doxorubicin 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)
Scientific Papers found: Click to Expand⟱
8879- MOR,  doxoR,    Synergistic Effects of Morin and Doxorubicin Overcome Chemoresistance in Ovarian Cancer: Preclinical Insights From in vitro and in vivo Models
- vitro+vivo, Ovarian, OVCAR-3 - NA, Melanoma, A2780S
Dose↝, ChemoSen↑, cycA1/CCNA1↓, cycD1/CCND1↓, TumVol↓, Apoptosis↑, TumCCA↑, ROS↝, chemoP↑, TumAuto↑, ROS↓, SOD↑, Catalase↑, GSH↑, MDA↓, cardioP↑, mTOR↓, PI3K↓, Akt↓, Bcl-2↓, Casp3↑, Casp9↑, LC3A↑, ATG5↑, Beclin-1/ATG6↑,
8886- MOR,  doxoR,    Morin overcomes doxorubicin resistance in human breast cancer by inducing DNA damage and modulating the LKB1/AMPK/mTORC1 signaling pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7
DNAdam↑, DNArepair↓, TumCCA↑, cycD1/CCND1↓, CDK4↓, cycE/CCNE↓, CycB/CCNB1↓, PARP↓, Bcl-xL↓, p‑AMPK↑, p‑STK11/LKB1↑, p‑mTOR↓, p‑Akt↓, p‑GSK‐3β↓, tumCV↓,
8772- MSM,  doxoR,    Methylsulfonylmethane sensitizes endometrial cancer cells to doxorubicin
- in-vitro, EC, NA
Apoptosis↑, ChemoSen↑, DNAdam↑, tumCV↓, ROS↑,
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↑,
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/ABCB1↓,
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↑,
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↓,
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↑,
1491- RES,  doxoR,  Cisplatin,    Resveratrol Augments Doxorubicin and Cisplatin Chemotherapy: A Novel Therapeutic Strategy
- in-vivo, Var, NA
RadioS↑, ChemoSen↑,
4738- Se,  doxoR,    Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway
- in-vivo, 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↝,
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, MCF7 - in-vitro, Nor, MCF10
CardioT↓, *GSH↑, *ROS↓, *NRF2↑, NRF2∅, HDAC↓, DNMTs↓, Casp3↑, ER-α36↓, Remission↑, ChemoSen↑, ROS↑, selectivity?,
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↓,
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↑,
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
ChemoSen↑, tumCV↓, TumCCA↑, ROS↑, MMP↓, eff↓, TumVol↓, eff↑, Ki-67↓,
2129- TQ,  doxoR,    Thymoquinone up-regulates PTEN expression and induces apoptosis in doxorubicin-resistant human breast cancer cells
- in-vitro, BC, MCF7
ChemoSen↑, PTEN↑, p‑Akt↓, TumCCA↑, P53↑, P21↑, Apoptosis↑, MMP↓, Casp↑, cl‑PARP↑, Bax:Bcl2↑, eff↓, DNAdam↓, p‑γH2AX↑, ROS↑,
3405- TQ,  doxoR,    Protective effect of thymoquinone against doxorubicin-induced cardiotoxicity and the underlying mechanism
- vitro+vivo, CardioV, NA
*cardioP↑, *NRF2↑, *HO-1↑, *ROS↓, *NQO1↑, *COX2/PTGS2↓, *NOX4↓, *GPx4↑, *FTH1↑, *p‑mTOR↓, *TGF-β↓,

Showing Research Papers: 51 to 68 of 68
Prev Page 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 68

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↓, 1,   Catalase↑, 1,   Fenton↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   HO-1↓, 2,   Iron↑, 1,   i-Iron↓, 1,   Keap1↓, 1,   lipid-P↑, 2,   MDA↓, 2,   MDA↑, 1,   i-MDA↑, 1,   mt-NADH↑, 1,   NRF2↓, 3,   NRF2∅, 1,   ROS↓, 3,   ROS↑, 22,   ROS↝, 3,   SOD↓, 1,   SOD↑, 1,   mt-SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↑, 2,   mt-OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

p‑AMPK↑, 1,   ATP↓, 1,   Glycolysis↓, 1,   p‑GSK‐3β↓, 1,   HK2↓, 1,   LDHA↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Apoptosis↑, 10,   Apoptosis∅, 1,   p‑BAD↓, 1,   BAX↓, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Bcl-2↑, 1,   Bcl-xL↓, 2,   Casp↑, 1,   Casp3↓, 1,   Casp3↑, 9,   cl‑Casp3↑, 1,   Casp7↓, 1,   Casp7↑, 1,   Casp9↑, 2,   Ferroptosis↑, 1,   necrosis↑, 2,   p38↑, 1,   survivin↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   p‑Akt↓, 4,   cMET↓, 1,   p‑EGFR↓, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   PI3K↓, 2,   PI3K/Akt↓, 1,   PTEN↓, 1,   PTEN↑, 1,   p‑STAT3↓, 1,   p‑STK11/LKB1↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

DNMTs↓, 1,   FOXM1↓, 1,   p‑H3↓, 1,   HDAC↓, 1,   other↑, 1,   other↝, 1,   other∅, 1,   tumCV↓, 10,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3A↑, 1,   LC3B↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   DNAdam↑, 5,   DNArepair↓, 1,   P53↑, 2,   PARP↓, 1,   PARP↝, 1,   cl‑PARP↑, 3,   PCNA↓, 1,   γH2AX↑, 2,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1?, 1,   CDK4↓, 1,   p‑CHK1↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 2,   E2Fs↓, 1,   Ki-67↓, 3,   P21↑, 2,   PLK1↓, 1,   TumCCA↑, 12,   TumCCA⇅, 1,  

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

ALDH↓, 1,   CD133↓, 1,   CSCs↓, 1,   Ki-67↓, 3,   TumCG↓, 3,   TumCG↑, 1,   TumCG∅, 2,   TumCP↓, 2,  

Migration(tgid=13) ⓘ

Ca+2↑, 2,   Na+↝, 1,   NeuroT↓, 1,   TumCI↓, 1,   TumCMig↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

CD31/PECAM-1↓, 1,   Hif1a↓, 1,   NO↑, 1,  

Barriers & Transport(tgid=15) ⓘ

EPR↑, 5,   MMP↓, 5,   Na+↝, 1,   TRPC1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   Imm↑, 2,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

BNP↓, 1,   ER-α36↓, 1,   PXR, NR1I2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   BioAv↝, 1,   BioEnh↑, 7,   ChemoSen?, 1,   ChemoSen↑, 36,   ChemoSen∅, 2,   CYP3A4↓, 1,   CYP3A4⇅, 1,   Dose?, 1,   Dose↓, 1,   Dose↝, 6,   eff↓, 3,   eff↑, 4,   eff↝, 1,   GSTA1↓, 1,   MDR1↓, 1,   MRP1/ABCC1↓, 2,   P-gp/ABCB1↓, 3,   RadioS↑, 1,   selectivity?, 1,   selectivity↑, 9,   Synergy↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

p‑EGFR↓, 1,   FOXM1↓, 1,   IL6↓, 1,   LDH↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   antiNeop↑, 1,   antiNeop∅, 1,   cardioP↑, 6,   CardioT↓, 1,   CardioT↝, 1,   chemoP↑, 6,   hepatoP↑, 2,   neuroP↑, 1,   OS↑, 3,   Remission↑, 1,   RenoP↑, 1,   toxicity↝, 1,   TumVol↓, 9,   TumW↓, 1,   Weight↑, 1,  
Total Targets: 171

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

4-HNE↓, 1,   antiOx↑, 5,   Catalase↑, 1,   GPx↑, 2,   GPx4↑, 2,   GSH↑, 5,   GSR↑, 1,   GSSG↓, 1,   HO-1↑, 2,   Iron↑, 1,   i-Iron↓, 1,   lipid-P↓, 3,   MDA↓, 2,   MPO↓, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 8,   ROS↓, 13,   ROS∅, 1,   SOD↑, 4,   SOD2↑, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↑, 1,   FTH1↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mitResp↑, 2,   SIRT3↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 3,   Ferroptosis↓, 2,   p38↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Mst1↓, 1,   p‑mTOR↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   TGF-β↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↑, 1,  

Barriers & Transport(tgid=15) ⓘ

MMP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   Inflam↓, 5,   NF-kB↓, 2,   NLRP3↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment(tgid=17) ⓘ

GGT/CD224↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARγ↑, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioEnh↑, 1,   Dose↝, 4,   eff↓, 2,   eff↑, 1,   GSTA1↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AST↓, 1,   CK/CK-MB↓, 1,   Ferritin↑, 1,   LDH↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 11,   CardioT↓, 1,   chemoP↑, 4,   toxicity↓, 3,  
Total Targets: 58

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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