Disulfiram / angioG Cancer Research Results

DSF, Disulfiram: Click to Expand ⟱
Features:
Disulfiram is a synthetic small-molecule drug best known for its use in the treatment of chronic alcohol use disorder. It is a thiuram disulfide compound with the chemical formula C₁₀H₂₀N₂S₄ and acts primarily as an aldehyde dehydrogenase (ALDH) inhibitor.
Main Actions:
-Potent copper-dependent pro-oxidant
-Targets ALDH⁺ cancer stem cells
-Strong clinical repurposing interest

Key pathways
-Cu-mediated redox cycling
-Proteasome inhibition
-Mitochondrial ROS

Chemo relevance
-Often synergistic
-Highly mechanism-dependent
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Metal chelation / Disulfiram–Cu complex formation ↑ DSF–Cu complex formation ↔ limited formation Driver Copper-dependent cytotoxic chemistry Elevated copper in cancer cells enables formation of cytotoxic DSF–Cu complexes; this is the initiating event for most anticancer effects
2 Proteasome / p97–NPL4 axis ↓ proteasome function; ↑ proteotoxic stress ↔ minimal disruption Driver Protein homeostasis collapse DSF–Cu disrupts protein degradation pathways, leading to accumulation of misfolded proteins and stress signaling
3 Reactive oxygen species (ROS) ↑ ROS (metal-dependent) ↔ buffered Secondary Oxidative stress amplification ROS rise follows DSF–Cu redox cycling and proteotoxic stress; not the primary trigger
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Secondary Execution of cell death Mitochondrial dysfunction and apoptosis occur downstream of proteostasis and redox stress
5 ALDH activity (ALDH1A1 / stemness) ↓ ALDH activity ↓ ALDH (clinically tolerated) Secondary Cancer stem-like cell targeting ALDH inhibition preferentially impacts cancer stem-like populations; normal cells tolerate inhibition at therapeutic exposure
6 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of survival transcription NF-κB inhibition reflects upstream proteotoxic and redox stress rather than direct targeting
7 Cell cycle progression ↓ proliferation / ↑ arrest ↔ largely spared Phenotypic Cytostatic growth control Growth inhibition reflects impaired protein turnover and metabolic stress
8 Apoptosis / non-apoptotic death ↑ apoptosis or proteotoxic death ↔ protected Phenotypic Threshold-dependent cell death Cell death modality depends on copper availability and stress magnitude


angioG, angiogenesis: Click to Expand ⟱
Source:
Type:
Process through which new blood vessels.
Angiogenesis, the process of new blood vessel formation from pre-existing vessels, plays a crucial role in cancer progression and metastasis. Tumors require a blood supply to grow beyond a certain size and to spread to other parts of the body.
Vascular Endothelial Growth Factor (VEGF): VEGF is one of the most important pro-angiogenic factors. It stimulates endothelial cell proliferation and migration, leading to the formation of new blood vessels. Many tumors overexpress VEGF, which correlates with poor prognosis.
Hypoxia-Inducible Factor (HIF): In response to low oxygen levels (hypoxia), tumors can activate HIF, which in turn promotes the expression of VEGF and other angiogenic factors. This mechanism allows tumors to adapt to their microenvironment and sustain growth.


Scientific Papers found: Click to Expand⟱
4914- DSF,  immuno,    Disulfiram and cancer immunotherapy: Advanced nano-delivery systems and potential therapeutic strategies
- Review, Var, NA
AntiTum↑, eff↑, ALDH↓, Dose↝, RadioS↑, angioG↓, TumMeta↓, BioAv↝, ROS↑, DNAdam↑, P-gp↓, CSCs↓, EMT↓, Imm↑, SOD↓, MAPK↓, NF-kB↓, ChemoSen↑, eff↑, toxicity↝, BioAv↑, *Inflam↓, Sepsis↓,
5008- DSF,  Cu,    Overcoming the compensatory elevation of NRF2 renders hepatocellular carcinoma cells more vulnerable to disulfiram/copper-induced ferroptosis
- in-vitro, HCC, NA
selectivity↑, TumCD↑, TumCMig↓, TumCI↓, angioG↓, mtDam↑, Iron↑, lipid-P↑, Ferroptosis↑, NF-kB↑, p‑p62↑, Keap1↓, eff↑, eff↓, ChemoSen↑,
5012- DSF,  Cu,    Advancing Cancer Therapy with Copper/Disulfiram Nanomedicines and Drug Delivery Systems
ROS↑, ALDH↓, TumCP↓, CSCs↓, angioG↓, TumMeta↓, DNAdam↑, Proteasome↓, SOD1↓, GSR↓, ox-GSSG↑, GSH/GSSG↓, MMP↓, Akt↓, cycD1/CCND1↓, NF-kB↓, CSCs↓, MAPK↓, angioG↓, DrugR↓, EMT↓, Vim↓, BioAv↑, eff↑,
5013- DSF,  Cu,  Z,    Disulfiram inhibits activating transcription factor/cyclic AMP-responsive element binding protein and human melanoma growth in a metal-dependent manner in vitro, in mice and in a patient with metastatic disease
- vitro+vivo, Melanoma, NA - Case Report, Melanoma, NA
P-gp↓, NF-kB↓, ChemoSen↑, angioG↓, TumCG↓, TumMeta↓, Remission↑, toxicity↓, ATF2↓, CREB↓, cycA1/CCNA1↓, TumCG↓, angioG↓, Dose↝, toxicity↝,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Ferroptosis↑, 1,   GSH/GSSG↓, 1,   GSR↓, 1,   ox-GSSG↑, 1,   Iron↑, 1,   Keap1↓, 1,   lipid-P↑, 1,   ROS↑, 2,   SOD↓, 1,   SOD1↓, 1,  

Mitochondria & Bioenergetics

MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis

CREB↓, 1,  

Cell Death

Akt↓, 1,   ATF2↓, 1,   Ferroptosis↑, 1,   MAPK↓, 2,   Proteasome↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes

p‑p62↑, 1,  

DNA Damage & Repair

DNAdam↑, 2,  

Cell Cycle & Senescence

cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State

ALDH↓, 2,   CSCs↓, 3,   EMT↓, 2,   TumCG↓, 2,  

Migration

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 3,   Vim↓, 1,  

Angiogenesis & Vasculature

angioG↓, 6,  

Barriers & Transport

P-gp↓, 2,  

Immune & Inflammatory Signaling

Imm↑, 1,   NF-kB↓, 3,   NF-kB↑, 1,  

Drug Metabolism & Resistance

BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 3,   Dose↝, 2,   DrugR↓, 1,   eff↓, 1,   eff↑, 4,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes

AntiTum↑, 1,   Remission↑, 1,   toxicity↓, 1,   toxicity↝, 2,  

Infection & Microbiome

Sepsis↓, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling

Inflam↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: angioG, angiogenesis
4 Disulfiram
3 Copper and Cu NanoParticles
1 immunotherapy
1 Zinc
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#:387  Target#:447  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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