ATM Cancer Research Results

ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
ATM is considered a moderate cancer risk gene. A mutation in a moderate risk gene is just one risk factor that can contribute to cancer development. ATM has traditionally been assigned the role of a tumor suppressor. However, in both humans and mice, lymphoma and leukemia are the only clear-cut examples of cancer development caused by ATM deficiency(13). Its roles in other types of cancer, especially solid tumors, are much less clear.
ATM, a master regulator of DNA damage response.


CRC, Colorectal Cancer: Click to Expand ⟱
Colorectal cancer is a broader term that encompasses both colon and rectal cancer.


Scientific Papers found: Click to Expand⟱
5109- SSE,    Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells
- in-vitro, CRC, HCT116
ROS↑, DNAdam↓, ATM↑, eff↓, TumCCA↑,

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

ROS↑, 1,  

DNA Damage & Repair

ATM↑, 1,   DNAdam↓, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Drug Metabolism & Resistance

eff↓, 1,  
Total Targets: 5

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated
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:6  Cells:%  prod#:%  Target#:20  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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