Abstract
The term "lymphoma" describes a heterogeneous group of disorders involving monoclonal proliferation of malignant lymphocytes. As a group, lymphomas are among the most common tumors of dogs. Yet our enumeration and understanding of the many subtypes of lymphoma have been relatively slow, perhaps in part because for many years lymphoma was treated as a singular entity rather than a group of distinct diseases. The recognition that the full spectrum of lymphoid malignancies seen in humans also occurs in dogs, and that these tumors retain not only morphologic similarities and biological behavior but also synonymous driver molecular abnormalities, sets an ideal stage for dual-purpose research that can accelerate progress for these diseases in both species. Specifically, dogs represent exceptional models for defining causality, understanding progression, and developing new treatments for lymphoma in comparatively brief windows of time. Unique advantages of canine models include (1) spontaneous disease occurring without an isogenic background or genetic engineering ; (2) chronology of disease adapted to lifespan, (3) shared environment and societal status that allows dogs to be treated as "patients," while at the same time being able to ethically explore translational innovations that are not possible in human subjects; and (4) organization of dogs into breeds with relatively homogeneous genetic backgrounds and distinct predisposition for lymphomas. Here, we will review recent studies describing intrinsic and extrinsic factors that contribute to the pathogenesis of canine and human lymphomas, as well as newly developed tools that will enhance the fidelity of these models to improve diagnosis and develop new treatments.
Original language | English (US) |
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Pages (from-to) | 192-201 |
Number of pages | 10 |
Journal | Veterinary immunology and immunopathology |
Volume | 159 |
Issue number | 3-4 |
DOIs | |
State | Published - 2014 |
Bibliographical note
Funding Information:The authors would like to thank Ms. Mitzi Lewellen and Ms. Ashley Graef for editorial assistance. We also wish to acknowledge the assistance of Dr. Aaron Sarver (University of Minnesota) for microarray data analysis. This work was supported in part by MAF First Award Grant D12CA-302 (DI), Morris Animal Foundation D13CA-033 (JFM), Masonic Cancer Center Internal Grants Program - Hematologic Malignancy Innovations Award (JFM), Skippy Frank Fund for Life Sciences and Translational Research (DI and JFM), the Starlight Fund, The Land of PureGold Foundation, the WillPower Fund, and other philanthropic donations to the University of Minnesota Animal Cancer Care and Research Program. AMF was supported by the DVM/PhD combined degree program of the College of Veterinary Medicine, University of Minnesota and by a pre-doctoral fellowship from Morris Animal Foundation (D09CA-405).