RAS Cancer Research Results

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↓, Synergy↑, ROS↑, Akt↑, Casp3↑,
6289- DL,    D-Limonene modulates inflammation, oxidative stress and Ras-ERK pathway to inhibit murine skin tumorigenesis
- in-vivo, Var, NA
COX2/PTGS2↓, *GSH↑, *GPx↑, *Catalase↑, Bcl-2↓, BAX↑, *chemoPv↑, *Inflam↓, *ROS↓, *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(tgid=1) ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

OXPHOS↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

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

Cell Death(tgid=5) ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↑, 1,   mTOR↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

IGF-1↓, 1,   IGFBP1↑, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   MMPs↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 2,   Synergy↑, 1,  

Functional Outcomes(tgid=23) ⓘ

ChemoSideEff↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   ROS↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   MAPK↓, 1,   PI3K↓, 1,   RAS↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,  
Total Targets: 10

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:1  prod#:%  Target#:269  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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