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.


Sepsis, Sepsis: Click to Expand ⟱
Sepsis is a potentially life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. This initial stage of sepsis is followed by suppression of the immune system. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion.


Scientific Papers found: Click to Expand⟱
2868- HNK,    Honokiol: A review of its pharmacological potential and therapeutic insights
- Review, Var, NA - Review, Sepsis, NA
*P-gp↓, *ROS↓, *TNF-α↓, *IL10↓, *IL6↓, eIF2α↑, CHOP↑, GRP78/BiP↑, BAX↑, cl‑Casp9↑, p‑PERK↑, ER Stress↑, Apoptosis↑, MMPs↓, cFLIP↓, CXCR4↓, Twist↓, HDAC↓, BMPs↑, p‑STAT3↓, mTOR↓, EGFR↓, NF-kB↓, Shh↓, VEGF↓, tumCV↓, TumCMig↓, TumCI↓, ERK↓, Akt↓, Bcl-2↓, Nestin↓, CD133↓, p‑cMET↑, RAS↑, chemoP↑, *NRF2↑, *NADPH↓, *p‑Rac1↓, *ROS↓, *IKKα↑, *NF-kB↓, *COX2↓, *PGE2↓, *Casp3↓, *hepatoP↑, *antiOx↑, *GSH↑, *Catalase↑, *RenoP↑, *ALP↓, *AST↓, *ALAT↓, *neuroP↑, *cardioP↑, *HO-1↑, *Inflam↓,

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:


Cell Death

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   cl‑Casp9↑, 1,   cFLIP↓, 1,  

Transcription & Epigenetics

tumCV↓, 1,  

Protein Folding & ER Stress

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   p‑PERK↑, 1,  

Proliferation, Differentiation & Cell State

CD133↓, 1,   p‑cMET↑, 1,   ERK↓, 1,   HDAC↓, 1,   mTOR↓, 1,   Nestin↓, 1,   RAS↑, 1,   Shh↓, 1,   p‑STAT3↓, 1,  

Migration

MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   Twist↓, 1,  

Angiogenesis & Vasculature

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling

CXCR4↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers

BMPs↑, 1,   EGFR↓, 1,  

Functional Outcomes

chemoP↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GSH↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 2,  

Core Metabolism/Glycolysis

ALAT↓, 1,   NADPH↓, 1,  

Cell Death

Casp3↓, 1,  

Migration

p‑Rac1↓, 1,  

Barriers & Transport

P-gp↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   IKKα↑, 1,   IL10↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   IL6↓, 1,  

Functional Outcomes

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 27

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:65  Cells:%  prod#:%  Target#:269  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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