Chemotherapy / GSTs 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.


GSTs, Glutathione S-transferases: Click to Expand ⟱
Source:
Type:
Glutathione S-transferases (GSTs) are a family of phase II detoxification enzymes that play key roles in catalyzing the conjugation of glutathione (GSH) to a wide range of electrophilic compounds. This family includes multiple isoenzymes (e.g., GST-α, GST-μ, GST-π) with tissue-specific expression patterns and overlapping as well as distinct substrate specificities.

-GSTs are important for detoxifying potentially harmful compounds, including products of oxidative stress, environmental toxins, and chemotherapeutic agents.
-They contribute to the cellular defense mechanism against oxidative damage and help maintain cellular redox balance.
-Beyond detoxification, GSTs can modulate cell signaling pathways, potentially affecting cell proliferation, apoptosis, and drug resistance.

-GST-π is commonly upregulated in several cancers such as breast, lung, colorectal, and hematologic malignancies.
-Elevated expression of specific GST isoenzymes—most notably GST-π—has been associated with a poorer prognosis in several cancer types. This is often linked to resistance to chemo- or radiotherapy, as higher GST activity can lead to more efficient detoxification of these agents, reducing their cytotoxic effects.
-In contrast, reduced GST expression in some contexts might indicate a less robust detoxification system, which can correlate with increased sensitivity to oxidative stress and possibly a less aggressive tumor phenotype.


Scientific Papers found: Click to Expand⟱
2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, *Inflam↓, *antiOx↑, *lipid-P↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *ROS↓, *ALAT↓, *AST↓, *MDA↓, *NRF2↑, *COX2↑, *NF-kB↓, *ICAM-1↓, *MCP1↓, *HO-1↑, CXCc↓,

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:


Immune & Inflammatory Signaling

CXCc↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis

ALAT↓, 1,  

Immune & Inflammatory Signaling

COX2↑, 1,   ICAM-1↓, 1,   Inflam↓, 1,   MCP1↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes

hepatoP↑, 1,  
Total Targets: 20

Scientific Paper Hit Count for: GSTs, Glutathione S-transferases
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#:1153  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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