cellSen Cancer Research Results

cellSen, cellular senescence: Click to Expand ⟱
Source:
Type:
Cellular senescence is a state in which cells cease to divide and grow, often in response to DNA damage or other forms of cellular stress.
On one hand, senescence can prevent cancer by:
-Halting the proliferation of damaged cells, thereby preventing the accumulation of mutations that can lead to cancer
-Activating immune responses that can eliminate senescent cells.
-Producing anti-tumor factors that can inhibit the growth of nearby cancer cells.

On the other hand, senescence can also promote cancer by:
-Creating a pro-tumorigenic microenvironment that can support the growth of nearby cancer cells
-Producing pro-inflammatory factors that can promote cancer progression
-Contributing to the development of a senescence-associated secretory phenotype (SASP), which can promote cancer cell growth and metastasis.


Nor, Normal Healthy: Click to Expand ⟱
Normal Healthy

Scientific Papers found: Click to Expand⟱
6896- FIS,    Fisetin is a senotherapeutic that extends health and lifespan
- in-vivo, Nor, NA
*AntiAge↑, *cellSen↑, *selectivity⇅,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling(tgid=16)

cellSen↑, 1,  

Drug Metabolism & Resistance(tgid=21)

selectivity⇅, 1,  

Functional Outcomes(tgid=23)

AntiAge↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: cellSen, cellular senescence
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:49  Cells:%  prod#:%  Target#:920  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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