TF-Ag Cancer Research Results

TF-Ag, Thomsen-Friedenreich Antigen / Galβ1-3GalNAc: Click to Expand ⟱
Source:
Type:

TF Antigen - Thomsen-Friedenreich Antigen / Galβ1-3GalNAc

Abbreviation: TF antigen, TF-Ag, T antigen, CD176

Type: Tumor-associated carbohydrate antigen / truncated O-glycan

Function: The Thomsen-Friedenreich antigen consists of galactose linked β1-3 to N-acetyl-D-galactosamine (Galβ1-3GalNAc), typically attached to serine or threonine residues of glycoproteins. In normal tissues this carbohydrate structure is usually further glycosylated or masked, whereas abnormal O-glycosylation in malignant cells can expose the TF antigen on the cell surface.

Cancer: ↑ Frequently increased or exposed in carcinomas. TF antigen expression is associated with abnormal tumor glycosylation, cell adhesion, galectin-3 interactions, invasion, endothelial attachment, and metastatic dissemination.
Scientific Papers found: Click to Expand⟱
7641- Ins,    Overview of Inositol and Inositol Phosphates on Chemoprevention of Colitis-Induced Carcinogenesis
- Review, CRC, NA
AntiCan↑, Dietary inositol and its phosphates, as well as phospholipid derivatives, are well known to benefit human health in diverse pathologies including cancer prevention.
p‑Akt↓, Specifically, mice receiving myo-inositol showed a 73% reduction in nuclear pAkt
TF-Ag↓, In colon cancer cells, InsP6 inhibits the expression of Galactose-N-acetyl-D-galactosamine (Gal-GalNAc), the most common cancer marker
*PI3K↓, InsP6 has been shown to block epidermal growth factor-mediated activation of PI3K and AP-1 suggesting that along with enhancing DNA repair
*AP-1↓,
*DNArepair↑,
*BioAv↑, Several studies in rodents and humans have now demonstrated that InsP6 is rapidly absorbed from the gastrointestinal tract, distributed through the plasma to various organs including the brain, and excreted from the lungs via exhaled air and through
*BBB↑, InsP6 crosses the blood-brain barrier and distributes to the brain
*other↑, inositol displays a strong effect to inhibit IBD-induced carcinogenesis, we further propose the potential mechanism of inositol on inhibiting IBD-induced multiple stage carcinogenesis (from initiation to promotion, finally to invasive cancer), as se
*PGE2↓, inositol will participate in an intracellular inositol pool (a) to block IP3/AKT signaling and (b) to inhibit PGE2 and LTB4 production


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

TF-Ag↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 3

Pathway results for Effect on Normal Cells:


Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNArepair↑, 1,  

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

PI3K↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

PGE2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: TF-Ag, Thomsen-Friedenreich Antigen / Galβ1-3GalNAc
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#:1676  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page