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Nalm6 (leukemia)

Description


Nalm6 is a B cell precursor leukemia cell line initiated from an adolescent male. It is a CD24-positive xenograft model of acute lymphoblastic leukemia.

Usage Information


Nalm6 cells are suitable for in vitro and in vivo experimentation. The cells will form tumors and spontaneous metastases in immunocompromised mice. Depending on the route of inoculation (see below), implanted Nalm6 cells can metastasize to the bone marrow, liver, spleen, and lymph nodes.

The following chart provides some examples of Nalm6 cells used for tumor formation and studies.

Route of Implantation Mice Tumor/Metastases References
Intravenous SCID-beige Bone marrow, liver, spleen, lymph nodes, periodontal region Santos et al. (2009) Nature Med 15: 338-344.

Brentjens et al. (2007) Clin Cancer Res 13: 5426-5435.

Intravenous NSG Live, bone marrow Barrett, et al. (2011) Blood 118: e112-e117.

Benito, et al. (2011) PLoS One 6:e23108.

Subcutaneous SCID-beige Subcutaneous tumor Santos et al. (2009) Nature Med 15: 338-344.
Note: The above information is based on available data from the indicated references. It is not meant to be comprehensive and Imanis has not directly tested each condition.

Stable reporter cell lines


Our Nalm6 reporter cell lines can be tracked in vivo, making them great tools for studying the mechanisms of tumor growth and metastasis, as well as evaluating the effects of various drugs or therapies in animals. Our Nalm6 cells are available with a variety of different reporters, including the human sodium iodide symporter (hNIS), firefly luciferase (Fluc), and enhanced green fluorescent protein (eGFP). Dual reporter Nalm6 cell lines are available to facilitate multimodal imaging.

In order to ensure high, constitutive expression of the reporter proteins, our cell lines are generated by lentivirus transduction. The lentivirus vectors used for these transductions are self-inactivating (SIN) vectors in which the viral enhancer and promoter has been deleted. This increases the biosafety of the lentiviruses by preventing mobilization of replication competent viruses (Miyoshi et al., J Virol. 1998).

 

 

 

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