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.


Colon, Colon Cancer: Click to Expand ⟱
Colon cancer can start anywhere in the colon, (5 feet long) and absorbs water from stool. Rectal cancer starts in the rectum, which is the last 12 centimeters.
Scientific Papers found: Click to Expand⟱
7690- IP6,  Ins,    Inositol Hexaphosphate (IP6) and Colon Cancer: From Concepts and First Experiments to Clinical Application
- Review, Colon, NA
AntiCan↑, Imm↑, antiOx↑, TumCP↓, Diff↑, TumCG↓, eff↑, P21↓, p27/CDKN1B↓, pRB↓, TumCCA↑, PI3K↓, Akt↓, PKCδ↓, RAS↓, ERK↓, NF-kB↓, Inflam↓, MMP9↓, IronCh↑, NK cell↑, selectivity↑, ChemoSen↑, chemoP↑, toxicity↓, Remission↑,

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(tgid=1) ⓘ

antiOx↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p27/CDKN1B↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

pRB↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,   TumCCA↑, 1,  

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

Diff↑, 1,   ERK↓, 1,   PI3K↓, 1,   RAS↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

MMP9↓, 1,   PKCδ↓, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 1,   Remission↑, 1,   toxicity↓, 1,  
Total Targets: 26

Pathway results for Effect on Normal Cells:


Total Targets: 0

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

 

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