Hyperthermia / ROS Cancer Research Results

HPT, Hyperthermia: Click to Expand ⟱
Features:
Mild Hyperthermia (Approximately 39°C to 41°C
Pathways and Effects:
-Heat Shock Protein (HSP) Induction: Mild heat stress triggers the production of HSPs (e.g., HSP70, HSP90) that help cells cope with stress, which can sometimes provide a transient protective effect. However, these proteins can also act as immunomodulators.
-Modulation of the Immune System: Mild hyperthermia can enhance dendritic cell activation and improve antigen presentation, leading to the stimulation of anti-tumor immune responses.
-Vasodilation: Increased blood flow and improved oxygenation can sensitize tumors to radiation therapy and certain chemotherapeutics.

Moderate Hyperthermia (Approximately 41°C to 43°C)
Pathways and Effects:
-Enhanced Cytotoxicity: At temperatures in this range, tumor cells become more vulnerable to radiation and some chemotherapeutic agents. This is partly due to the inhibition of DNA repair pathways.
-Increased Permeability: Moderate heat can increase the permeability of cellular membranes, aiding in drug delivery and the uptake of chemotherapeutic agents.
-Induction of Apoptosis: Elevated temperatures can trigger apoptotic signaling pathways in cancer cells, sometimes in conjunction with other therapies.

High Hyperthermia / Thermal Ablation (Approximately 43°C to 50°C and above)
Pathways and Effects:
-Direct Cytotoxicity: High temperatures can lead to protein denaturation, membrane disruption, and direct cell death.
-Coagulative Necrosis: Sustained high temperatures cause irreversible cell injury leading to necrosis of tumor tissues.
-Vascular Damage: Hyperthermia in this range can damage tumor vasculature, reducing blood supply and indirectly causing tumor cell death.
-Enhanced Immune Response: Although high temperatures can cause immediate cell death, the release of tumor antigens and damage-associated molecular patterns (DAMPs) can stimulate an anti-tumor immune response


Hyperthermia — a physical anticancer treatment modality in which tumor tissue is deliberately heated, usually to approximately 39–43°C for tens of minutes, using electromagnetic energy, ultrasound, infrared heating, heated perfusate, or related techniques. It is formally classified as a thermal therapy rather than a drug and is most commonly abbreviated HT; the Nestronics database uses HPT. Local, superficial, interstitial, and regional hyperthermia are distinct from thermal ablation, where substantially greater thermal doses are intended to directly destroy tissue. Therapeutic hyperthermia is primarily used as an adjunct to radiotherapy or chemotherapy rather than as a stand-alone systemic cancer treatment. Its biological activity depends strongly on temperature, duration, spatial temperature distribution, tumor perfusion, and timing relative to other therapy.

Primary mechanisms (ranked):

  1. Radiosensitization through inhibition of DNA-damage repair, particularly transient suppression of homologous recombination through BRCA2 degradation and impaired RAD51-dependent repair.
  2. Proteotoxic stress and disruption of protein folding, macromolecular complexes, membranes, and cytoskeletal structures as thermal dose increases.
  3. Tumor perfusion and oxygenation modulation; mild hyperthermia can increase blood flow and reduce hypoxia, thereby increasing radiation sensitivity.
  4. Chemosensitization through increased tumor perfusion and drug delivery, membrane permeability, impaired DNA repair, and heat-dependent enhancement of cytotoxic drug activity.
  5. Mitochondrial and cellular stress leading to apoptosis and, at greater thermal doses, irreversible necrotic cell injury.
  6. Heat-shock response with HSF1-driven HSP70/HSP90 induction; this is an important adaptive counter-response that can produce thermotolerance and partially oppose therapeutic cytotoxicity.
  7. Immune modulation through stress-protein signaling, antigen release, DAMP-associated signaling, and altered immune-cell trafficking and antigen presentation.
  8. ROS and oxidative-stress amplification as a secondary, temperature- and model-dependent contributor to mitochondrial injury, apoptosis, and radiosensitization.

Bioavailability / PK relevance: Not applicable in the conventional pharmacokinetic sense because hyperthermia is a locally delivered physical modality rather than a circulating drug. The analogous exposure variable is thermal dose, commonly characterized by achieved temperature, treatment duration, spatial coverage, and metrics such as cumulative equivalent minutes at 43°C. Clinical effectiveness depends on adequate and reasonably homogeneous heating of the target while limiting normal-tissue hot spots. Tumor depth, perfusion, tissue composition, applicator geometry, coupling, thermometry, and treatment planning are therefore major delivery constraints.

In-vitro vs systemic exposure relevance: Hyperthermia is not concentration-driven. In-vitro temperature exposures can be tightly controlled and spatially uniform, whereas clinical tumors commonly exhibit substantial temperature heterogeneity. Mechanistic findings obtained at 41–43°C are clinically relevant when comparable intratumoral thermal doses are actually achieved; experiments at higher temperatures or prolonged exposures increasingly model thermal ablation rather than conventional oncologic hyperthermia.

Clinical evidence status: RCT-supported adjunct treatment in selected cancers, particularly in combination with radiotherapy, re-irradiation, or chemotherapy. Randomized studies demonstrate improved local response or progression-related outcomes in settings including superficial or recurrent breast tumors, locally advanced pelvic tumors, and high-risk soft-tissue sarcoma. Survival benefit is disease- and regimen-dependent and has not been demonstrated uniformly. Hyperthermia remains specialized and is not widely available. FDA-regulated RF/microwave hyperthermia systems have been cleared or approved for defined oncologic indications. Major practical limitations are achieving adequate target thermal dose, avoiding normal-tissue hot spots, specialized equipment and expertise, and integration with radiotherapy or chemotherapy. Local adverse effects include discomfort, pain, burns and blistering; regional perfusion and whole-body techniques have additional systemic risks.

Hyperthermia Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 DNA repair inhibition and radiosensitization BRCA2 ↓; RAD51-dependent HR ↓; radiation sensitivity ↑ DNA repair may also be heat-sensitive, but normally perfused tissue is generally more thermally protected R Radiosensitization ↑ One of the best-defined molecular mechanisms. Approximately 41–43°C can transiently impair homologous recombination, creating a period of increased sensitivity to ionizing radiation and potentially other DNA-damaging therapies.
2 Proteotoxic stress and protein stability Protein unfolding ↑; aggregation ↑; proteostasis stress ↑ Proteotoxic stress ↑ (dose-dependent) P, R Cellular stress and thermal cytotoxicity ↑ Heat directly alters protein conformation and macromolecular complexes. Direct cytotoxicity becomes progressively more important as thermal dose increases.
3 Tumor perfusion and oxygenation Blood flow ↑; oxygenation ↑; hypoxia ↓ (mild hyperthermia, context-dependent) Perfusion ↑ P, R Radiation response ↑; drug delivery may ↑ Often strongest around mild temperatures near 39–42°C. At excessive thermal doses vascular function can instead deteriorate, so the direction is temperature- and tissue-dependent.
4 Chemosensitization Drug delivery ↑; drug cytotoxicity ↑; DNA repair capacity ↓ (drug-dependent) Drug exposure or toxicity may ↑ locally R, G Chemotherapy efficacy ↑ Synergy is agent-specific. Mechanisms include improved perfusion, altered membrane transport and protein function, and interference with repair of chemotherapy-induced DNA damage.
5 Heat shock response and thermotolerance HSF1 ↑; HSP70/HSP90 ↑; thermotolerance ↑ HSPs ↑; cytoprotection ↑ R, G Adaptive resistance ↑ A major counter-regulatory mechanism rather than a purely anticancer effect. Prior heat exposure can reduce sensitivity to subsequent heating, making treatment interval and thermal history important.
6 Mitochondrial injury and intrinsic apoptosis Mitochondrial dysfunction ↑; membrane potential ↓; cytochrome c release ↑; apoptosis ↑ Mitochondrial injury ↑ at excessive thermal dose R, G Programmed cell death ↑ Importance rises with temperature and exposure duration. Tumor susceptibility varies substantially among cell types.
7 Membrane and cytoskeletal disruption Membrane fluidity and permeability ↑; trafficking disruption ↑; cytoskeletal stress ↑ Similar changes ↑ (dose-dependent) P, R Cell stress and drug uptake ↑ Provides one contributor to heat-mediated chemosensitization but is not selectively confined to malignant cells.
8 Immune and DAMP signaling DAMP release ↑; extracellular HSP signaling ↑; tumor-antigen availability ↑ Immune-cell trafficking and activation ↝ (context-dependent) G Antitumor immune visibility ↑ Potentially useful for combination with radiotherapy and immunotherapy, but clinical magnitude depends strongly on thermal regimen, tumor type, immune context, and concurrent treatment.
9 Oxidative and mitochondrial ROS stress ROS ↑ (secondary, dose-dependent); oxidative damage ↑ ROS ↑ at sufficient thermal stress P, R Stress signaling and cell death ↑ Mechanistically relevant in multiple experimental systems but less central and less universal than DNA-repair inhibition, proteotoxicity, and perfusion-mediated radiosensitization.
10 Direct thermal cell death Apoptosis ↑; necrosis ↑ as thermal dose rises Collateral thermal injury ↑ at excessive dose R, G Tumor cell survival ↓ Conventional hyperthermia emphasizes sensitization and sublethal thermal stress. At substantially greater temperature-time exposures direct coagulative injury dominates and treatment should more appropriately be classified as thermal ablation.
11 Clinical Translation Constraint Therapeutic effect depends on temperature coverage, duration, tumor perfusion, depth, and combination-treatment timing Hot spots can cause pain, burns, blistering, or deeper tissue injury P, R, G Reproducibility and therapeutic window limitation No conventional PK applies. Thermal heterogeneity, applicator geometry, thermometry, treatment planning, patient anatomy, tumor perfusion, and specialized equipment are major determinants of clinical efficacy. Evidence supports selected adjunct applications rather than universal use across cancers.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr

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ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
7620- HPT,    Hyperthermia and radiotherapy: physiological basis for a synergistic effect
- Review, Var, NA
RadioS↑, DNArepair↓, Hypoxia↓, CSCs↓, Imm↑, pH↝, HSPs↑, ROS↑, eff↑,
7622- HPT,    A Review of the Current Clinical Evidence for Loco-Regional Moderate Hyperthermia in the Adjunct Management of Cancers
- Review, Var, NA
LC↑, OS↑, QoL↑, toxicity↓, Dose↝, Dose↝, ROS↑, DNArepair↓, EPR↑, DNAdam↑, HSP70/HSPA5↑, BloodF↑, Hypoxia↓,
886- HPT,    Impact of hyper- and hypothermia on cellular and whole-body physiology
- Analysis, NA, NA
MMP↓, OXPHOS↓, ATP↓, ROS↑, Apoptosis↑, Cyt‑c↑,
7572- HPT,  Rad,    The effect of thermal dose on hyperthermia-mediated inhibition of DNA repair through homologous recombination
- in-vitro, Cerv, HeLa - in-vitro, Laryn, FaDu
RadioS↑, TumCD↑, BRCA2↓, Dose↝, BloodF↑, ROS↑, Imm↑,
5054- HPT,    Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification
- Review, Var, NA
eff↓, ROS↑, Apoptosis↑,
5053- HPT,  Rad,  Chemo,    Association of elevated reactive oxygen species and hyperthermia induced radiosensitivity in cancer stem-like cells
- in-vitro, Var, NA
CSCs↓, TumCP↓, ROS↑, RadioS↑,
5052- HPT,    Hyperthermia Induces Apoptosis through Endoplasmic Reticulum and Reactive Oxygen Species in Human Osteosarcoma Cells
- in-vitro, OS, U2OS
Apoptosis↑, ROS↑, Casp3↑, mtDam↑, Cyt‑c↑, Bcl-2↓, Bcl-xL↓, Bak↑, BAX↓, ER Stress↑, Ca+2↝, cal2↑,
5051- HPT,  doxoR,    Hyperthermia Enhances Doxorubicin Therapeutic Efficacy against A375 and MNT-1 Melanoma Cells
- in-vitro, Melanoma, A375
tumCV↓, TumCCA↑, ROS↑, eff↑,
5050- HPT,    Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review
- Review, Nor, NA
*ROS↑, *SOD1↓, *GSH↓, other↑, HIF-1↑, ROS↑,
5049- HPT,    Nanoparticle-based hyperthermia distinctly impacts production of ROS, expression of Ki-67, TOP2A, and TPX2, and induction of apoptosis in pancreatic cancer
- vitro+vivo, PC, Panc02 - vitro+vivo, PC, Bxpc-3
tumCV↓, proCasp↑, ROS↑, Ki-67↓, TOP2↓, TumVol↓,
1674- PBG,  SDT,  HPT,    Study on the effect of a triple cancer treatment of propolis, thermal cycling-hyperthermia, and low-intensity ultrasound on PANC-1 cells
- in-vitro, PC, PANC1 - in-vitro, Nor, H6c7
tumCV↓, ROS↑, eff↑, Dose∅, selectivity↑, MMP↓, mtDam↑, cl‑PARP↑, p‑ERK↓, p‑JNK↑, p‑p38↑, eff↓, ChemoSen↑,

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

LC↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

OXPHOS↓, 1,   ROS↑, 11,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   MMP↓, 2,   mtDam↑, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 3,   Bak↑, 1,   BAX↓, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   proCasp↑, 1,   Casp3↑, 1,   Cyt‑c↑, 2,   p‑JNK↑, 1,   p‑p38↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   tumCV↓, 3,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 1,   HSPs↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA2↓, 1,   DNAdam↑, 1,   DNArepair↓, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CSCs↓, 2,   p‑ERK↓, 1,   TOP2↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↝, 1,   cal2↑, 1,   Ki-67↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EPR↑, 1,   HIF-1↑, 1,   Hypoxia↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 3,   Dose∅, 1,   eff↓, 2,   eff↑, 3,   RadioS↑, 3,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 2,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

OS↑, 1,   QoL↑, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 52

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,   SOD1↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
11 Hyperthermia
2 Radiotherapy/Radiation
1 Chemotherapy
1 doxorubicin
1 Propolis -bee glue
1 SonoDynamic Therapy UltraSound
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#:98  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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