Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research
Abstract
:1. Introduction
2. FAB Classification and Diagnostic Process
3. WHO Classification
4. AML Cell Lines and Types
4.1. AML with Minimal Differentiation (M0)
4.1.1. Kasumi-3
4.1.2. MOLM-16
4.2. AML without Maturation (M1)
4.2.1. CTS
4.2.2. UoC-M1
4.2.3. KG-1
4.2.4. K-562
4.3. AML with Maturation (M2)
4.3.1. Kasumi-1
4.3.2. Kasumi-6
4.3.3. SKNO-1
4.3.4. HL-60
4.3.5. PLB-985
4.4. Acute Promyelocytic Leukemia (M3)
4.4.1. NB4
4.4.2. PL-21
4.4.3. UF-1
4.4.4. HT93
4.4.5. AP-1060
4.5. Acute Myelomonocytic Leukemia (M4)
4.5.1. OCI-AML2 and OCI-AML3
4.5.2. MUTZ-11
4.5.3. MUTZ-8
4.5.4. MUTZ-3
4.5.5. ME-1
4.6. Acute Monoblastic and Monocytic Leukemia (M5)
4.6.1. THP-1
4.6.2. U-937
4.6.3. MOLM-13 and MV4-11
4.7. Acute Erythroid Leukemia (M6)
4.7.1. HEL
4.7.2. OCI-M1
4.7.3. OCI-M2
4.7.4. F-36P
4.7.5. TF-1
4.7.6. AS-E2
4.8. Acute Megakaryoblastic Leukemia (M7)
4.8.1. CMK
4.8.2. ELF-153
4.8.3. UT-7
4.8.4. M-07
4.8.5. MEG-01
4.8.6. MEGAL
4.9. Cell-Line Markers
Disease | Cell Line | Markers | Use |
---|---|---|---|
M0 | Kasumi-3 | CD2−, cy/smCD3−, CD4+, CD5−, CD7+, CD8−, CD13+, CD14+, CD15−, CD19−, CD20−, CD22+, CD25+, CD33+, CD34+,CD38+, CD56+, cyCD68+, HLA-DR+, c-Kit+ | EVI1 and BET inhibitors research; |
Drug response in AML; | |||
Engraftment studies | |||
MOLM-16 | CD3−, CD9+, CD13+, CD19−, CD22+ CD31+, CD33+, CD34+, CD36+, CD38+, CD41+, CD47+, CD56+, CD61+, CD62P+, CD63+, CD71+, CD110+, CD117+, CD119+ CD151+, CD235A+, thrombospondin+, vWf+, fibrinogen+, HLA-DR- | t(6;8) (q21;q24.3) model; | |
PIM/FLT3 signaling; | |||
JAK2 V617F function research; | |||
PMS2 and RSPH10B2 deletion | |||
M1 | CTS | CD1+, CD2+, CD3+, CD4+, CD5+, CD7+, CD8+, CD10+, CD13+, CD14+, CD19+, CD20+, CD25+, CD33+, CD34+, HLA-DR+, D2-10+, P2+, HPCA-1+ | t(6;11) (q27;q23) model; |
KMT2/AF6 research model; | |||
GM-CSF and G-CSF differentiation; | |||
Pluripotent stem cell research | |||
UoC-M1 | CD7+, CD24+, CD34+, CD38+, CD45+, HLA-DR+ CD61+ | Monosomy 7 and 5q loss model; | |
High KMT2A mRNA level | |||
KG1 | CD3−, CD13+, CD14−, CD15+, CD19−, CD33+, CD34+, HLA-DR+ | Cell maturation studies; | |
KMT2A and WT DNMT3A research; | |||
Toxicology and drug testing; | |||
Macrophage differentiation; | |||
K-562 | CD3−, CD14−, CD15+, CD19−, CD33+, CD71+, CD235a+ | BCR-ABL1 fusion, Ph1 chromosome; | |
Platelet-formation; | |||
p53-deficient | |||
M2 | Kasumi-1 | CD3−, CD4+, CD13+, CD14−, CD15+, CD19−, CD33+, CD34+, CD38+, CD71+, HLA-DR+ | t(8;21) model; |
RUNX1-RUNX1T1 fusion research; | |||
c-kit, TP53 mutations; | |||
Granulocytic and macrophage differentiation; | |||
Il-5 and TPA-induced differentiation; | |||
Kasumi-6 | CD3−, CD4−, CD13+, CD14−, CD19−, CD33+, CD34−, cyCD68−, HLA-DR+ | FLT3, CEBPA, TP53 mutations; | |
Model for differentiation research | |||
TPA-induced differentiation | |||
SKNO-1 | CD3−, CD4+, CD13+, CD14−, CD15−, CD19-, CD33+ CD1, CD2, CD3, CD4, CD5, CD6, CD7, CD8, CD11, CD13, CD14, CD15, CD19, CD20, CD33, CD34, HLA-DR | t(8;21) (q22;q22) research; | |
RUNX1/RUNX1T1 fusion; | |||
Myeloid leukemogenesis studies; | |||
HL-60 | CD3−, CD4+, CD13+, CD14−, CD15+, CD19−, CD33+, CD34−, HLA-DR- | t(15;17) model; | |
Granulocytic and mononuclear maturation; Chemotherapeutics influence; | |||
Proliferation, apoptosis, and cell cycle study; | |||
Chemotactic response; | |||
miRNA studies | |||
PLB-985 | CD3−, CD4+, CD13+, CD14−, CD15+, CD19−, CD33+, CD34− | Granulocytic, monocytic, macrophage maturation, proliferation; | |
Neutrophil differentiation; | |||
Maturation studies of cells in early stage | |||
M3 | NB4 | CD3−, CD4+, CD11b−, CD13+, CD14−, CD15+, CD19−, CD33+, CD34−, CD38+, HLA-DR- | ATRA resistance mechanisms |
PML-RARAPro900Ser mutation; | |||
Retinoic acid, DMSO, TPA differentiation; | |||
Drug screening | |||
PL-21 | CD3−, CD4 (+), CD14−, CD15+, CD19−, CD33+, cyCD68+, HLA-DR- | Lack of t(15;17) | |
KRAS, FLT3 mutations and WT P53; | |||
Kinase inhibitors studies | |||
UF-1 | CD3−, CD4−, CD5−, CD8−, CD11b−, CD10−, CD7+, CD13+, CD19−, CD20−, CD33+, CD34−, CD38+, CD41− [82] | WT RARA; | |
PML-RARA research; | |||
ATRA-resistance studies; | |||
Multi-drug screening with ATRA | |||
HT93 | CD3−, CD19−, CD33+, CD34+, cyCD68+, HLA-DR− | t(15;17) and t(1;12) model with PML-RARA and | |
ETV6-ABL2 fusion; | |||
TP53 mutation; | |||
Differentiation, proliferation, cytokine studies | |||
AP-1060 | CD3−, CD14−, CD15+, CD19−, CD33+, cyCD68+, HLA-DR− | t(15;17) and unique t(3;14) model; | |
PML-RARAPro900Leu mutation; | |||
ATRA and ATO resistance; | |||
Cytokine-dependent growth research; | |||
ETV6-NTRK3 fusion model; | |||
Neutrophil maturation | |||
M4 | OCI-AML2 | CD3−, CD4+, CD13+, CD15+, CD19−, CD33+, CD34−, cyCD68+, HLA-DR+ | Mutated DNMT3A role in leukemogenesis; |
xenograft models | |||
OCI-AML3 | CD3−, CD4+, CD13+, CD14−, CD15+, CD19−, cyCD68+, HLA-DR- | Mutated DNMT3A role in leukemogenesis; xenograft models; | |
NPM1 mutation; | |||
MUTZ-11 | CD4+, CD7+, CD13+, CD15+, CD33+, CD65+, CD68+ [102] | Response to cytokines; | |
Dendritic cell myeloid differentiation; | |||
KMT2A and FLT3 mutations | |||
MUTZ-8 | CD3−, CD4−, CD13+, CD19−, CD33+, CD34+, HLA-DR+ | t(5;11) model; | |
JAK2 V617F mutation; | |||
Cytokine response | |||
MUTZ-3 | CD3−, CD4+, CD5−, CD7−, CD8−, CD13+, CD14+, CD15+, CD19−, CD34+, HLA-DR+ | Role of FLT3 in leukemia pathogenesis; Cytokine response; | |
Dendritic cell myeloid differentiation | |||
M5 | THP-1 | CD3−, CD4+, CD13+, CD15+, CD19−, CD34−, cyCD68+, HLA-DR+ | t(9;11) (p22;q23) with KMT2A/MLLT3(AF9) fusion model; |
Immune and inflammatory response; inflammation; | |||
Susceptible to genetic modifications; | |||
Skin sensitization model; | |||
Cytokine response; | |||
U-937 | CD3−, CD4+, CD14−, CD15+, CD19−, CD33+, CD34−, CD54+ | Monocyte and macrophage differentiation; Response to ROS; | |
Skin sensitization model; | |||
Model for cell apoptotic disintegration | |||
MOLM-13 | CD3−, CD4+, CD14−, CD15+, CD19−, CD33+, CD34−, CD68+, HLA-DR− | Drug resistance research; Leukemia xenograft models; | |
WT TP53, FLT3-ITD+ in AML | |||
MV4-11 | CD3−, CD4+, CD5−, CD8−, CD10−, CD14−, CD15+, CD19−, CD33+, CD34− | t(4;11) (q21;q23) model; | |
Mechanisms of FLT3-ITD+ AML Leukemia; Xenograft models; | |||
WT TP53, FLT3-ITD+ in AML | |||
M6 | HEL | CD3−, CD13+, CD14−, CD19−, CD33+, CD41a+, CD71+, CD235a+ | JAK/STAT signaling pathway, |
Differential globins expression | |||
JAK2 mutation | |||
OCI-M1 | CD3−, CD4−, CD15+, CD19−, CD33+, CD34−, CD41−, CD42−, CD71+, HLA-DR+ | Model for the EPO receptors studies, | |
OCI-M2 | CD3+, CD14+, CD19−, CD33 (+), CD71+ | Studying NFkB inhibitors; | |
NKX2-4 expression | |||
F-36P | CD3−, CD13+, CD14−, CD15−, CD19−, CD33+, CD34+, CD41−, CD42−, CD71+, CD235a+ | Study of IL-3 and GM-CSF dependence; | |
Primitive progenitor cell model; | |||
Myeloid cell differentiation; | |||
Oncogenesis | |||
TF-1 | CD3−, CD13+, CD14−, CD15−, CD19−, CD33+, CD34+, CD71+, HLA-DR+ | TNFR2 expression; | |
TPA macrophage differentiation; | |||
Cytokines response; | |||
Anti-IL-6R nanobody ALX-0061 | |||
AS-E2 | CD2−, CD3−, CD10−, CD11b+, CD13+, CD19−, CD25−, CD33+, CD36+, CD41−, Glycophorin A+, CD71+ [199] | Erythroid progenitor cells; | |
EPO-dependent growth; | |||
GATA-1 expression | |||
M7 | CMK | CD3−, CD13+, CD14−, CD15−, CD19−, CD33+, CD34+, CD71+, CD235a+ | der(17)t(11:17) model; |
JAK2 V617F mutation; | |||
Megakaryocytopoiesis research; | |||
ELF-153 | CD3−, CD4+, CD13+, CD14−, CD15−, CD19−, CD33+, CD34+, HLA-DR+ | High GATA level; | |
Megakaryocytopoiesis research | |||
UT-7 | CD3−, CD13+, CD14−, CD15−, CD19−, CD33+, CD34−, cyCD68+ | Response to cytokines; | |
EPO-response; | |||
GATA expression, | |||
M-07 | Non disclosed | Cytokine response | |
M-07e | CD3−, CD13+, CD14−, CD19−, CD33+, HLA-DR- | Cytokine response | |
MEG-01 | CD3−, CD13+, CD15+, CD19−, CD33+ | t(9;22) model; | |
BCR/CBL fusion; | |||
Megakaryocytic differentiation/maturation | |||
MEGAL | CD3−, CD13−, CD14−, CD19−, CD33+, CD34+, CD71+, CD235a− | SET-NUP214 fusion |
4.10. Controls from Healthy Donors
5. Conclusions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Skopek, R.; Palusińska, M.; Kaczor-Keller, K.; Pingwara, R.; Papierniak-Wyglądała, A.; Schenk, T.; Lewicki, S.; Zelent, A.; Szymański, Ł. Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research. Int. J. Mol. Sci. 2023, 24, 5377. https://doi.org/10.3390/ijms24065377
Skopek R, Palusińska M, Kaczor-Keller K, Pingwara R, Papierniak-Wyglądała A, Schenk T, Lewicki S, Zelent A, Szymański Ł. Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research. International Journal of Molecular Sciences. 2023; 24(6):5377. https://doi.org/10.3390/ijms24065377
Chicago/Turabian StyleSkopek, Rafał, Małgorzata Palusińska, Katarzyna Kaczor-Keller, Rafał Pingwara, Anna Papierniak-Wyglądała, Tino Schenk, Sławomir Lewicki, Artur Zelent, and Łukasz Szymański. 2023. "Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research" International Journal of Molecular Sciences 24, no. 6: 5377. https://doi.org/10.3390/ijms24065377