Document Type
Article
Publication Date
1-1-2020
Keywords
JMG
JAX Source
Genes Cancer 2020; 11(1-2):83-94.
Volume
11
Issue
1-2
First Page
83
Last Page
94
ISSN
1947-6019
PMID
32577159
DOI
https://doi.org/10.18632/genesandcancer.198
Grant
The Linda Tallen and David Kane Educational Foundation, CA034196,OD210259
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.
Recommended Citation
Branca J,
Low BE,
Saxl RL,
Sargent J,
Doty RA,
Wiles MV,
Dumont B,
Hasham MG.
Loss of TRP53 (p53) accelerates tumorigenesis and changes the tumor spectrum of SJL/J mice. Genes Cancer 2020; 11(1-2):83-94.
Comments
We thank Byrant Perkins, Caitlin Lewis, and Cindy Avery for mouse care and genotyping. Susanne Sattler and Stephen Krasinski for advice and manuscript review.
We gratefully acknowledge the contribution of Microinjection, JAX Sanger Sequencing, Histopathological Sciences and Microscopy Service at The Jackson Laboratory for expert assistance with the work described in this publication.
This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0
(CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.