diet FMD Fasting Mimicking Diet / PI3K Cancer Research Results

dietFMD, diet FMD Fasting Mimicking Diet: Click to Expand ⟱
Features:
5-day diet to mimic fasting without fasting.
FMDs are caloric-restricted plant–based diets containing low proteins, low sugar and high fats which represent a more feasible and safer option to water-only fasting.
Fasting modality                         Approx CRIS
--------------------------------------   ----------
Time-restricted eating (12–16 h)          –3 to –4
Early time-restricted eating (eTRE)        –4
Intermittent fasting (24 h 1–2x/week)     –4
Periodic fasting / FMD                    –4 to –5*
Calorie restriction (chronic)             –3 (risk tradeoffs)

Compare STF(short term Fasting) to FMD
IGF-1 / insulin suppression (core driver)
| Aspect            | STF                 | FMD      |
| ----------------- | ------------------- | -------- |
| Depth             | **Very deep**       | Moderate |
| Speed             | **Rapid (24–48 h)** | Gradual  |
| Tumor stress      | **High**            | Medium   |
| Normal protection | High                | High     |
Fasting-Mimicking Diet (FMD; ~5-day low-protein, low-calorie cycle) Cancer vs Normal Cell Effects
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Insulin / IGF-1 signaling ↓ IGF-1 signaling (chronic stress) ↓ IGF-1 with regenerative priming Driver Sustained growth factor suppression Repeated IGF-1 lowering impairs tumor growth programs
2 AMPK → mTOR nutrient sensing ↓ mTOR; ↑ AMPK (growth inhibition) ↓ mTOR; ↑ AMPK (maintenance mode) Driver Prolonged anabolic suppression More sustained but less acute than STF
3 Autophagy / mitophagy ↑ autophagy → loss of tumor robustness ↑ autophagy → rejuvenation Driver Cellular renewal vs destabilization Repeated cycles promote organelle quality control
4 Mitochondrial metabolism ↓ metabolic resilience ↑ mitochondrial fitness Secondary Energy efficiency divergence Normal cells adapt better across cycles
5 Inflammatory signaling (NF-κB / cytokines) ↓ pro-tumor inflammation ↓ systemic inflammation Secondary Anti-inflammatory milieu Inflammation reduction contributes to chemopreventive effects
6 Reactive oxygen species (ROS) ↑ ROS (secondary, context-dependent) ↓ ROS Secondary Metabolism-linked redox shift ROS effects are indirect and less pronounced than STF
7 NRF2 antioxidant response ↔ modest activation ↑ NRF2 (protective) Adaptive Stress adaptation NRF2 supports normal-cell recovery between cycles
8 Cell cycle / regeneration ↓ proliferation ↑ regeneration post-cycle Phenotypic Degrowth vs regeneration FMD uniquely promotes regeneration upon refeeding


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⟱
1860- dietFMD,  Chemo,    Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape
- in-vitro, BC, SUM159 - in-vitro, BC, 4T1
PI3K↑, Akt↑, mTOR↑, CDK4↑, CDK6↑, hyperG↓, TumCG↓, TumVol↓, Casp3↑, BG↓, eff↑, eff∅, PKA↓, KLF5↓, p‑GSK‐3β↑, Nanog↓, OCT4↓, KLF2↓, eff↑, ROS↑, BIM↑, ASK1↑, PI3K↑, Akt↑, mTOR↑, CDK1↓, CDK4↑, CDK6↑, eff↑,
1844- dietFMD,    Unlocking the Potential: Caloric Restriction, Caloric Restriction Mimetics, and Their Impact on Cancer Prevention and Treatment
- Review, NA, NA
Risk↓, AMPK↑, Akt↓, mTOR↓, SIRT1↑, Hif1a↓, NRF2↓, SOD↑, ROS↑, IGF-1↓, p‑Akt↓, PI3K↑, GutMicro↑, OS↑, eff↝, ROS↑, TumCCA↑, *DNArepair↑, DNAdam↑,

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 ⓘ

hyperG↓, 1,   NRF2↓, 1,   ROS↑, 3,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

KLF5↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 2,   p‑Akt↓, 1,   ASK1↑, 1,   BIM↑, 1,   Casp3↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK4↑, 2,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,   IGF-1↓, 1,   mTOR↓, 1,   mTOR↑, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↑, 3,   TumCG↓, 1,  

Migration ⓘ

KLF2↓, 1,   PKA↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 2,  

Drug Metabolism & Resistance ⓘ

eff↑, 3,   eff↝, 1,   eff∅, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

OS↑, 1,   Risk↓, 1,   TumVol↓, 1,  
Total Targets: 37

Pathway results for Effect on Normal Cells:


DNA Damage & Repair ⓘ

DNArepair↑, 1,  
Total Targets: 1

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#:79  Target#:252  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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