A20 (Lymphoma)

A20 (ATCC® TIB-208™) is a murine lymphoma cell line derived from a spontaneous reticulum cell neoplasm of a Balb/c mouse.

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Usage Information

A20 cells are suitable for in vitro and in vivo experimentation. The cells will form tumors and spontaneous metastases in immunocompromised and syngeneic Balb/c mice. Depending on the route of inoculation (see below), implanted A20 cells can metastasize to numerous sites including the bone marrow, liver, spleen, lymph nodes, ovaries, and peritoneal cavity.

The following chart provides some examples of A20 cells used for tumor formation and studies.

Route of ImplantationMiceTumor/MetastasesReferences
SubcutaneousBalb/cSubcutaneous tumorEdinger, et al. (2003) Blood 101: 640-648
Palmieri et al. (2010) Blood 116: 226-238
SubcutaneousBalb/cSubcutaneous tumor, liver and lymph node metastasesBascuas et al. (2016) J Translational Med 14: 323
IntravenousBalb/c
(irradiated)
Bone marrow, spinal cordEdinger, et al. (2003) Blood 101: 640-648
IntracranialBalb/cBrain tumors and metastasesShichkin and Moriev (2014) The Scientific World Journal vol. 2014
IntravenousBalb/cLiver, ovaries, lymph nodes, bone marrow, spleen, peritoneal cavityWen et al. (2010) Lab Animal Res 26: 415-423
Lin et al. (2010) Oncogene 29: 608-615
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 A20 reporter cells expressing firefly luciferase (Fluc) 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.

In order to ensure high, constitutive expression of the reporter proteins, our cell lines are generated by lentiviral vector transduction. The lentiviral 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 lentiviral vectors by preventing mobilization of replication competent viruses (Miyoshi et al., J Virol. 1998).

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