Chemotherapy / H2O2 Cancer Research Results

Chemo, Chemotherapy: Click to Expand ⟱
Features: treatment category
Chemotherapy is a treatment approach that uses drugs to target and kill rapidly dividing cells, primarily cancer cells. However, because many normal cells also divide quickly (such as those in the bone marrow, digestive tract, and hair follicles), chemotherapy can also affect these cells, leading to a range of side effects.

Main Classes of Chemotherapy Agents and Examples
Alkylating Agents:
-work by adding alkyl groups to DNA, which interferes with the DNA’s structure and prevents replication.
Examples: Cyclophosphamide, Ifosfamide, Melphalan, Chlorambucil, Busulfan.

Anti-metabolites:
-interfere with DNA and RNA synthesis by substituting for the normal building blocks of nucleic acids.
Examples: Methotrexate, 5-Fluorouracil (5-FU), Cytarabine, Gemcitabine, 6-Mercaptopurine.

Anti-microtubule Agents:
-interfere with the structures that separate chromosomes during cell division (mitosis). Examples: Paclitaxel, Docetaxel, Vincristine, Vinblastine.

Topoisomerase Inhibitors:
-target the enzymes topoisomerase I and II, which control the changes in DNA structure required for replication.
Examples: Etoposide (topoisomerase II inhibitor), Irinotecan (topoisomerase I inhibitor), Topotecan.

Cytotoxic Antibiotics:
-intercalate into DNA, inhibiting the replication of cancer cells.
Examples: Doxorubicin, Daunorubicin, Bleomycin, Mitoxantrone.

Platinum-Based Agents:
-contain platinum and cause cross-linking of DNA, which interferes with DNA repair and replication. Examples: Cisplatin, Carboplatin, Oxaliplatin.

Many chemotherapy agents exert their effects, at least in part, by inducing oxidative stress in cancer cells. They can increase ROS levels through several mechanisms:
-Direct generation of free radicals.
-Disruption of mitochondrial function, leading to increased production of ROS.
-Interference with the cell’s antioxidant systems.

-May want to avoid antioxidants 7 days bef
ore and 7 days after chemo.
Examples: NAC, Glutathione, Alpha Lipoic Acid, Vitamin E
-anti-oxidants known to have pro-oxidant effects (like Quercetin, Curcumin, etc.) should not be taken 2-3 days before and after chemo
-pro-oxidants known to bring good benefit to chemo can be continued during chemo. Examples are: Omega 3, Aremisia Annua, Silver NanoParticles.
H2O2, Hydrogen peroxide (H2O2): Click to Expand ⟱
Source:
Type:
H2O2 is a reactive oxygen species (ROS) that can induce oxidative stress in cells. While low levels of ROS can promote cell signaling and proliferation, high levels can lead to DNA damage, apoptosis (programmed cell death), and other cellular dysfunctions. This dual role means that H2O2 can contribute to cancer development and progression, as oxidative stress can lead to mutations and genomic instability.
H2O2 can enhance the effectiveness of certain chemotherapeutic agents by increasing oxidative stress in cancer cells. Additionally, localized delivery of H2O2 has been explored as a means to selectively target and kill cancer cells while sparing normal cells.
Cancer cells often exhibit altered metabolism, leading to increased production of reactive oxygen species, including H2O2. This can result from enhanced mitochondrial activity, increased glycolysis, or other metabolic adaptations that are characteristic of cancer.


Reported H2O2 concentrations for representative compounds.
   Prooxidant          Dose                   Cell Line            H2O2 Produced
EGCG50 µMJurkat~1 µM
EGCG10 µMHCT116 and HT291.5 µM
EGCG100 µMJurkat20 µM
Quercetin70 µMHT292 µM
Menadione10 µMJurkat20 µM
Plumbagin4 µMSiHA and HeLa1 mM
β-Lap1 µMHL-6070 µM
Doxorubicin1 µMPC338 pM
Ascorbic Acid 1 mMHL-60161 µM
Ascorbic Acid0.2–2.0 mMLymphoma20–120 µM
Ascorbic Acidi.v. 0.5 mg/gRats0–20 µM
Ascorbic Acidi.p. 4.0 g/kgMice tumor> 125 µM
TiO210 µg/mLHepG2150 nmol/mL
Paclitaxel100 nMMCF7600 nM
Paclitaxel100 nMHL-601100 nM

Note: many products at lower concentrations act as antioxidants, instead of Prooxidants.

Generally, increased hydrogen peroxide and oxidative stress are associated with poor outcomes, while the specific context and cellular environment can modulate its effects.
Scientific Papers found: Click to Expand⟱
2309- EGCG,  Chemo,    Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HPNE - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumCG↓, eff↑, ROS↑, ECAR↓, ChemoSen↑, selectivity↑, Glycolysis↓, PFK↓, PKA↓, HK2∅, LDHA∅, PFKP↓, PKM2↓, H2O2↑, TumW↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   HK2∅, 1,   LDHA∅, 1,   PFK↓, 1,   PFKP↓, 1,   PKM2↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

PKA↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

TumW↓, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: H2O2, Hydrogen peroxide (H2O2)
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#:233  Target#:138  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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