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.


GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
5912- CAR,    Inhibition of TRPM7 by carvacrol suppresses glioblastoma cell proliferation migration and invasion
- in-vitro, GBM, U87MG - in-vitro, Nor, HEK293
TRPM7↓, tumCV↓, TumCMig↓, TumCI↓, MMP2↓, p‑Cofilin↑, RAS↓, MEK↓, MAPK↓, PI3K↓, Akt↓,
2127- TQ,    Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways
- Review, GBM, NA
chemoP↑, ChemoSen↑, BioAv↑, PTEN↑, PI3K↓, Akt↓, TumCCA↓, NF-kB↓, p‑Akt↓, p65↓, XIAP↓, Bcl-2↓, COX2↓, VEGF↓, mTOR↓, RAS↓, Raf↓, MEK↓, ERK↓, MMP2↓, MMP9↓, TumCMig↓, TumCI↓, Casp↑, cl‑PARP↑, ROS⇅, ROS↑, MMP↓, eff↑, Telomerase↓, DNAdam↑, Apoptosis↑, STAT3↓, RadioS↑,

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 ⓘ

ROS↑, 1,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 2,   MMP↓, 1,   Raf↓, 1,   XIAP↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   MAPK↓, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   mTOR↓, 1,   PI3K↓, 2,   PTEN↑, 1,   RAS↓, 2,   STAT3↓, 1,   TRPM7↓, 1,  

Migration ⓘ

p‑Cofilin↑, 1,   MMP2↓, 2,   MMP9↓, 1,   TumCI↓, 2,   TumCMig↓, 2,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   eff↑, 1,   RadioS↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 38

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

 

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