The Immunohistochemical Characterization of Devil Facial Tumor Disease (DFTD) in the Tasmanian Devil (<i>Sarcophilus harrisii</i>)

Loh, Richmond; Hayes, Dane; Mahjoor, A.A.; O’Hara, A.J.; Pyecroft, Stephen; Raidal, Shane R.

doi:10.1354/vp.43-6-896

Cited by 74 publications

(73 citation statements)

References 30 publications

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“…Although undifferentiated in appearance, DFTD has been characterized histologically as a tumor of neuroendocrine origin due to its expression of vimentin, S100, Melan A, CgA, NSE and synaptophysin, and the absence of expression of epithelial, neural, endothelial and hematopoietic markers (Table 1; Loh et al, 2006a, b). Only 32% of DFTD cases showed evidence of immune cell infiltration (Loh et al, 2006b).…”

Section: Dftdmentioning

confidence: 98%

Clonally transmissible cancers in dogs and Tasmanian devils

2008

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Tasmanian devil facial tumor disease (DFTD) and canine transmissible venereal tumor (CTVT) are the only known naturally occurring clonally transmissible cancers. These cancers are transmitted by the physical transfer of viable tumor cells that can be transplanted across histocompatibility barriers into unrelated hosts. Despite their common etiology, DFTD and CTVT have evolved independently and have unique life histories and host adaptations. DFTD is a recently emerged aggressive facial tumor that is threatening the Tasmanian devil with extinction. CTVT is a sexually transmitted tumor of dogs that has a worldwide distribution and that probably arose thousands of years ago. By contrasting the biology, molecular genetics and immunology of these two unusual cancers, I highlight the common and unique features of clonally transmissible cancers, and discuss the implications of clonally transmissible cancers for host-pathogen evolution.

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Section: Dftdmentioning

confidence: 98%

Clonally transmissible cancers in dogs and Tasmanian devils

2008

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“…It is not yet clear why DFTD-affected devils fail to develop effective immunological rejection for the facial tumor allografts that establish through devil-to-devil transfer of viable tumor cells. In a histological survey of DFTD-affected tumors, Loh et al (2006b) reported a paucity of lymphocyte infiltration in association with the tumors and this may be explained by low MHC diversity in the devil populations where high prevalence of DFTD has been detected . The apparent inability of DFTD-affected devils to recognize these neoplasms and develop a tumor-specific immunological response, coupled with the absence of any free-ranging devil cases demonstrating tumor regression reinforces the need to continue research into the immunogenetic aspects of this serious disease.…”

Section: Lymphoid Tissues Of the Tasmanian Devilmentioning

confidence: 99%

A Histological and Immunohistochemical Analysis of Lymphoid Tissues of the Tasmanian Devil

Kreiss

Obendorf

Hemsley

et al. 2009

The Anatomical Record

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Tasmanian devil lymphoid tissues (thymus, spleen, and lymph node) from seven animals, including pouch young, juvenile, and adult devils, were investigated using histological and immunohistochemical techniques. Antibodies against the conserved intracytoplasmic portion of CD3 and CD79b (T-and B-cell markers, respectively) and MHC II were used to label immune cells. The thymus from the juvenile devils and the pouch young had CD3þ cells that were primarily located in the medulla of the organ. The spleen consisted of red and white pulp areas with characteristic lymphoid follicles with CD79bþ and MHC IIþ cells and nonfollicular T-cell-dominated periarteriolar lymphoid sheaths. Peripheral lymph nodes presented three distinct regions, outer cortex and medulla (both with primarily CD79bþ and MHC IIþ cells) and paracortex (mainly CD3þ cells). Tissue architecture and distribution of the immune cells were similar to that seen in eutherian mammals and other marsupials, indicating that the Tasmanian devil has all the structural elements necessary for effective adaptive immunity. Anat Rec, 292:611-620, 2009. V V C 2009 Wiley-Liss, Inc.

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“…Devils affected by DFTD develop lesions around the face and neck (Loh et al 2006b), which can metastasize. Mortality of affected devils occurs owing to organ failure, secondary infection or an inability to feed (Loh et al 2006a;Pyecroft et al 2007).…”

Section: Introductionmentioning

confidence: 99%

MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer

et al. 2010

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Tasmanian devils face extinction owing to the emergence of a contagious cancer. Devil facial tumour disease (DFTD) is a clonal cancer spread owing to a lack of major histocompatibility complex (MHC) barriers in Tasmanian devil populations. We present a comprehensive screen of MHC diversity in devils and identify 25 MHC types and 53 novel sequences, but conclude that overall levels of MHC diversity at the sequence level are low. The majority of MHC Class I variation can be explained by allelic copy number variation with two to seven sequence variants identified per individual. MHC sequences are divided into two distinct groups based on sequence similarity. DFTD cells and most devils have sequences from both groups. Twenty per cent of individuals have a restricted MHC repertoire and contain only group I or only group II sequences. Counterintuitively, we postulate that the immune system of individuals with a restricted MHC repertoire may recognize foreign MHC antigens on the surface of the DFTD cell. The implication of these results for management of DFTD and this endangered species are discussed.

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The Immunohistochemical Characterization of Devil Facial Tumor Disease (DFTD) in the Tasmanian Devil (Sarcophilus harrisii)

Cited by 74 publications

References 30 publications

Clonally transmissible cancers in dogs and Tasmanian devils

Clonally transmissible cancers in dogs and Tasmanian devils

A Histological and Immunohistochemical Analysis of Lymphoid Tissues of the Tasmanian Devil

MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer

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