OCI-AML-3Homo sapiens (Human)Cancer cell line

Also known as: Ontario Cancer Institute-Acute Myeloid Leukemia-3, OCIAML3, OCI AML3, OCI/AML3, OCI-AML3, OCI/AML-3, OCI-Aml-3

🤖 AI SummaryBased on 15 publications

OCI-AML3

Quick Overview

OCI-AML3 is a human acute myeloid leukemia cell line with NPM1 mutation and DNMT3A mutation, used in cancer research.

Detailed Summary

OCI-AML3 is a human acute myeloid leukemia (AML) cell line derived from a patient with AML. It is characterized by a mutation in the NPM1 gene (type A) and a mutation in the DNMT3A gene (R882H). These genetic alterations are associated with specific molecular features and may contribute to the pathogenesis of AML. The cell line is widely used in research to study the mechanisms of leukemogenesis, drug sensitivity, and the role of epigenetic modifications in cancer progression. OCI-AML3 has been utilized in studies involving BET inhibitors, CRISPR-Cas9 screens, and investigations into the effects of genetic mutations on cellular behavior and therapeutic responses. It is also part of the Cancer Cell Line Encyclopedia (CCLE) and has been used in various high-throughput screening efforts to identify potential therapeutic targets.

Research Applications

Study of NPM1 and DNMT3A mutations in AMLInvestigation of epigenetic modifications in cancerScreening for therapeutic targets using CRISPR-Cas9Evaluation of drug sensitivity to BET inhibitorsAnalysis of genetic and molecular mechanisms of leukemogenesis

Key Characteristics

NPM1 gene mutation (type A)DNMT3A R882H mutationUsed in high-throughput screeningPart of the Cancer Cell Line Encyclopedia (CCLE)Relevant for studying epigenetic and genetic alterations in AML
Generated on 6/17/2025

Basic Information

Database IDCVCL_1844
SpeciesHomo sapiens (Human)
Tissue SourcePeripheral blood[UBERON:UBERON_0000178]

Donor Information

Age57
Age CategoryAdult
SexMale

Disease Information

DiseaseAcute myeloid leukemia
LineageMyeloid
SubtypeAcute Myeloid Leukemia
OncoTree CodeAML

DepMap Information

Source TypeDSMZ
Source IDACH-000336_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
MutationSimpleNPM1p.Trp288Cysfs*12 (c.860_863dupTCTG)Heterozygous-from parent cell line OCI-AML-3
MutationSimpleNRASp.Gln61Leu (c.182A>T)Unspecified-PubMed=26214590
MutationSimpleDNMT3Ap.Arg882Cys (c.2644C>T)Heterozygous-from parent cell line OCI-AML-3

Haplotype Information (STR Profile)

Short Tandem Repeat (STR) profile for cell line authentication.

Amelogenin
X
CSF1PO
11,12
D13S317
8,13
D16S539
11,13
D18S51
12,18
D19S433
15,17
D21S11
29,30
D2S1338
17,21
D3S1358
16
D5S818
11,13
D7S820
9,10
D8S1179
10,12
FGA
22
Penta D
12,13
Penta E
11,13
TH01
8,9.3
TPOX
8,11
vWA
17,18
Gene Expression Profile
Gene expression levels and statistical distribution
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Full DepMap dataset with combined data across cell lines

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Publications

DNMT3A R882H mutation in acute myeloid leukemia cell line SET-2.";

Uphoff C.C., Zaborski M., Drexler H.G.

Leuk. Res. 88:106270.1-106270.3(2020).

The LL-100 panel: 100 cell lines for blood cancer studies.";

MacLeod R.A.F., Nagel S., Steube K.G., Uphoff C.C., Drexler H.G.

Sci. Rep. 9:8218-8218(2019).

Next-generation characterization of the Cancer Cell Line Encyclopedia.

Sellers W.R.

Nature 569:503-508(2019).

Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens.

Stronach E.A., Saez-Rodriguez J., Yusa K., Garnett M.J.

Nature 568:511-516(2019).

An interactive resource to probe genetic diversity and estimated ancestry in cancer cell lines.

Dutil J., Chen Z.-H., Monteiro A.N.A., Teer J.K., Eschrich S.A.

Cancer Res. 79:1263-1273(2019).

Screening human cell lines for viral infections applying RNA-Seq data analysis.

Uphoff C.C., Pommerenke C., Denkmann S.A., Drexler H.G.

PLoS ONE 14:E0210404-E0210404(2019).

Profiling the B/T cell receptor repertoire of lymphocyte derived cell lines.

Yang H.H., Koeffler H.P.

BMC Cancer 18:940.1-940.13(2018).

The novel BET bromodomain inhibitor BI 894999 represses super-enhancer-associated transcription and synergizes with CDK9 inhibition in AML.

Gerstberger T., Zuber J., Savarese F., Kraut N.

Oncogene 37:2687-2701(2018).

Hh/Gli antagonist in acute myeloid leukemia with CBFA2T3-GLIS2 fusion gene.

Pigazzi M., Martelli A.M., Basso G., Locatelli F., Pession A.

J. Hematol. Oncol. 10:26.1-26.5(2017).

A landscape of pharmacogenomic interactions in cancer.";

Wessels L.F.A., Saez-Rodriguez J., McDermott U., Garnett M.J.

Cell 166:740-754(2016).

TCLP: an online cancer cell line catalogue integrating HLA type, predicted neo-epitopes, virus and gene expression.

Loewer M., Sahin U., Castle J.C.

Genome Med. 7:118.1-118.7(2015).

DNMT3A mutations mediate the epigenetic reactivation of the leukemogenic factor MEIS1 in acute myeloid leukemia.

Esteller M.

Oncogene 35:3079-3082(2016).

Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies.

Golub T.R., Root D.E., Hahn W.C.

Sci. Data 1:140035-140035(2014).

A resource for cell line authentication, annotation and quality control.

Neve R.M.

Nature 520:307-311(2015).

A comprehensive transcriptional portrait of human cancer cell lines.

Settleman J., Seshagiri S., Zhang Z.-M.

Nat. Biotechnol. 33:306-312(2015).

The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.

Morrissey M.P., Sellers W.R., Schlegel R., Garraway L.A.

Nature 483:603-607(2012).

Survey of activated FLT3 signaling in leukemia.";

Druker B.J., Heinrich M.C., Rush J., Polakiewicz R.D.

PLoS ONE 6:E19169-E19169(2011).

JAK2 V617F tyrosine kinase mutation in cell lines derived from myeloproliferative disorders.

Quentmeier H., MacLeod R.A.F., Zaborski M., Drexler H.G.

Leukemia 20:471-476(2006).

Cell line OCI/AML3 bears exon-12 NPM gene mutation-A and cytoplasmic expression of nucleophosmin.

Martelli M.F., Mecucci C., Drexler H.G., Falini B.

Leukemia 19:1760-1767(2005).

Low levels of ABCG2 expression in adult AML blast samples.";

Andreeff M., Sorrentino B.P.

Blood 100:4594-4601(2002).

Expression of a retinoic acid receptor gene in myeloid leukemia cells.

Wang C., Curtis J.E., Minden M.D., McCulloch E.A.

Leukemia 3:264-269(1989).