Database Query Results : , , IDH1

IDH1, isocitrate dehydrogenase 1 (NADP+), soluble: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
An enzyme that plays a crucial role in the citric acid cycle (Krebs cycle), which is essential for cellular metabolism. Mutations in the IDH1 gene have been implicated in various types of cancer, particularly gliomas and acute myeloid leukemia (AML).
Expression in Cancers: IDH1 is expressed in various tissues, and its expression can be altered in cancer. Mutations in the IDH1 gene, particularly the R132H mutation, are commonly found in certain types of tumors, including gliomas and secondary glioblastomas, as well as in a subset of acute myeloid leukemia cases.
Prognostic Implications: The presence of IDH1 mutations is associated with distinct clinical outcomes. In gliomas, IDH1 mutations are generally linked to a better prognosis compared to wild-type IDH1. Patients with IDH1-mutant gliomas often have longer survival rates and respond differently to treatment. In AML, IDH1 mutations can also influence prognosis, with some studies suggesting that they may be associated with a favorable response to certain therapies.
Oncogenic Potential: Mutant IDH1 is considered an oncogene due to its role in altering cellular metabolism. The R132H mutation leads to a neomorphic enzyme activity that converts alpha-ketoglutarate to 2-hydroxyglutarate (2-HG), an oncometabolite that can inhibit various α-ketoglutarate-dependent dioxygenases, including those involved in DNA and histone demethylation. This alteration in metabolism and epigenetic regulation contributes to tumorigenesis and the development of cancer.

IDH1 (Isocitrate Dehydrogenase 1) is not classified as a traditional oncogene. Instead, it is considered a mutated metabolic enzyme that can contribute to oncogenesis when mutated. Here’s a more detailed explanation:
Scientific Papers found: Click to Expand⟱
1180- Ash,    Withaferin A Inhibits Liver Cancer Tumorigenesis by Suppressing Aerobic Glycolysis through the p53/IDH1/HIF-1α Signaling Axis
- in-vitro, Liver, HepG2
IDH1↑, Glycolysis↓, P53↑, Hif1a↓,
2384- MET,    Integration of metabolomics and transcriptomics reveals metformin suppresses thyroid cancer progression via inhibiting glycolysis and restraining DNA replication
- in-vitro, Thyroid, BCPAP - in-vivo, NA, NA - in-vitro, Thyroid, TPC-1
Glycolysis↓, OXPHOS↑, tumCV↓, TumCI↓, TumCMig↓, EMT↓, Apoptosis↑, TumCCA↑, LDHA↓, PKM2↓, IDH1↑, TumCG↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↑, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 2,   IDH1↑, 2,   LDHA↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: IDH1, isocitrate dehydrogenase 1 (NADP+), soluble
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:%  Cells:%  prod#:%  Target#:152  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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