Abstract
Mouse plasma cell tumors (PCT) arise in BALB/cAn and NZB mice due to a protracted series of events culminating in tumor incidences of 60 and 30%, respectively, over a period of 220–360 days[l,2]. These incidences are due to both genetic and environmental factors. During the past several years, we have documented that at least two genes, Pctr1 and Pctr2, on the distal half of mouse Chr 4 play a determining role in the susceptibility of BALB/cAn mice to PCT formation [3–6]. Additional congenic strain analyses are in support of a third locus, Pctr3, also residing on Chr 4 between Pctr1 and Pctr2.
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© 1999 Springer-Verlag Berlin Heidelberg
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Zhang, S., Mock, B.A. (1999). The Role of p16INK4a (Cdkn2a) in Mouse Plasma Cell Tumors. In: Melchers, F., Potter, M. (eds) Mechanisms of B Cell Neoplasia 1998. Current Topics in Microbiology and Immunology, vol 246. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60162-0_44
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DOI: https://doi.org/10.1007/978-3-642-60162-0_44
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