IL1β Cancer Research Results

IL1β, interleukin-1 beta: Click to Expand ⟱
Source:
Type:
The term "IL-1" is often used as an umbrella term for the interleukin-1 family, which includes multiple cytokines. The two best-known members are IL-1α and IL-1β.
IL-1β is secreted from cells and plays a major systemic role in inflammation. It is a crucial mediator in the inflammatory response and is involved in the fever response, activation of endothelial cells, and leukocyte recruitment.
Its increased expression is commonly linked to:
  – Promotion of a pro-inflammatory microenvironment that supports tumor growth.
  – Enhanced angiogenesis, invasion, and metastasis.
  – Recruitment of myeloid cells that may further suppress antitumor immunity.

High expression of either tends to be associated with a more aggressive phenotype and worse prognosis in many cancer types.


AML, Acute Myeloid Leukemia: Click to Expand ⟱
Acute Myeloid Leukemia

Scientific Papers found: Click to Expand⟱
2972- PL,    Piperlongumine Is an NLRP3 Inhibitor With Anti-inflammatory Activity
- in-vitro, AML, THP1
NLRP3↓, IL1β↓, LDH↓, cl‑Casp1↓, 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:


Core Metabolism/Glycolysis

LDH↓, 1,  

Cell Death

cl‑Casp1↓, 1,  

Immune & Inflammatory Signaling

IL1β↓, 1,   Inflam↓, 1,  

Protein Aggregation

NLRP3↓, 1,  

Clinical Biomarkers

LDH↓, 1,  
Total Targets: 6

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: IL1β, interleukin-1 beta
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:2  Cells:%  prod#:%  Target#:978  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

Home Page