Loss of TRP53 (p53) accelerates tumorigenesis and changes the tumor spectrum of SJL/J mice
Jane A. Branca1, Benjamin E. Low1, Ruth L. Saxl1, Jennifer K. Sargent1, Rosalinda A. Doty1, Michael V. Wiles1, Beth L. Dumont1 and Muneer G. Hasham1
1 The Jackson Laboratory, Bar Harbor, Maine, USA
Correspondence:
Muneer G. Hasham, email:
Keywords: TRP53, p53, SJL/J, tumorigenesis
Received: November 07, 2019 Accepted: January 06, 2020 Published: January 21, 2020
Abstract
Known as the guardian of the genome, transformation-related protein 53 (TRP53) is a well -known tumor suppressor. Here, we describe a novel TRP53 deficient mouse model on a tumor prone background—SJL/J mice. The absence of TRP53 (TRP53 nullizygosity) leads to a shift in the tumor spectrum from a non-Hodgkin’s-like disease to thymic lymphomas and testicular teratomas at a very rapid tumor onset averaging ~12 weeks of age. In haplotype studies, comparing tumor prone versus tumor resistant Trp53 null mouse strains, we found that other tumor suppressor, DNA repair and/or immune system genes modulate tumor incidence in TRP53 null strains, suggesting that even a strong tumor suppressor such as TRP53 is modulated by genetic background. Due to their rapid development of tumors, the SJL/J TRP53 null mice generated here can be used as an efficient chemotherapy or immunotherapy screening mouse model.
