CEA Cancer Research Results

CEA, Carcinoembryonic antigen: Click to Expand ⟱
Source:
Type: tumor marker
Carcinoembryonic antigen (CEA) is a glycoprotein involved in cell adhesion and is one of the most widely used tumor markers, especially in gastrointestinal malignancies.

CEA is commonly overexpressed in several cancers, most notably colorectal cancer, but also in cancers of the lung, pancreas, breast, and others.
– Both tissue expression and serum CEA levels can be monitored; serum measurements are frequently used in clinical practice.
Scientific Papers found: Click to Expand⟱
5432- AG,    Astragalus polysaccharides combined with radiochemotherapy for cervical cancer: a systematic review and meta-analysis of randomized controlled studies
- Review, Cerv, NA
ChemoSen↑, review aims to determine the clinical efficacy and safety of Astragalus Polysaccharide Injection (APS) combined with chemoradiotherapy for cervical cancer based on existing data.
eff↑, APS combined with chemoradiotherapy improved the objective response rate (ORR, RR = 1.43, 95% CI: 1.24–1.64) and disease control rate (
RadioS↑, APS can enhance the clinical efficacy of radiotherapy and chemotherapy for cervical cancer, respectively.
CEA↓, APS further reduced tumor marker levels: CEA (MD = −1.24, 95% CI: −1.58 to −0.89, p < 0.00001; heterogeneity: χ2 = 1.75, p = 0.19, I2 = 43%), SCC (
Wnt↓, Specifically, APS inhibits the cisplatin resistance pathway and regulates the cell cycle by suppressing the Wnt/β-catenin pathway via the PPARD/CDC20 axis (Liu et al., 2025)
β-catenin/ZEB1↓,
γH2AX↑, APS also influences autophagy and upregulates γH2AX expression, thereby enhancing cervical cancer sensitivity to radiotherapy
ER Stress↑, APS alleviates endoplasmic reticulum stress and promotes mitochondrial autophagy, thereby enhancing apoptosis and mitigating cisplatin-induced toxicity
mt-TumAuto↑,
QoL↑, suggested that APS combination therapy improves short-term clinical efficacy, quality of life, and immune function
Imm↑,

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↓,
*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↓,

6385- Eug,    Anticancer potential of eugenol in hepatocellular carcinoma through modulation of oxidative stress, inflammation, apoptosis, and proliferation mechanisms
- in-vivo, HCC, HepG2
tumCV↓, eugenol reduced cell viability (IC50 of 189.29 µg/mL) and inhibited cell migration in the HCC cell line HepG2.
TumCMig↓,
*ALAT↓, Eugenol treatment significantly reduced the activity levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), along with the levels of total bilirubin (TBIL), alpha-fetoprotein (AFP),
*AST↓,
*ALP↓,
*Bil↓,
*CEA↓, carcinoembryonic antigen (CEA), carbohydrate antigen 19–9 (CA 19–9), lipid peroxides (LPO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β).
*lipid-P↓,
*TNF-α↓,
*IL1β↓,
NF-kB↓, (NF-κB), interleukin-8, C-X-C Motif Chemokine Receptor 3 (CXCR3), B-cell lymphoma 2 (Bcl-2), IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), IQ Motif Containing GTPase Activating Protein 3 (IQGAP3), Harvey rat sarcoma viral oncogene homolo
CXCR3↓,
HRAS↓, Harvey rat sarcoma viral oncogene homolog (HRAS), Kirsten rat sarcoma viral oncogene homolog (KRAS), and Ki-67 were downregulated following eugenol
KRAS↓,
Ki-67↓,
*GSH↑, eugenol supplementation significantly enhanced glutathione (GSH) content, as well as the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the levels of nuclear factor erythroid 2-related factor 2 (Nrf2).
*GPx↑,
*SOD↑,
*NRF2↑,
P53↑, expressions of tumor suppressor gene p53, Bcl-2-associated X protein (BAX), death receptor 4 (DR4), death receptor 5 (DR5), decoy receptor 1 (DcR1), programmed cell death 5 (PDCD5), and IQ Motif Containing GTPase Activating Protein 2 (IQGAP2) were ma
BAX↑,
DR4↑,
DR5↑,

2503- H2,    Brain Metastases Completely Disappear in Non-Small Cell Lung Cancer Using Hydrogen Gas Inhalation: A Case Report
- Case Report, Lung, NA
TumVol↓, Hydrogen-gas monotherapy was started to control the tumor a month later. After 4 months, the size of multiple brain tumors was reduced significantly
OS↑, After 1 year, all brain tumors had disappeared, and there were no significant changes in metastases in the liver and lung.
Dose↝, The hydrogen oxygen nebulizer (AMS-H-03, Asclepius Meditec, Shanghai, China) generates 3 L/min hydrogen gas by hydrocephalus electrolysis. As measured by gas chromatography, the gas generated consisted of 67% hydrogen and 33% oxygen.
Dose↝, Using a special mask, the patient continued to inhale hydrogen for 3–6 hrs a day at rest, with no interruption even after the obvious relief of symptoms.
CEA↓, dropped from 29.44 to 12 ng/mL in 12 months (figure 3)
CA125↓, dropped from 150 to 60 u/mL (figure 3)
CYFRA21-1↓, dropped from 12 to 6 ng/mL (figure 3)
SIRT1↓, several scholars have demonstrated that hydrogen can suppress SIRT1 signaling in different model
COX2↓, hydrogen exerts neuroprotective effects by reducing cyclooxygenase-2 activity25 or activating expression of anti-apoptotic protein kinase B.
IL1β↓, Hydrogen inhalation can down-regulate the expression of various pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α, intracellular adhesion molecule-1, high mobility group box-1, nuclear factor-kappa B, and prosta
IL6↓,
TNF-α↓,
HMGB1↓,
NF-kB↓,
EP2↓, and prostaglandin-E2

2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration

1251- RT,  OLST,    Rutin and orlistat produce antitumor effects via antioxidant and apoptotic actions
- in-vitro, BC, MCF7 - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumVol↓, Our results have shown that both rutin and orlistat exerted an in vivo anticancer activity as evidenced by the decrease in tumor volume
*CEA↓, CEA level, cholesterol content, FAS
*FASN↓, inhibition of FASN by orlistat resulted in a significant reduction of PANC-1 proliferation and enhanced apoptosis of these cells
*ROS↓, and the exerted antioxidant action (reduced MDA level and increased GSH content)**assume this means tissue as opposed to in tumor. (see figure 3)
*MDA↓, rutin decreased tissue MDA and increased tissue GSH.
*GSH↑, reduced MDA level and increased GSH content
Apoptosis↑, both were cytotoxic to MCF-7 and Panc-1 cell lines by promoting apoptosis


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CXCR3↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   CYP1A1↓, 1,   GPx↓, 1,   GSH↓, 2,   GSR↓, 1,   GSTs↓, 1,   HO-1↓, 1,   NQO1↓, 1,   NRF2↓, 1,   ROS↑, 1,   SOD↓, 1,   SOD2↓, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   Bak↓, 1,   BAX↑, 2,   Bcl-2↓, 2,   BID↑, 1,   Casp1↓, 1,   Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 1,   Cyt‑c↑, 2,   DR4↑, 1,   DR5↑, 2,   Fas↑, 2,   FasL↑, 1,   HGF/c-Met↓, 1,   p‑JNK↑, 1,   MAPK↓, 1,   p‑MDM2↓, 1,   p‑p38↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

H3↓, 1,   H4↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3II↑, 1,   mt-TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 2,   PARP↑, 2,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CD34↓, 1,   cFos↑, 1,   EMT↓, 1,   EP2↓, 1,   FGF↓, 1,   HDAC↓, 1,   HRAS↓, 1,   mTOR↓, 1,   NOTCH1↓, 1,   p‑PI3K↓, 1,   PTEN↓, 1,   p‑Src↓, 1,   STAT3↓, 1,   p‑STAT6↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AXL↓, 1,   Cdc42↓, 1,   CEA↓, 4,   CLDN1↓, 1,   E-cadherin↓, 1,   FAK↓, 1,   ITGB1↓, 1,   Ki-67↓, 1,   KRAS↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP2↓, 1,   N-cadherin↓, 1,   Rac1↓, 1,   Rho↓, 1,   Snail↓, 1,   TIMP2↑, 1,   TumCMig↓, 1,   Tyro3↓, 1,   Vim↑, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↑, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ASC↓, 1,   COX2↓, 2,   HMGB1↓, 1,   ICAM-1↓, 1,   IKKα↓, 1,   IL1β↓, 1,   IL2↑, 1,   IL6↓, 2,   Imm↑, 1,   NF-kB↓, 3,   NF-kB↑, 1,   p‑p65↓, 1,   PD-1↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   CA125↓, 1,   CEA↓, 4,   CYFRA21-1↓, 1,   EGFR↑, 2,   HER2/EBBR2↓, 1,   IL6↓, 2,   Ki-67↓, 1,   KRAS↓, 1,   NSE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cachexia↓, 1,   chemoP↑, 1,   OS↑, 1,   QoL↑, 1,   TumVol↓, 2,  
Total Targets: 129

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Bil↓, 1,   Catalase↑, 3,   GPx↑, 2,   GSH↑, 5,   GSTs↑, 1,   Keap1↑, 1,   lipid-P↓, 3,   MDA↓, 2,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 4,   TBARS↓, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   FASN↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↓, 2,   Cyt‑c↓, 1,   iNOS↓, 2,  

Migration(tgid=13) ⓘ

CEA↓, 2,   MMP13↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2↓, 2,   IL10↑, 1,   IL1β↓, 3,   IL6↓, 1,   IL6↑, 1,   Imm↑, 1,   Inflam↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   eff↑, 2,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   Bil↓, 1,   CEA↓, 2,   creat↓, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   motorD↑, 1,   neuroP↑, 1,   Pain↓, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   CD8+↑, 1,  
Total Targets: 61

Scientific Paper Hit Count for: CEA, Carcinoembryonic antigen
1 Astragalus
1 α-Bisabolol / Chamomile oil
1 Eugenol
1 Hydrogen Gas
1 Luteolin
1 Rutin
1 Orlistat
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#:1056  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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