Author:
Grosse Nicole,van Loon Barbara,Rohrer Bley Carla
Abstract
Abstract
Background
Companion animals like dogs frequently develop tumors with age and similarly to human malignancies, display interpatient tumoral heterogeneity. Tumors are frequently characterized with regard to their mutation spectra, changes in gene expression or protein levels. Among others, these changes affect proteins involved in the DNA damage response (DDR), which served as a basis for the development of numerous clinically relevant cancer therapies. Even though the effects of different DNA damaging agents, as well as DDR kinetics, have been well characterized in mammalian cells in vitro, very little is so far known about the kinetics of DDR in tumor and normal tissues in vivo.
Discussion
Due to (i) the similarities between human and canine genomes, (ii) the course of spontaneous tumor development, as well as (iii) common exposure to environmental agents, canine tumors are potentially an excellent model to study DDR in vivo. This is further supported by the fact that dogs show approximately the same rate of tumor development with age as humans. Though similarities between human and dog osteosarcoma, as well as mammary tumors have been well established, only few studies using canine tumor samples addressed the importance of affected DDR pathways in tumor progression, thus leaving many questions unanswered.
Summary
Studies in humans showed that misregulated DDR pathways play an important role during tumor development, as well as in treatment response. Since dogs are proposed to be a good tumor model in many aspects of cancer research, we herein critically investigate the current knowledge of canine DDR and discuss (i) its future potential for studies on the in vivo level, as well as (ii) its possible translation to veterinary and human medicine.
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Genetics,Oncology
Reference59 articles.
1. Gamulin M, Garaj-Vrhovac V, Kopjar N: Evaluation of DNA damage in radiotherapy-treated cancer patients using the alkaline comet assay. Coll Antropol. 2007, 31 (3): 837-845.
2. Nascimento PA, da Silva MA, Oliveira EM, Suzuki MF, Okazaki K: Evaluation of radioinduced damage and repair capacity in blood lymphocytes of breast cancer patients. Braz J Med Biol Res. 2001, 34 (2): 165-176. 10.1590/S0100-879X2001000200003.
3. Palyvoda O, Polanska J, Wygoda A, Rzeszowska-Wolny J: DNA damage and repair in lymphocytes of normal individuals and cancer patients: studies by the comet assay and micronucleus tests. Acta Biochim Pol. 2003, 50 (1): 181-190.
4. Smith TR, Miller MS, Lohman KK, Case LD, Hu JJ: DNA damage and breast cancer risk. Carcinogenesis. 2003, 24 (5): 883-889. 10.1093/carcin/bgg037.
5. Walczak A, Rusin P, Dziki L, Zielinska-Blizniewska H, Olszewski J, Majsterek I: Evaluation of DNA double strand breaks repair efficiency in head and neck cancer. DNA and cell biology. 2012, 31 (3): 298-305. 10.1089/dna.2011.1325.
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