Unexpected effects of the severe combined immunodeficiency mutation on murine lymphomagenesis

doi:10.1084/jem.176.2.399

This Article

	Full Text (PDF, 681K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Lieberman, M.
	Articles by Sen-Majumdar, A.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Lieberman, M.
	Articles by Sen-Majumdar, A.


Social Bookmarking

	What's this?

ARTICLES

Unexpected effects of the severe combined immunodeficiency mutation on murine lymphomagenesis

M Lieberman, GA Hansteen, EK Waller, IL Weissman and A Sen-Majumdar
Department of Radiation Oncology, Stanford University School of Medicine, California 94305.

Strain C.B17 scid/scid (SCID) mice, which lack functional T and B lymphocytes, show heightened susceptibility to the induction of thymic lymphomas by x-irradiation. Susceptibility is highest in thymus- chimeric SCID-BL mice (thymectomized SCID mice bearing a C57BL thymus graft). All SCID-BL lymphomas originate in the cells of the thymic graft (C57BL type) and lack murine leukemia virus expression. Both SCID and SCID-BL lymphomas are phenotypically CD4-8+ and/or CD4+8+, but only the SCID-BL tumors express CD3. Injection of C57BL or BALB/c bone marrow into irradiated SCID-BL mice prevents lymphoma development, but SCID marrow is completely ineffective. The results suggest that the scid condition enhances the activity of a putative lymphomagenic agent induced in the bone marrow by x-irradiation and that C57BL thymic cells are highly sensitive targets. Moreover, the failure of SCID bone marrow to protect against lymphomagenesis vs. the efficacy of marrow from immunocompetent donors points to involvement of T or B lineage cells in this process.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Mortellaro, A., Hernandez, R. J., Guerrini, M. M., Carlucci, F., Tabucchi, A., Ponzoni, M., Sanvito, F., Doglioni, C., Serio, C. D., Biasco, L., Follenzi, A., Naldini, L., Bordignon, C., Roncarolo, M. G., Aiuti, A. (2006). Ex vivo gene therapy with lentiviral vectors rescues adenosine deaminase (ADA)-deficient mice and corrects their immune and metabolic defects. Blood 108: 2979-2988 [Abstract] [Full Text]
Zenger, E., Abbey, N. W., Weinstein, M. D., Kapp, L., Reis, J., Gofman, I., Millward, C., Gascon, R., Elbaggari, A., Herndier, B. G., McGrath, M. S. (2002). Injection of Human Primary Effusion Lymphoma Cells or Associated Macrophages into Severe Combined Immunodeficient Mice Causes Murine Lymphomas. Cancer Res. 62: 5536-5542 [Abstract] [Full Text]
Williams, C. J., Grandal, I., Vesprini, D. J., Wojtyra, U., Danska, J. S., Guidos, C. J. (2001). Irradiation Promotes V(D)J Joining and RAG-Dependent Neoplastic Transformation in SCID T-Cell Precursors. Mol. Cell. Biol. 21: 400-413 [Abstract] [Full Text]
Brayton, C., Justice, M., Montgomery, C. A. (2001). Evaluating Mutant Mice: Anatomic Pathology. Vet Pathol 38: 1-19 [Abstract] [Full Text]
Kemp, C. J., Vo, K., Gurley, K. E. (1999). Resistance to skin tumorigenesis in DNAPK-deficient SCID mice is not due to immunodeficiency but results from hypersensitivity to TPA-induced apoptosis. Carcinogenesis 20: 2051-2056 [Abstract] [Full Text]
Ristevski, S., Purcell, D. F.�J., Marshall, J., Campagna, D., Nouri, S., Fenton, S. P., McPhee, D. A., Kannourakis, G. (1999). Novel Endogenous Type D Retroviral Particles Expressed at High Levels in a SCID Mouse Thymic Lymphoma. J. Virol. 73: 4662-4669 [Abstract] [Full Text]
Danska, J., Pflumio, F, Williams, C., Huner, O, Dick, J., Guidos, C. (1994). Rescue of T cell-specific V(D)J recombination in SCID mice by DNA-damaging agents. Science 266: 450-455 [Abstract]