doxorubicin / ChemoSen 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)

ChemoSen, chemo-sensitization: Click to Expand ⟱

Source:

Type:

The effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them, which is known as “chemo-sensitization”.

Chemo-Sensitizers:
-Curcumin
-Resveratrol
-EGCG
-Quercetin
-Genistein
-Berberine
-Piperine: alkaloid from black pepper
-Ginsenosides: active components of ginseng
-Silymarin
-Allicin
-Lycopene
-Ellagic acid
-caffeic acid phenethyl ester
-flavopiridol
-oleandrin
-ursolic acid
-butein
-betulinic acid

Scientific Papers found: Click to Expand⟱

4431-

AgNPs,

doxoR,

Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy

in-vitro,

BC,

4T1

PA-AgNPs have an average hydrodynamic diameter of 130 nm

in-vivo,

BC,

4T1

in-vitro,

Nor,

3T3

AntiCan↑, ROS↑, TumVol↓, EPR↑, selectivity↑, ChemoSen↑,

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↑,

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,

in vivo xenograft model of ovarian cancer.

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↝,

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↓,

1965-

GamB,

doxoR,

Gambogic acid sensitizes ovarian cancer cells to doxorubicin through ROS-mediated apoptosis

in-vitro,

Ovarian,

SKOV3

eff↑, AntiCan↑, ROS↑, 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↑,

506-

MF,

doxoR,

Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells

in-vitro,

OS,

LM8

5 mT, 200 Hz

x2 fold improved

The IC50 for combined PEMF and doxorubicin was about 2-fold lower than that of doxorubicin alone, suggesting that PEMF enhanced the antiproliferative activity of doxorubicin.

TumCP↓, p‑CHK1↓, Ca+2↑, Casp3↓, Casp7↓, p‑BAD↓, ChemoSen↑,

5610-

NaHCO3,

doxoR,

Sodium bicarbonate nanoparticles modulate the tumor pH and enhance the cellular uptake of doxorubicin

vitro+vivo,

BC,

4T1

mice bearing orthotropic 4T1 breast cancer tumors

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↑,

89-

QC,

doxoR,

Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c-met

in-vitro,

Pca,

PC3

 10 uM

 PC3/R

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

100uM

51.42 uM

in-vivo,

NA,

quercetin 100 mg/kg day or DOX 5 mg/kg

mice

cardioP↑, hepatoP↑, TumCG↓, OS↑, ChemoSen↑, chemoP↑, Hif1a↓, *Hif1a↑, selectivity↑, TumVol↓, OS↑,

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

 75 uM

in-vitro,

NA,

CD133+

CSC

Bcl-2↓, TumCCA↑, CD133↓, CSCs↓, ChemoSen↑, CycB/CCNB1↑, cycE/CCNE↓, cycD1/CCND1↓, E2Fs↓,

4504-

SeNPs,

Chit,

FA,

doxoR,

pH-responsive selenium nanoparticles stabilized by folate-chitosan delivering doxorubicin for overcoming drug-resistant cancer cells

in-vitro,

Var,

ChemoSen↑, Apoptosis↑, Casp3↑, PARP↝,

2129-

TQ,

doxoR,

Thymoquinone up-regulates PTEN expression and induces apoptosis in doxorubicin-resistant human breast cancer cells

in-vitro,

BC,

MCF-7

25, 50 or 100 µM TQ

ChemoSen↑, PTEN↑, p‑Akt↓, TumCCA↑, P53↑, P21↑, Apoptosis↑, MMP↓, Casp↑, cl‑PARP↑, Bax:Bcl2↑, eff↓, DNAdam↓, p‑γH2AX↑, ROS↑,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,
Total Targets: 1

Scientific Paper Hit Count for: ChemoSen, chemo-sensitization

15 doxorubicin
3 Quercetin
2 Magnetic Fields
1 Silver-NanoParticles
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Baicalein
1 Baicalin
1 Chrysin
1 Gambogic Acid
1 Bicarbonate(Sodium)
1 Piperine
1 Selenium NanoParticles
1 chitosan
1 Folic Acid, Vit B9
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#:1106  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

doxorubicin / ChemoSen Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Angiogenesis & Vasculature ⓘ

Home Page