AFP Cancer Research Results

AFP, α-fetal protein: Click to Expand ⟱
Source:
Type: biomarker
α-fetal protein (AFP) is a protein that is typically produced by the liver and yolk sac of a developing fetus. In adults, high levels of AFP in the blood can be a sign of certain types of cancer, particularly those of the liver, testes, and ovaries.

-AFP is primarily known as a serum biomarker in hepatocellular carcinoma (HCC), but its expression and prognostic significance can also extend to other malignancies.


Scientific Papers found: Click to Expand⟱
5887- CAR,  TV,    Antitumor Effects of Carvacrol and Thymol: A Systematic Review
- Review, Var, NA
Apoptosis↑, It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity,
TumCCA↑, accumulation of cells in the G1 phase, together with a reduction of cells in the S phase, slowing cell cycle/mitosis and provoking cell death.
TumMeta↓,
TumCP↓, antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
eff↑, carvacrol appears to be more potent than thymol
*Inflam↓, these compounds present anti-inflammatory (Li et al., 2018; Chamanara et al., 2019) and antioxidant
*antiOx↑,
AXL↓, These effects occurred mainly through the inhibition of tyrosine kinase receptor (AXL) expression and an increase in malondialdehyde (MDA
MDA↑,
Casp3↑, caspase-3 activation and Bcl-2 inhibition
Bcl-2↓,
MMP2↓, promoted a decrease in Bcl-2, metalloproteinase-2 and -9 (MMP-2 and MMP-9), p-ERK, p-Akt, cyclin B1 levels and an increase in p-JNK, Bax levels, resulting in cell cycle arrest at the G2/M phase
MMP9↓,
p‑JNK↑,
BAX↑,
MDA↓, In respect of breast cancer, treatment with carvacrol decreases MDA-MB231 (Jamali et al., 2018; Li et al., 2021) and MCF-7 cells line viability
TRPM7↓, TRPM7 pathway is one of the suggested pharmacological mechanisms of action
MMP↓, decreased mitochondrial membrane potential, cytochrome C release, caspase activation, PARP cleavage
Cyt‑c↑,
Casp↑,
cl‑PARP↑,
ROS↑, Carvacrol also induced cytotoxicity and apoptosis (via caspase-3 and reactive oxygen species—ROS) of human oral squamous cell carcinoma (OC2 cell line)
CDK4↓, In tongue cancer (Tca-8113, SCC-25 cell lines), Dai et al. (2016) reported that carvacrol effectively inhibited cell proliferation through the negative regulation of CCND1 and CDK4 expression, and the positive regulation of p21 expression,
P21↑,
F-actin↓, A blockade of TRPM7 channels, reduced expression of MMP-2 and F-actin, was also observed, together with the inhibition of PI3K/Akt and MAPK
GSH↓, by increasing ROS, Bax, Caspase-3, -9 levels and reducing Bcl-2 and GSH levels.
*SOD↑, Moreover, carvacrol was able to increase the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH), along with a reduction of lipid peroxides and the enzymes AST, ALT, AL
*Catalase↑,
*GPx↑,
*GSR↑,
*GSH↑,
*lipid-P↓,
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
DNAdam↑, hepatocellular carcinoma induced by diethylnitrosamine (DEN), carvacrol treatment promoted DNA fragmentation
AFP↓, carvacrol showed a reduction in serum levels of alpha-fetoprotein (AFP), alpha l-fucosidase (AFU), vascular endothelial growth factor (VEGF
VEGF↓,
Weight↑, Carvacrol supplementation significantly improved the weight gain and growth rate of animals with colon cancer
*chemoP↑, reduction in oxidative stress damage (higher levels of GSH, GPx, GR, SOD and CAT), suggesting that carvacrol presents chemopreventive effects
ROS↑, In vitro, carvacrol and thymol increased the generation of reactive oxygen species in 24.63% (n = 17) of the studies, a fact that is also observed in chemotherapeutics

5894- CAR,    Targeting Gastrointestinal Cancers with Carvacrol: Mechanistic Insights and Therapeutic Potential
- Review, Var, NA
AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.

5891- CAR,  SRF,    Carvacrol enhances anti-tumor activity and mitigates cardiotoxicity of sorafenib in thioacetamide-induced hepatocellular carcinoma model through inhibiting TRPM7
- in-vivo, HCC, NA
eff↑, CARV/Sora combination significantly improved survival rate, and liver functions, reduced Alpha-Fetoprotein level, and attenuated HCC progression compared with Sora group
OS↑,
hepatoP↑,
AFP↓,
NOTCH↓, downregulating ATP-binding cassette subfamily G member 2, NOTCH1, Spalt like transcription factor 4, and CD133.
cycD1/CCND1↓, decreasing cyclin D1 and B-cell leukemia/lymphoma 2 and increasing BCL2-Associated X and caspase-3.
Bcl-xL↑,
Casp3↑,
TRPM7↓, CARV/Sora is a promising combination for tumor suppression and overcoming Sora resistance and cardiotoxicity in HCC by modulating TRPM7
Dose↝, CARV (15 mg/kg/day; orally) (Rats)

655- EGCG,    A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cells
- in-vitro, HCC, HepG2
AFP↓, EGCG can effectively reduce AFP secretion and simultaneously induce AFP aggregation in human HCC HepG2 cells.
TumAuto↑,
LC3II↑, promoting the synthesis of LC3-II, a characteristic autophagosomal marke
TumCG↓,
MMP↓,

5228- EMD,    Evaluating anticancer activity of emodin by enhancing antioxidant activities and affecting PKC/ADAMTS4 pathway in thioacetamide-induced hepatocellular carcinoma in rats
- in-vivo, HCC, NA
OS↑, Emodin increased the survival percentage and reduced the number of hepatic nodules compared to the HCC group. Therefore, emodin extended the survival percentage of the HCC group by about 45%
PKCδ↓, emodin reduced the elevated expression of both mRNA and proteins of all PKC, ERK5, ADAMTS4, MMP3, and VEGF compared with the HCC group
ERK5↓,
MMP3↓,
VEGF↓,
NRF2↑, emodin increased the expression of mRNA and proteins of Nrf2, HO-1, and aggrecan compared with the HCC group.
HO-1↑,
MDA↓, HCC rats exhibited a 4.71-fold increase in hepatic levels of MDA and a 61% reduction in the hepatic concentration of reduced glutathione compared to the control rats. Treatment with emodin reversed these effects
AFP↓, emodin succeeded in significantly decreasing the upregulated serum AFP (about 71% reduction), restoring it to its normal level in the control group

2489- metroC,  capec,    Long-lasting response with metronomic capecitabine in advanced hepatocellular carcinoma
- Case Report, HCC, NA
Dose↝, We report a case of metastatic HCC associated with Child-Pugh class B cirrhosis that was treated with low, "metronomic" doses of capecitabine (1000 mg/day continuously).
OS↑, This treatment was effective and well tolerated and the response was maintained for 18 months.
TumVol↓, After 3 months of capecitabine treatment, CT examination showed a decrease in the number and size of peritoneal metastases, which had reduced to 1 nodule with a maximum diameter of 6 mm in the left lower quadrant.
AFP↓, AFP had dropped to 1480 ng/mL.

2486- metroC,  capec,    Sustained complete response of advanced hepatocellular carcinoma with metronomic capecitabine: a report of three cases
- Case Report, HCC, NA
OS↑, We describe three cases of advanced HCC treated with metronomic capecitabine where a complete response CR was obtained.
eff↝, However, the effects of metronomic chemotherapy appear to vary according to solid tumour type.
Dose↝, the patient started metronomic capecitabine (500 mg twice daily, continuous administration), which was well-tolerated.
AFP↓, AFP level had fallen to 3.3 ng/mL
Dose↝, AFP (47,137 ng/mL), the patient was switched to capecitabine therapy (500 mg twice daily, continuous administration).
TumVol↓, CT scanning performed every 3 months showed the progressive reduction of pulmonary metastases, recanalization of the median hepatic vein, and progressive improvement in inferior cava vein invasion
AFP↓, Serum AFP levels decreased to 4583 ng/mL in May 2016, 5.5 ng/mL in September 2016, 2.5 ng/mL in November 2016, and 1.5 ng/mL in October 2017.


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 2,   HO-1↑, 1,   MDA↓, 2,   MDA↑, 1,   NRF2↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 3,   Bcl-xL↑, 1,   Casp↑, 1,   Casp3↑, 3,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 2,   FADD↑, 1,   Fas↑, 1,   p‑JNK↑, 1,   MAPK↓, 1,   p38↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   ERK5↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   TRPM7↓, 2,   TumCG↓, 1,  

Migration ⓘ

AXL↓, 1,   E-cadherin↑, 1,   F-actin↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   PKCδ↓, 1,   TIMP2↑, 1,   TIMP3↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 3,   ZEB2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 5,   eff↑, 2,   eff↝, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AFP↓, 8,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   hepatoP↑, 2,   OS↑, 5,   TumVol↓, 2,   Weight↑, 1,  
Total Targets: 75

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   LDH↓, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   ALP↓, 2,   AST↓, 2,   LDH↓, 2,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 15

Scientific Paper Hit Count for: AFP, α-fetal protein
3 Carvacrol
2 metronomic chemo
2 capecitabine
1 Thymol-Thymus vulgaris
1 Sorafenib (brand name Nexavar)
1 EGCG (Epigallocatechin Gallate)
1 Emodin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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