diet FMD Fasting Mimicking Diet / RAS 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


RAS, RAS: Click to Expand ⟱
Source: CGL-CS
Type: oncogene
Family of RAS proteins (KRAS, NRAS, and HRAS) have been well described to cause oncogenic transformation.

- The expression and mutational status of RAS isoforms are critical in several cancers and are generally linked with a poorer prognosis when mutated.
RAS is one of the most frequently activated oncogenic drivers in human cancer. Mutations lock RAS in its GTP-bound active state, making signaling:
-Constitutive
-Growth-factor independent
-Resistant to normal feedback control

Key framing: RAS is a true driver oncogene, not just an amplifier.

Core Oncogenic Pathways Downstream of RAS
RAS sits at the apex of multiple essential signaling cascades:
a. MAPK Pathway (RAF–MEK–ERK)
-Drives proliferation
-Induces cell-cycle genes (Cyclin D, MYC, FOS/AP-1)
-Supports invasion and differentiation blockade

b. PI3K–AKT–mTOR
-Promotes survival and metabolic reprogramming
-Enhances resistance to apoptosis
-Supports protein synthesis and growth

c. RAL-GDS and Others
-Cytoskeletal remodeling
-Vesicle trafficking
-Metastatic behavior

Together, these create a multi-axis growth and survival program.


Scientific Papers found: Click to Expand⟱
1854- dietFMD,    How Far Are We from Prescribing Fasting as Anticancer Medicine?
- Review, Var, NA
ChemoSideEff↓, ChemoSen↑, IGF-1↓, IGFBP1↑, adiP↑, glyC↓, E-cadherin↑, MMPs↓, Casp3↑, ROS↑, ATP↓, AMPK↑, mTOR↓, ROS↑, Glycolysis↓, NADPH↓, OXPHOS↝, eff↑, eff↑, *RAS↓, *MAPK↓, *PI3K↓, *Akt↓, eff↑, ROS↑, Akt↑, Casp3↑,
5067- dietFMD,    Fasting-mimicking diet potentiates anti-tumor effects of CDK4/6 inhibitors against breast cancer by suppressing NRAS- and IGF1-mediated mTORC1 signaling
- in-vitro, BC, NA
mTORC1↓, IGF-1↓, RAS↓,

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 ⓘ

OXPHOS↝, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 1,   AMPK↑, 1,   glyC↓, 1,   Glycolysis↓, 1,   NADPH↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Casp3↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 2,   IGFBP1↑, 1,   mTOR↓, 1,   mTORC1↓, 1,   RAS↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMPs↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 3,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Akt↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   RAS↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: RAS, RAS
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#:269  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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