1
Discover top-quality products tailored for scientific and medical research. Request a personalized quote today
to enhance your projects.
Species | Human |
Cat.No | ABC-TC3023 |
Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
Product Category | Primary Cells |
Size/Quantity | 1 vial |
Cell Type | Mononuclear Cell |
Shipping Info | Dry Ice |
Growth Conditions | 37 ℃, 5% CO2 |
Source Organ | Peripheral Blood |
Disease | Acute Myeloid Leukemia |
Biosafety Level | 1 |
Storage | Liquid Nitrogen |
Product Type | Diseased Human Peripheral Blood Mononuclear Cells |
Human Acute Myeloid Leukemia Peripheral Blood Mononuclear Cells (Relapsed/Refractory) are derived from the peripheral blood of patients with relapsed/refractory acute myeloid leukemia (AML). They are peripheral blood mononuclear cells primarily composed of leukemic myeloblasts.These cells achieve unlimited proliferation by abnormally activating signaling pathways such as RTK-RAS-MAPK and WNT/β-catenin, and inhibit the expression of myeloid differentiation genes through epigenetic remodeling (such as DNMT3A mutation) to maintain the original state . These cells frequently exhibit complex karyotypic abnormalities, including monosomy 7, trisomy 8, or translocations such as t(8;21).They often express CD33, CD34, and CD117, confirmed via flow cytometry.At the same time, they highly express CD47 and secrete immunosuppressive factors such as IL-6/TGF-β, which can inhibit macrophage phagocytosis and induce T cell exhaustion, and cooperate with stromal cells (MSCs) in the bone marrow microenvironment to build an immune escape niche.
When you publish your research, please cite our product as "AcceGen Biotech Cat.# XXX-0000". In return, we’ll give you a $100 coupon. Simply click here and submit your paper’s PubMed ID (PMID).
Human Acute Myeloid Leukemia Peripheral Blood Mononuclear Cells (Relapsed/Refractory) can serve as an in vitro cell model to study AML pathogenesis and develop novel therapies. They can also be used to study constitutive activation of survival pathways (RTK-RAS, WNT/β-catenin), chemoresistance mechanisms (ABC transporter upregulation), and metabolic adaptations (OXPHOS dependency).