doxorubicin / TumVol Cancer Research Results

doxoR, doxorubicin: Click to Expand ⟱
Features:
Doxorubicin, (brand name Adriamycin) is a chemotherapy medication used to treat breast cancer, bladder cancer, Kaposi's sarcoma, lymphoma, and acute lymphocytic leukemia. Often used together with other chemotherapy agents. Given by injection into a vein.
Doxorubicin is an anthracycline chemotherapy whose core anticancer activity is driven by DNA intercalation and topoisomerase II poisoning (DNA double-strand break stress), with additional contributions from redox cycling/iron-linked oxidative injury in some contexts. Its major clinical limitations are myelosuppression and cumulative dose–dependent cardiomyopathy, plus severe tissue injury if extravasated (leaks outside the vein).
-Cumulative cardiomyopathy risk is real and dose-dependent; labels note higher risk at higher cumulative doses (often cited around >550 mg/m², with lower limits in higher-risk patients).
-Mechanism split: tumor kill is primarily Topo II + DNA damage, while cardiotoxicity is strongly linked to TOP2β/mitochondrial pathways (redox/iron biology remains discussed, but not the only story).
-Administration hazard: extravasation can cause severe local injury;

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Topoisomerase II poisoning (DNA double-strand break stress) Topo II–DNA cleavage complexes ↑ → DNA breaks ↑ → apoptosis/senescence ↑ (context) Also affects normal proliferating tissues (marrow, mucosa) P, R Core cytotoxic mechanism Primary anticancer mechanism: stabilization of Topo II–DNA cleavage complexes blocks repair and drives lethal DNA damage responses.
2 DNA intercalation → replication/transcription disruption DNA/RNA synthesis ↓; replication stress ↑ Off-target in normal dividing cells P, R Replication/transcription blockade Intercalation contributes to replication fork stress and complements Topo II poisoning.
3 Redox cycling / iron-associated oxidative injury (context-dependent) ROS / oxidative damage ↑ (reported; model-dependent) Oxidative injury risk in sensitive tissues (esp. heart) ↑ P, R, G Stress amplification Often described as semiquinone redox cycling and iron interactions; the relative importance vs Topo II varies by tissue/model.
4 Cardiotoxicity axis (TOP2β + mitochondrial injury; cumulative-dose dependent) — Risk of cardiomyopathy/heart failure ↑ with cumulative exposure R, G Major dose-limiting toxicity Clinically important boxed-warning toxicity; risk increases with cumulative dose (labels cite higher risk above ~550 mg/m²; higher-risk patients often use lower limits).
5 Myelosuppression (bone marrow progenitors) — Neutropenia/anemia/thrombocytopenia risk ↑ R, G Dose-limiting toxicity Expected on-target effect in rapidly dividing marrow cells; infection risk increases when neutrophils are low.
6 p53 / DNA-damage response programs DDR signaling ↑; p53 pathway engagement ↑ (context) DDR activation in normal tissues contributes to toxicity R, G Cell fate commitment Downstream of DNA breaks: checkpoint activation, apoptosis, senescence, or mitotic catastrophe depending on genotype and dose.
7 Immunogenic cell death signals (DAMP exposure; context-dependent) Potential ICD features ↑ (reported in some systems) — G Immune engagement (conditional) Anthracyclines are often discussed as capable of immunogenic cell death in certain settings; not universal across regimens.
8 Extravasation tissue injury (local) — Severe local tissue damage risk if IV leakage occurs P, R Administration hazard Boxed warning emphasizes severe tissue injury with extravasation; requires strict IV administration controls.
9 Secondary malignancy risk (therapy-related AML/MDS; exposure-dependent) — Rare long-term risk signal ↑ — Late toxicity constraint Listed in boxed warnings/labels as a potential late effect, especially with combination regimens.
10 Cardioprotection strategy (dexrazoxane; selected settings) — Cardiotoxicity risk ↓ (when used appropriately) R, G Risk mitigation Dexrazoxane is used to reduce anthracycline cardiotoxicity; mechanistic literature includes TOP2β-linked protection and other hypotheses.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (direct DNA/Topo interactions begin rapidly)
  • R: 30 min–3 hr (acute DNA-damage response + stress signaling)
  • G: >3 hr (gene programs, apoptosis/senescence, phenotype-level outcomes)
TumVol, Tumor Volume: Click to Expand ⟱
Source:
Type:
Tumor Volume
Scientific Papers found: Click to Expand⟱
4431- AgNPs,  doxoR,    Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1 - in-vitro, Nor, 3T3
AntiCan↑, ROS↑, TumVol↓, EPR↑, selectivity↑, ChemoSen↑,
4354- MF,  doxoR,    Modulated TRPC1 Expression Predicts Sensitivity of Breast Cancer to Doxorubicin and Magnetic Field Therapy: Segue Towards a Precision Medicine Approach
- in-vivo, BC, MDA-MB-231 - in-vivo, BC, MCF-7
selectivity↑, Apoptosis↑, TumCI↓, tumCV↓, TumVol↓, eff↓, eff↑, ROS↑, Ca+2↑, TumCMig↓,
5610- NaHCO3,  doxoR,    Sodium bicarbonate nanoparticles modulate the tumor pH and enhance the cellular uptake of doxorubicin
- vitro+vivo, BC, 4T1
pH↑, Imm↑, eff↑, ChemoSen↑, TumVol↓, eff↑,
5216- PI,  doxoR,    Piperine enhances doxorubicin sensitivity in triple-negative breast cancer by targeting the PI3K/Akt/mTOR pathway and cancer stem cells
- vitro+vivo, BC, MDA-MB-231
ChemoSen↑, necrosis↑, PTEN↓, PI3K↓, p‑Akt↓, mTOR↓, ALDH↓, TumVol↓, OS↑, cardioP↑, cl‑PARP↑,
2303- QC,  doxoR,    Quercetin greatly improved therapeutic index of doxorubicin against 4T1 breast cancer by its opposing effects on HIF-1α in tumor and normal cells
- in-vitro, BC, 4T1 - in-vivo, NA, NA
cardioP↑, hepatoP↑, TumCG↓, OS↑, ChemoSen↑, chemoP↑, Hif1a↓, *Hif1a↑, selectivity↑, TumVol↓, OS↑,
1931- TQ,  doxoR,    Thymoquinone enhances the anticancer activity of doxorubicin against adult T-cell leukemia in vitro and in vivo through ROS-dependent mechanisms
- in-vivo, AML, NA
eff↑, tumCV↓, TumCCA↑, ROS↑, MMP↓, eff↑, TumVol↓, eff↑, Ki-67↓,

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:


Redox & Oxidative Stress ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   necrosis↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,   Ki-67↓, 1,   TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

EPR↑, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,  

Cellular Microenvironment ⓘ

pH↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   eff↓, 1,   eff↑, 6,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 2,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 3,   TumVol↓, 6,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: TumVol, Tumor Volume
6 doxorubicin
1 Silver-NanoParticles
1 Magnetic Fields
1 Bicarbonate(Sodium)
1 Piperine
1 Quercetin
1 Thymoquinone
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#:179  Target#:530  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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