Figure 5
Figure 5. Concomitant increase of serum CXCL1/KC and skin hyperplasia are a prerequisite to NPM-ALK+ lymphoma cell epidermotropism. (A-H) Histological analysis of lymphoma cell dissemination in a conditional mouse transgenic model. Conditional NPM-ALK lymphoma mouse models develop ALK+ B-cell (B220+) lymphomas. Images show normal architecture and negative lymphoma cell staining of spleen (A) and skin 10 (B) and 15 days (D) after birth. Lymphoma cells positive for ALK staining are observed in the spleen 15 (C), 20 (E), and 30 (G) days after birth. Note that the skin presents a hyperplasia of the epidermis and is negative for lymphoma cells staining (B220−; F). In contrast, 30 days after birth, 30% of the animals display B220+ tumoral cells infiltrated below the skin lesions (H; right inset shows magnification of bracket). Original magnification was 400× for the spleen and 100× for the skin, except in panel H, where the original magnification was 50× and 640×, respectively (right inset).

Concomitant increase of serum CXCL1/KC and skin hyperplasia are a prerequisite to NPM-ALK+ lymphoma cell epidermotropism. (A-H) Histological analysis of lymphoma cell dissemination in a conditional mouse transgenic model. Conditional NPM-ALK lymphoma mouse models develop ALK+ B-cell (B220+) lymphomas. Images show normal architecture and negative lymphoma cell staining of spleen (A) and skin 10 (B) and 15 days (D) after birth. Lymphoma cells positive for ALK staining are observed in the spleen 15 (C), 20 (E), and 30 (G) days after birth. Note that the skin presents a hyperplasia of the epidermis and is negative for lymphoma cells staining (B220; F). In contrast, 30 days after birth, 30% of the animals display B220+ tumoral cells infiltrated below the skin lesions (H; right inset shows magnification of bracket). Original magnification was 400× for the spleen and 100× for the skin, except in panel H, where the original magnification was 50× and 640×, respectively (right inset).

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