Chemotherapy / PI3K 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.
PI3K, Phosphatidylinositide-3-Kinases: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS
Type:
Phosphatidylinositol 3-kinase (PtdIns3K or PI3K) is a family of enzymes that play a crucial role in cell signaling pathways, particularly in the regulation of cell growth, survival, and metabolism. The PI3K pathway is one of the most frequently altered pathways in human cancer. Inhibition of the PI3K pathway has been explored as a therapeutic strategy for cancer treatment. Several PI3K inhibitors have been developed and are currently being tested in clinical trials. These inhibitors can target specific components of the pathway, such as PI3K, AKT, or mTOR.

Class I phosphoinositide 3-kinase (PI3K)
Class III PtdIns3K
In contrast to the class III PtdIns3K as a positive regulator of autophagy, class I PI3K-AKT signaling has an opposing effect on the initiation of autophagy.

PI3K inhibitors include:
-Idelalisib , Copanlisib, Alpelisib
-LY294002?
-Wortmannin: potent PI3K inhibitor, has some associated toxicity.
-Quercetin:
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)
Scientific Papers found: Click to Expand⟱
2584- Api,  Chemo,    The versatility of apigenin: Especially as a chemopreventive agent for cancer
- Review, Var, NA
ChemoSen↑, RadioS↑, eff↝, DR5↑, selectivity↑, angioG↓, selectivity↑, chemoP↑, MAPK↓, PI3K↓, Akt↓, mTOR↓, Wnt↓, β-catenin/ZEB1↓, GLUT1↓, radioP↑, BioAv↓, chemoPv↑,
1861- dietFMD,  Chemo,    Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models
- in-vitro, Colon, CT26 - in-vivo, NA, NA
selectivity↑, ChemoSen↑, BG↓, AminoA↓, Warburg↓, OCR↑, ATP↓, ROS↑, Apoptosis↑, GlucoseCon↓, PI3K↓, PTEN↑, GLUT1↓, GLUT2↓, HK2↓, PFK1↓, PKA↓, ATP:AMP↓, Glycolysis↓, lactateProd↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

AminoA↓, 1,   ATP:AMP↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PFK1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   DR5↑, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   PI3K↓, 2,   PTEN↑, 1,   Wnt↓, 1,  

Migration ⓘ

PKA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

BG↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   radioP↑, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PI3K, Phosphatidylinositide-3-Kinases
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#:252  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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