γH2AX Cancer Research Results

γH2AX, gamma-H2AX: Click to Expand ⟱
Source:
Type:
γH2AX (gamma-H2AX) is a histone protein that plays a crucial role in the repair of DNA double-strand breaks (DSBs). It is a phosphorylated form of the H2AX protein, which is a component of chromatin.

γH2AX is often used as a biomarker for DNA damage and genomic instability. When DNA is damaged, the H2AX protein is phosphorylated, forming γH2AX, which recruits and activates DNA repair proteins to the site of damage.
γ-H2AX, a marker for DNA double-strand breaks.

Cancer cells often exhibit increased levels of γH2AX due to their high rate of DNA replication and repair errors.

Gamma-H2AX, on the other hand, refers to a phosphorylated form of H2AX.
Nor, Normal Healthy: Click to Expand ⟱
Normal Healthy
Scientific Papers found: Click to Expand⟱
4400- AgNPs,  Rad,    Differential cytotoxic and radiosensitizing effects of silver nanoparticles on triple-negative breast cancer and non-triple-negative breast cells
- in-vitro, BC, MCF7 - in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, BC, MDA-MB-231
ROS↑, DNAdam↑, selectivity↑, TumCG↓, RadioS↑, Dose↝, selectivity↑, other↝, eff↓, eff↑, γH2AX↑, Dose↓, eff↑,
1864- DCA,  MET,    Dichloroacetate Enhances Apoptotic Cell Death via Oxidative Damage and Attenuates Lactate Production in Metformin-Treated Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, BC, T47D - in-vitro, Nor, MCF10
PDKs↓, eff↑, ROS↑, PDK1 / PDPK1↓, lactateProd↓, p‑PDH↑, Dose∅, OCR↑, DNA-PK↑, γH2AX↑, cl‑PARP↑, selectivity↑, *toxicity∅,
6848- EVO,    Evodiamine: A Extremely Potential Drug Development Candidate of Alkaloids from Evodia rutaecarpa
- Review, Nor, NA
AntiTum↑, cardioP↑, Inflam↓, TumCP↓, TumCCA↑, Apoptosis↑, TumAuto↑, BioAv↓, toxicity↑, NF-kB↓, MAPK↓, NOD1↓, p‑Akt↓, BAX↑, cl‑Casp3↑, γH2AX↑, cl‑PARP↑, ROS↑, BBB↑, neuroP↑, BioAv↑,
8090- KAE,    A systematic review of anti-cancer roles and mechanisms of kaempferol as a natural compound
- Review, Nor, NA
*cardioP↑, *AntiCan↑, *Inflam↓, *neuroP↑, *BioAv↓, selectivity?, p‑Akt↓, p‑cycD1/CCND1↓, p‑CDK4↓, p‑BID↓, p‑Mcl-1↓, p‑BRCA1↑, ATM↑, P53↑, P21↑, p38↑, BAX↑, BID↑, MMP↓, Casp3↑, Casp7↑, Casp9↑, AIF↑, ER Stress↑, TumMeta↓, ERK↓, AP-1↓, JNK↓, p38↓, GLUT1↓, GlucoseCon↓, MMP9↓, CYP1A1↓, ChemoSen↑, OCT4↓, Nanog↓, P-gp/ABCB1↓, ALDH1A1↓, TumCCA↑, DNAdam↑, γH2AX↑, COX2/PTGS2↓, i-ROS↓, Ca+2↓, eff↑, DR5↑, ChemoSen↑, Akt↓, PI3K↓, ROS↑, EMT↓, survivin↓,
2258- MFrot,  MF,    EXTH-68. ONCOMAGNETIC TREATMENT SELECTIVELY KILLS GLIOMA CANCER CELLS BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
- in-vitro, GBM, GBM - in-vitro, Nor, SVGp12
TumVol↓, OS↑, γH2AX↑, DNAdam↑, selectivity↑, ROS↑, TumCD↑, eff↑, eff↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NOD1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

CYP1A1↓, 1,   ROS↑, 5,   i-ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   MMP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↓, 1,   lactateProd↓, 1,   p‑PDH↑, 1,   PDK1 / PDPK1↓, 1,   PDKs↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 2,   BID↑, 1,   p‑BID↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp9↑, 1,   DR5↑, 1,   JNK↓, 1,   MAPK↓, 1,   p‑Mcl-1↓, 1,   p38↓, 1,   p38↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑BRCA1↑, 1,   DNA-PK↑, 1,   DNAdam↑, 3,   P53↑, 1,   cl‑PARP↑, 2,   γH2AX↑, 5,  

Cell Cycle & Senescence(tgid=11) ⓘ

p‑CDK4↓, 1,   p‑cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ALDH1A1↓, 1,   EMT↓, 1,   ERK↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   Ca+2↓, 1,   MMP9↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT1↓, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 2,   Dose↓, 1,   Dose↝, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 5,   RadioS↑, 1,   selectivity?, 1,   selectivity↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

p‑BRCA1↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,   cardioP↑, 1,   neuroP↑, 1,   OS↑, 1,   toxicity↑, 1,   TumVol↓, 1,  
Total Targets: 80

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cardioP↑, 1,   neuroP↑, 1,   toxicity∅, 1,  
Total Targets: 6

Scientific Paper Hit Count for: γH2AX, gamma-H2AX
1 Silver-NanoParticles
1 Radiotherapy/Radiation
1 Dichloroacetate
1 Metformin
1 Evodiamine
1 Kaempferol
1 Magnetic Field Rotating
1 Magnetic Fields
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#:667  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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