Lactobacillus.
T-Cell↑, improved the function of effector T cells
Treg lymp↓,

1021-

HNK,

Honokiol suppress the PD-L1 expression to improve anti-tumor immunity in lung cancer

in-vivo,

Lung,

PD-L1↓, in cells with high PD-L1 expression
T-Cell↑, facilitates T cell killing of tumor cells
CD4+↑,
CD8+↑,
TumCG↓, mice

7653-

IP,

Generation of systemic antitumour immunity via the in situ modulation of the gut microbiome by an orally administered inulin gel

in-vivo,

Var,

mice

GutMicro↑, inulin — a widely consumed dietary fibre — formulated as a colon-retentive orally administered gel can effectively modulate the gut microbiome in situ
T-Cell↑, induce systemic memory-T-cell responses, and amplify the antitumour activity of the checkpoint inhibitor anti-programmed-cell-death-protein-1 (anti-PD-1)
AntiTum↑,
eff↑, Inulin improves the efficacy of α-PD-1 therapy
TumCG↓, inulin gel plus α-PD-1 combo-therapy markedly delayed the tumor growth and increased the rate of complete tumor regression by 2-fold

8237-

LCA,

Role of Licochalcone A in Potential Pharmacological Therapy: A Review

Review,

Var,

*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↑,

8212-

LCA,

Licochalcone A inhibits proliferation and promotes apoptosis of colon cancer cell by targeting programmed cell death-ligand 1 via the NF-κB and Ras/Raf/MEK pathways

in-vitro,

Colon,

HepG3

in-vitro,

Lung,

A549

in-vitro,

Cerv,

HeLa

vitro+vivo,

CRC,

HCT116

mice

PD-L1↓, we found that licochalcone A suppressed the expression of programmed cell death ligand-1 (PD-L1), which plays a key role in regulating the immune response.
p65↓, licochalcone A inhibited the expressions of p65 and Ras.
RAS?,
NF-kB↓, Licochalcone A (LCA) inhibits TNF-α induced NF-κB signaling pathways activation in HCT116 cells
T-Cell↑, The results showed that licochalcone A (LCA) significantly enhanced the killing of T cells to HCT116 cell
p‑MEK↓, Licochalcone A (LCA) also inhibited TNF-α-induced p-MEK and p-Raf expressions without affecting MEK and Raf total protein levels
p‑Raf↓,

8129-

LF,

Study on the Therapeutic Benefit on Lactoferrin in Patients with Colorectal Cancer Receiving Chemotherapy

Trial,

CRC,

Dose↝, Test group (15 patients) received oral bLF 250 mg/day beside chemotherapy for three months. Control group (15 patients) received chemotherapy only.
toxicity↓, 3 months after treatment indicates that no significant difference in mean values of serum creatinine, AST, ALT, serum LF, serum GST enzyme, INF-γ, WBCs count, platelet count, CEA, RBCs count, neutrophil count, and Hb level of patients
INF-γ↝, Mean percent of change of main parameters (serum LF, serum GST enzyme, and INF-γ) after than before treatment among the studied patients indicate significant improvement in patients who received oral bLF 3 months
other↑, The results of this trial indicate that oral bLF made a significant increase in serum LF levels of patients in the test group 3 months after treatment compared to patients in the control group (P ≤ 0.05).
*ROS↓, Iron is essential as a catalyst for the production of reactive oxygen species. Therefore, lactoferrin can diminish the harmful influence of reactive oxygen species produced by leukocytes at the sites of inflammation
Imm↑, This result indicates that oral bLF enhances the immune system of colorectal cancer patients.
WBC↑, As a result of this increase in WBCs and neutrophil count patients disease state may be improved, because the body immune system can fight the disease more efficiently compatible with some previous studies
Neut↑,
T-Cell↑, These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status
*antiOx↑, The effect of antioxidants such as LF increase intracellular glutathione (GSH) levels in vascular endothelial cells by modulation of the GSH redox
*GSH↑,
*chemoP↑, On the other hand, oral bLF administration decreased chemotherapy related side effects as it enhances both renal and hepatic function tests.
*RenoP↑, Also, LF decreased chemotherapy related side effects by protecting liver and kidney from toxicity and improving their function test values
*hepatoP↑, Oral lactoferrin may increase liver functions and protect it from damage by reactive oxygen species since LF can function as an antioxidant, reducing intracellular levels of ROS
BUN↓, mean serum BUN decreased from 16.23 mg/dL before treatment to 11.43 mg/dL after 3 months of treatment in patients in the test group
creat↓, This decrease in BUN and serum creatinine may be due to the antioxidant effect of LF as mentioned in a former preclinical study on rat model of ferric nitrilotriacetate- (Fe-NTA-) induced renal tubular oxidative injury.
ALAT↓, Also, there was a significant decrease in serum ALT and AST in patients in test group 3 months after treatment compared to patients in the control group
AST↓,
RBC↑, Oral bLF administration enhanced anemia which is a very common chemotherapy related side effect; as results have shown, there were significant increases in RBCs count and serum Hb in patients in test group 3 months after treatment compared to patient
PC↑, There was a significant increase in platelets count in patients in test group after 3 months compared to control group
Mucositis↓, Patients in test group had less severed mucositis than patients in control group after every chemotherapy cycle;
*AntiBio↑, As mentioned before, lactoferrin has protective effects that range from direct antimicrobial activities against a large panel of microorganisms, including bacteria, viruses, fungi, and parasites, to anti-inflammatory and anticancer activities [
*AntiViral↑,
*AntiFungal↑,
*Inflam↓,

1782-

MEL,

Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities

Review,

Var,

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/CA9↑,
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

220-

MFrot,

MF,

Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation

in-vitro,

Melanoma,

B16-F10

 0.4 T, 7.5 Hz

 mouse cell line

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+↑,

1573-

MushReishi,

Ganoderma lucidum (Reishi mushroom) for cancer treatment

Review,

NA,

A total of five RCTs with 373 subjects were included in this review

ChemoSen↑, lucidum could be administered as an alternative adjunct to conventional treatment
CR3↝, beta‐glucans act on complement receptor type 3 (CR‐3) triggering a series of molecular pathway
eff↑, tudy patients who received G. lucidum treatment in combination with conventional chemotherapy generally responded more positively than those in the standard treatment group.
NK cell↑, use of G. lucidum and showed an increase in NK‐cell activity
T-Cell↑, findings also showed that G. lucidum could be capable of enhancing immunity in cancer patients by stimulating T‐lymphocyte proliferation
QoL↑, QoL was relatively improved in cancer patients with G. lucidum treatment than without.

MushShi,

AHCC Activation and Selection of Human Lymphocytes via Genotypic and Phenotypic Changes to an Adherent Cell Type: A Possible Novel Mechanism of T Cell Activation

*LAT↑, AHCC possibly induces upregulation of LAT and promotes cell adhesion to activate resting lymphocytes.
*FLRT2↑,
*GIT1↑,
*T-Cell↑,

103-

RES,

CUR,

QC,

The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice

vitro+vivo,

BC,

4T1

 Mice: 24 mg/kg
Res, 24 mg/kg
Cur, 12 mg/kg
Que
Translated into an edible human dose of 738 mg/day (including 295.2 mg Res, 295.2 mg Cur, and 147.6 mg Que)

 8.5mg/L

 mice

ROS↑, RCQ significantly increased reactive oxygen species (ROS), reduce mitochondrial membrane potentials in cancer cells, and modulate pro-apoptotic Bcl-2 family members
MMP↓,
Bcl-2↓,
BAX↑,
Casp9↑,
T-Cell↑, (CD4+CD8+)
TGF-β↓,

871-

RES,

CUR,

QC,

The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice

in-vitro,

BC,

4T1

8.55mg/L

 Res:Cur:Que = 1:1:0.5

in-vivo,

BC,

4T1

tumor bearing mice- subcutaneous injection of 4T1 breast cancer cells

T-Cell↑, in tumor microenviroment
Neut↓,
Macrophages↓,
ROS↑, RCQ significantly increased reactive oxygen species
MMP↓, in cancer cells
other↓, alleviate immunosuppression of the tumor microenvironment to enhance the anti-tumor effect.
AntiTum↑, at least nearly 5 times higher than that of a single Res/Cur/Que = 1:1:0.5
TumVol↓, 35-47% tumor inhibition rate

1195-

SM,

Salvia miltiorrhiza polysaccharide activates T Lymphocytes of cancer patients through activation of TLRs mediated -MAPK and -NF-κB signaling pathways

in-vitro,

Lung,

A549

in-vitro,

Liver,

HepG2

in-vitro,

CRC,

HCT116

T-Cell↑,
TumCP∅, SMP showed no effect on the proliferation of the tumor cells
IL4↑,
IL6↑,
IFN-γ↑,
TLR4↑,
TLR1↑,
TLR2↑,
p‑JNK↑,
p‑ERK↑,
IKKα↑,

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 3,
Total Targets: 168

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1, AntiBio↑, 1, AntiP↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↑, 2, lipid-P↓, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↝, 1, LAT↑, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,

Migration(tgid=13) ⓘ

FLRT2↑, 1, GIT1↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 3, NF-kB↓, 1, T-Cell↑, 1,

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1, hepatoP↑, 1, neuroP↑, 1, RenoP↑, 1, toxicity∅, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 27

Scientific Paper Hit Count for: T-Cell, T lymphocytes

5 Curcumin
3 immunotherapy
2 Licochalcone A
2 Resveratrol
2 Quercetin
1 Apigenin (mainly Parsley)
1 Baicalein
1 Baicalin
1 Chlorogenic acid
1 Citric Acid
1 Fucoidan
1 Honokiol
1 Inulin Prebiotic
1 Lactoferrin/Talactoferrin
1 Melatonin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Mushroom Reishi
1 Mushroom Shiitake, AHCC
1 Salvia miltiorrhiza

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#:300  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

T-Cell Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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