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What a dog transmissible tumor can teach us about cancer regression

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Article: e1472059 | Received 24 Apr 2018, Accepted 25 Apr 2018, Published online: 06 Aug 2018

Figures & data

Figure 1. Mechanisms underlying the regression of ocular canine transmissible venereal tumor (CTVT) upon chemotherapy in mixed breed dog.

Upper left, ocular CTVT treated with vincristine. Treatment induces activation and differentiation of host epithelial cells surrounding (or within) the tumour, an acute inflammatory response and a strong upregulation of Chemokine (C-C motif) ligand 5 (CCL5), which recruits and retains immune cells into the tumor. This early response is followed by infiltration of CD8 and CD4 T lymphocytes, natural killer (NK) cells, B lymphocytes and upregulation of C-C chemokine receptor type 5 (CCR5). Lastly, at regression (upper right), there is upregulation of genes for cell migration and tissue repair.

Figure 1. Mechanisms underlying the regression of ocular canine transmissible venereal tumor (CTVT) upon chemotherapy in mixed breed dog.Upper left, ocular CTVT treated with vincristine. Treatment induces activation and differentiation of host epithelial cells surrounding (or within) the tumour, an acute inflammatory response and a strong upregulation of Chemokine (C-C motif) ligand 5 (CCL5), which recruits and retains immune cells into the tumor. This early response is followed by infiltration of CD8 and CD4 T lymphocytes, natural killer (NK) cells, B lymphocytes and upregulation of C-C chemokine receptor type 5 (CCR5). Lastly, at regression (upper right), there is upregulation of genes for cell migration and tissue repair.

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