Database Query Results : doxorubicin, ,

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)
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↑,
256- AL,  doxoR,    Allicin Overcomes Doxorubicin Resistance of Breast Cancer Cells by Targeting the Nrf2 Pathway
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
NRF2↓, HO-1↓, p‑Akt↓,
301- ALA,  PacT,  doxoR,    Role of alpha-lipoic acid in counteracting paclitaxel- and doxorubicin-induced toxicities: a randomized controlled trial in breast cancer patients
- Human, BC, NA
BNP↓, TNF-α↓, MDA↓, NeuroT↓,
2586- Api,  doxoR,    Apigenin sensitizes doxorubicin-resistant hepatocellular carcinoma BEL-7402/ADM cells to doxorubicin via inhibiting PI3K/Akt/Nrf2 pathway
- in-vitro, HCC, Bel-7402
NRF2↓, ChemoSen↑,
1999- Api,  doxoR,    Apigenin ameliorates doxorubicin-induced renal injury via inhibition of oxidative stress and inflammation
- in-vitro, Nor, NRK52E - in-vitro, Nor, MPC5 - in-vitro, BC, 4T1 - in-vivo, NA, NA
neuroP↑, ChemoSen∅, RenoP↑, selectivity↑, chemoP↑, ROS↑, *ROS∅, *antiOx↑, *toxicity↓,
591- Api,  doxoR,    Polyphenols act synergistically with doxorubicin and etoposide in leukaemia cell lines
- in-vitro, AML, Jurkat - in-vitro, AML, THP1
ATP↓, Casp3↑, γH2AX↑,
938- Api,  doxoR,    Apigenin and hesperidin augment the toxic effect of doxorubicin against HepG2 cells
- vitro+vivo, HCC, HepG2
LDHA↓, HK2↓,
4991- ART/DHA,  doxoR,    Dihydroartemisinin alleviates doxorubicin-induced cardiotoxicity and ferroptosis by activating Nrf2 and regulating autophagy
- in-vivo, Nor, H9c2
*cardioP↑, *ROS↓, *Ferroptosis↓, *NRF2↑, Keap1↓,
1363- Ash,  doxoR,    Withaferin A Synergizes the Therapeutic Effect of Doxorubicin through ROS-Mediated Autophagy in Ovarian Cancer
- in-vitro, Ovarian, A2780S - in-vitro, Ovarian, CaOV3 - in-vivo, NA, NA
ChemoSen↑, ROS↑, DNAdam↑, TumCCA↑, LC3B↑, TumCG↓, cl‑Casp3↑,
5248- Ba,  BA,  doxoR,    Baicalin and Baicalein Enhance Cytotoxicity, Proapoptotic Activity, and Genotoxicity of Doxorubicin and Docetaxel in MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, HUVECs
toxicity↝, ChemoSen↑, selectivity↑, Apoptosis↑, necrosis↑, MMP↓, DNAdam↑, cl‑PARP↑, MRP1↓, Bcl-2↓, hepatoP↑, cardioP↑, BioAv↝,
1380- BBR,  doxoR,    treatment with ROS scavenger N-acetylcysteine (NAC) and JNK inhibitor SP600125 could partially attenuate apoptosis and DNA damage triggered by DCZ0358.
- in-vivo, Nor, NA
*ROS↓, *MDA↓, *SOD↑, *NRF2↑, *HO-1↑,
2591- CHr,  doxoR,    Chrysin enhances sensitivity of BEL-7402/ADM cells to doxorubicin by suppressing PI3K/Akt/Nrf2 and ERK/Nrf2 pathway
- in-vitro, HCC, Bel-7402
NRF2↓, ChemoSen↑, HO-1↓,
4763- CoQ10,  Chemo,  doxoR,    Effect of Coenzyme Q10 on Doxorubicin Cytotoxicity in Breast Cancer Cell Cultures
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549
ChemoSen∅, antiNeop∅, *cardioP↑, Dose↝, selectivity↑, TumCG∅, TumCG∅, Apoptosis∅,
1965- GamB,  doxoR,    Gambogic acid sensitizes ovarian cancer cells to doxorubicin through ROS-mediated apoptosis
- in-vitro, Ovarian, SKOV3
eff↑, AntiCan↑, ROS↑, ChemoSen↑,
1972- GamB,  doxoR,    Gambogic acid sensitizes resistant breast cancer cells to doxorubicin through inhibiting P-glycoprotein and suppressing survivin expression
- in-vitro, BC, NA
eff↑, P-gp↓, ROS↑, survivin↓, p38↑,
2901- HNK,  doxoR,    Honokiol protects against doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts
- in-vivo, Nor, NA
*mitResp↑, *PPARγ↑, *Inflam↓, *ROS↓, *cardioP↑, *SOD2↑, *LDH↓,
2893- HNK,  doxoR,    Honokiol protects against doxorubicin cardiotoxicity via improving mitochondrial function in mouse hearts
- in-vivo, Nor, NA
*mitResp↑, *PPARγ↑, *cardioP↑, *SIRT3↑, *ROS↓, *GSH↑, *SOD2↑,
2889- HNK,  doxoR,    Honokiol, an activator of Sirtuin-3 (SIRT3) preserves mitochondria and protects the heart from doxorubicin-induced cardiomyopathy in mice
- in-vivo, Nor, NA
*SIRT3↑, chemoP↑, *cardioP↑, mtDam↑, ROS↑, *ROS↓, *MMP↑,
5051- HPT,  doxoR,    Hyperthermia Enhances Doxorubicin Therapeutic Efficacy against A375 and MNT-1 Melanoma Cells
- in-vitro, Melanoma, A375
tumCV↓, TumCCA↑, ROS↑, eff↑,
986- LT,  doxoR,    Luteolin as a glycolysis inhibitor offers superior efficacy and lesser toxicity of doxorubicin in breast cancer cells
- in-vitro, BC, 4T1 - in-vitro, BC, MCF-7
SOD↓, Catalase↓, Glycolysis↓,
2534- M-Blu,  doxoR,  PDT,    Methylene Blue-Mediated Photodynamic Therapy in Combination With Doxorubicin: A Novel Approach in the Treatment of HT-29 Colon Cancer Cells
- in-vitro, CRC, HT-29
LDH↑, ROS↑,
506- MF,  doxoR,    Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells
- in-vitro, OS, LM8
TumCP↓, p‑CHK1↓, Ca+2↑, Casp3↓, Casp7↓, p‑BAD↓, ChemoSen↑,
4425- MF,  doxoR,    Brief Magnetic Field Exposure Stimulates Doxorubicin Uptake into Breast Cancer Cells in Association with TRPC1 Expression: A Precision Oncology Methodology to Enhance Chemotherapeutic Outcome
- in-vitro, BC, 4T1 - in-vitro, BC, MCF-7
ChemoSen↑, TRPC1↑, Dose↓, selectivity↑,
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↓,
508- MF,  doxoR,    Synergistic cytotoxic effects of an extremely low-frequency electromagnetic field with doxorubicin on MCF-7 cell line
- in-vitro, BC, MCF-7
ROS↑, Apoptosis↑, TumCCA↑,
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↑,
89- QC,  doxoR,    Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met
- in-vitro, Pca, PC3
PI3K/Akt↓, cMET↓, Casp3↑, Casp9↑, MMP↓, ChemoSen↑, ROS↑,
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↑,
926- QC,  PacT,  doxoR,  Tam,    Bioenhancers from mother nature and their applicability in modern medicine
- Review, Nor, NA
*BioEnh↑, BioEnh↑, BioEnh↑, BioEnh↑, BioEnh↑, BioEnh↑, BioEnh↑, P-gp↓,
58- QC,  doxoR,    Quercetin induces cell cycle arrest and apoptosis in CD133+ cancer stem cells of human colorectal HT29 cancer cell line and enhances anticancer effects of doxorubicin
- in-vitro, CRC, HT-29 - in-vitro, NA, CD133+
Bcl-2↓, TumCCA↑, CD133↓, CSCs↓, ChemoSen↑, CycB/CCNB1↑, cycE/CCNE↓, cycD1/CCND1↓, E2Fs↓,
4738- Se,  doxoR,    Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway
- NA, Nor, NA
*NRF2↑, *NLRP3↓, *cardioP↑,
4504- SeNPs,  Chit,  FA,  doxoR,    pH-responsive selenium nanoparticles stabilized by folate-chitosan delivering doxorubicin for overcoming drug-resistant cancer cells
- in-vitro, Var, NA
ChemoSen↑, Apoptosis↑, Casp3↑, PARP↝,
1495- SFN,  doxoR,    Sulforaphane protection against the development of doxorubicin-induced chronic heart failure is associated with Nrf2 Upregulation
- in-vivo, Nor, NA
*CardioT↓, *NRF2↑, *eff↓, *ROS↓,
1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
CardioT↓, *GSH↑, *ROS↓, *NRF2↑, NRF2∅, HDAC↓, DNMTs↓, Casp3↑, ER-α36↓, Remission↑, eff↑, ROS↑, selectivity?,
2215- SK,  doxoR,    Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice
- in-vivo, Nor, NA
*cardioP↑, *ROS↓, *Inflam↓, *Mst1↓, *NRF2↑, *eff↓, *antiOx↑, *SOD↑, *GSH↑, *TNF-α↓, BAX↓, Bcl-2↑,
3405- TQ,  doxoR,    Protective effect of thymoquinone against doxorubicin-induced cardiotoxicity and the underlying mechanism
- vitro+vivo, NA, NA
*cardioP↑, *NRF2↑, *HO-1↑, *ROS↓, *NQO1↑, *COX2↓, *NOX4↓, *GPx4↑, *FTH1↑, *p‑mTOR↓, *TGF-β↓,
2129- TQ,  doxoR,    Thymoquinone up-regulates PTEN expression and induces apoptosis in doxorubicin-resistant human breast cancer cells
- in-vitro, BC, MCF-7
ChemoSen↑, PTEN↑, p‑Akt↓, TumCCA↑, P53↑, P21↑, Apoptosis↑, MMP↓, Casp↑, cl‑PARP↑, Bax:Bcl2↑, eff↓, DNAdam↓, p‑γH2AX↑, ROS↑,
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↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 38

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   HO-1↓, 2,   Keap1↓, 1,   MDA↓, 1,   NRF2↓, 3,   NRF2∅, 1,   ROS↑, 14,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 4,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   HK2↓, 1,   LDH↑, 1,   LDHA↓, 1,   PI3K/Akt↓, 1,  

Cell Death ⓘ

p‑Akt↓, 3,   Apoptosis↑, 5,   Apoptosis∅, 1,   p‑BAD↓, 1,   BAX↓, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-2↑, 1,   Casp↑, 1,   Casp3↓, 1,   Casp3↑, 4,   cl‑Casp3↑, 1,   Casp7↓, 1,   Casp9↑, 1,   necrosis↑, 2,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 3,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,  

DNA Damage & Repair ⓘ

p‑CHK1↓, 1,   DNAdam↓, 1,   DNAdam↑, 2,   DNMTs↓, 1,   P53↑, 1,   PARP↝, 1,   cl‑PARP↑, 3,   γH2AX↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   E2Fs↓, 1,   P21↑, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD133↓, 1,   cMET↓, 1,   CSCs↓, 1,   HDAC↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↓, 1,   PTEN↑, 1,   TumCG↓, 2,   TumCG∅, 2,  

Migration ⓘ

Ca+2↑, 2,   ER-α36↓, 1,   Ki-67↓, 1,   NeuroT↓, 1,   TRPC1↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

EPR↑, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

BNP↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   BioEnh↑, 6,   ChemoSen↑, 14,   ChemoSen∅, 2,   Dose↓, 1,   Dose↝, 1,   eff↓, 2,   eff↑, 8,   MRP1↓, 1,   selectivity?, 1,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,   LDH↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   antiNeop∅, 1,   cardioP↑, 3,   CardioT↓, 1,   chemoP↑, 3,   hepatoP↑, 2,   neuroP↑, 1,   OS↑, 3,   Remission↑, 1,   RenoP↑, 1,   toxicity↝, 1,   TumVol↓, 5,  
Total Targets: 99

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Ferroptosis↓, 1,   GPx4↑, 1,   GSH↑, 3,   HO-1↑, 2,   MDA↓, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 7,   ROS↓, 9,   ROS∅, 1,   SIRT3↑, 2,   SOD↑, 2,   SOD2↑, 2,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,  

Mitochondria & Bioenergetics ⓘ

mitResp↑, 2,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,   PPARγ↑, 2,  

Cell Death ⓘ

Ferroptosis↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Mst1↓, 1,   p‑mTOR↓, 1,  

Migration ⓘ

TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   TNF-α↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   eff↓, 2,  

Clinical Biomarkers ⓘ

LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 8,   CardioT↓, 1,   toxicity↓, 1,  
Total Targets: 34

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#:%  State#:%  Dir#:%
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