diet Methionine-Restricted Diet / TS Cancer Research Results

dietMet, diet Methionine-Restricted Diet: Click to Expand ⟱
Features:
Methionine (MET) restriction (MR) has been shown to arrest cancer growth and sensitizes tumors to chemotherapy.
-Many cancer cells rely heavily on exogenous methionine to sustain rapid growth and proliferation because they often have impaired methionine salvage pathways.
-Methionine contributes to the synthesis of glutathione, a key antioxidant. (Methionine is a precursor of glutathione, a tripeptide that reduces reactive oxygen species.)
-MR diets might influence the redox state of cancer cells, increasing oxidative stress and thereby leading to cell death in metabolically compromised tumor cells.
-Proliferation and growth of several types of cancer cells are inhibited by MR, while normal cells are unaffected by limiting methionine as long as homocysteine is present.
-Methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media. methionine is the precursor for cysteine which is essential for the formation of GSH.
-Malignant cells lack the enzyme required to recycle homocysteine therefore giving methionine restriction the capacity to alter cancer cells while maintaining normal, healthy cells.

While vegan diets are typically low in methionine, some nuts and legumes (such as Brazil nuts and kidney beans) are rich in methionine.

Foods to avoid for MR diet:
Animal Proteins:
-Red Meat (Beef, Pork, Lamb):
-Poultry (Chicken, Turkey):
-Fish and Seafood:
-Eggs: Both the egg whites and yolks are protein rich.
-Dairy Products: Milk, cheese, and yogurt
Certain Plant Proteins:
-Soy Products:
-Legumes:
Protein Supplements:

Foods Lower in Methionine (Often Favorable on an MR Diet)
Fruits & Vegetables: leafy greens, berries, apples, and citrus fruits.
Grains & Cereals: rice, oats, and barley
Nuts and Seeds: can vary in methionine content.
Alternative Protein Sources: emphasize protein sources with a lower methionine-to-cysteine ratio.

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 One-carbon metabolism (methionine cycle → folate cycle coupling) ↓ one-carbon flux (Met/SAM-linked metabolites) Core metabolic constraint Nature study shows dietary MR produces controlled, reproducible changes to one-carbon metabolism that alter cancer outcomes (ref)
2 Nucleotide biosynthesis (purines/thymidylate via one-carbon units) ↓ nucleotide synthesis capacity DNA/RNA synthesis limitation Same MR Nature paper links MR-driven one-carbon changes to pathways needed for proliferation and therapy response (ref)
3 Therapy sensitivity (chemo / targeted one-carbon therapy synergy) ↑ sensitivity / ↑ efficacy Therapeutic potentiation Dietary MR influences outcomes and can enhance responses to standard therapies through one-carbon metabolic rewiring (ref)
4 mTORC1 nutrient sensing (Met/SAM → SAMTOR mechanism) ↓ mTORC1 signaling when Met/SAM low Reduced anabolic growth signaling Mechanistic review: SAMTOR senses SAM (derived from methionine) and, when SAM is low, inhibits mTORC1 signaling (ref)
5 Integrated Stress Response (ISR; ATF4 induction under MR) ↑ ISR / ↑ ATF4 Amino-acid stress adaptation MR activates ISR in TNBC cells (eIF2α phosphorylation; ATF4 and targets up), demonstrating stress signaling engagement under methionine restriction (ref)
6 Glutathione (GSH) / ferroptosis coupling (CHAC1 axis) ↑ CHAC1 / ↓ GSH / ↑ ferroptosis (context-dependent) Redox vulnerability Intermittent dietary methionine deprivation augments tumoral ferroptosis; paper links effect to CHAC1 upregulation (CHAC1 promotes GSH degradation) (ref)
7 Epigenetic methylation capacity (SAM-dependent methylation) ↓ methylation potential (via ↓ SAM availability) Altered gene regulation Review focused on dietary methionine and cancer: MR impacts SAM-dependent methylation processes central to biosynthesis/regulation in tumors (ref)
8 Systemic growth signaling (IGF-1) ↓ IGF-1 Lower systemic pro-growth cue Intermittent MR reduces circulating IGF-1 (healthspan paper, but the endocrine direction is explicit and relevant to tumor growth biology) (ref)
9 Radiation sensitization (clinical feasibility context) ↑ RT sensitivity (preclinical); feasible in humans Translational evidence Phase I pilot: MR diet given concurrently with radiation—supports feasibility/safety; paper states preclinical evidence of MRD sensitizing cancer to RT (ref)
10 In vivo tumor growth ↓ tumor growth / ↓ progression (model-dependent) Demonstrated anti-tumor effect Nature MR paper demonstrates MR can influence tumor outcomes in mouse cancer models (ref)


TS, thymidylate synthase: Click to Expand ⟱
Source:
Type:
Thymidylate synthase (TS) is a key enzyme responsible for catalyzing the methylation of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), a crucial step in the synthesis of thymidine—one of the four nucleotides required for DNA replication and repair.
Due to its essential role in DNA synthesis, TS is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and other antifolates.
Many cancers exhibit elevated levels of TS expression compared to normal tissues.
High TS expression can contribute to rapid cell proliferation and tumor growth by ensuring a sufficient supply of thymidine for DNA synthesis.

Thymidylate synthase (TS) plays a central role in DNA synthesis and cell proliferation, making it a critical enzyme in cancer biology. Overexpression of TS is commonly observed in a range of tumor types and is associated with increased cellular proliferation, drug resistance, and generally poorer clinical outcomes. As both a therapeutic target and a prognostic marker, TS levels offer insight into tumor aggressiveness and potential responsiveness to chemotherapeutic agents.
Scientific Papers found: Click to Expand⟱
2264- dietMet,    Methionine restriction for cancer therapy: From preclinical studies to clinical trials
- Review, Var, NA
TumCP↓, *ROS?, ChemoSen↑, RadioS↑, eff↑, ROS↑, selectivity↑, TS↓, eff↑,
2263- dietMet,    Methionine Restriction and Cancer Biology
- Review, Var, NA
AntiCan↑, TumCP↓, TumCG↓, selectivity↑, ChemoSen↓, RadioS↑, Insulin↓, *GlucoseCon↑, *ROS↓, *antiOx↑, *GSH↑, GSH↑, eff↑, polyA↓, TS↓, Raf↓, Akt↓, Casp9↑, Bak↑, P21↑, p27↑, Insulin↓, IGF-1↓,

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 ⓘ

GSH↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

Insulin↓, 2,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

polyA↓, 1,   TS↓, 2,  

Cell Death ⓘ

Akt↓, 1,   Bak↑, 1,   Casp9↑, 1,   p27↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   ROS?, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↑, 1,  
Total Targets: 5

Scientific Paper Hit Count for: TS, thymidylate synthase
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#:292  Target#:1064  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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