diet FMD Fasting Mimicking Diet / PTEN 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


PTEN, phosphatase and tensin homolog; phosphatase and tensin homolog pseudogene 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
PTEN (Phosphatase and Tensin Homolog) is a crucial tumor suppressor gene that plays a significant role in regulating cell growth, proliferation, and survival. It encodes a protein that functions as a phosphatase, which means it removes phosphate groups from specific molecules, thereby regulating various signaling pathways, particularly the PI3K/AKT pathway.
PTEN is mutated, deleted, or otherwise inactivated. This loss of function can lead to increased cell proliferation and survival, contributing to tumorigenesis. PTEN mutations are commonly found in various cancers, including:
Prostate cancer
Breast cancer
Endometrial cancer
Glioblastoma
Scientific Papers found: Click to Expand⟱
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 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 ⓘ

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 ⓘ

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

PKA↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PTEN, phosphatase and tensin homolog; phosphatase and tensin homolog pseudogene 1
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#:267  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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