Fig. 5.
Fig. 5. Comparative histopathological findings in TEL-ABL–induced andBCR-ABL–induced hematologic diseases. / Photomicrographs of Wright-Giemsa–stained PB (panels A, F, K, and P); hematoxylin-eosin–stained spleen (panels B, G, L, and Q), small bowel (panels C, H, M, and R), and hematoxylin-eosin–stained liver (panels D, I, N, and S); and ORO-stained liver (panels E, J, O, and T) from mice with TEL-ABL–induced SBS (panels F-J),TEL-ABL–induced CML-like disease (panels K-O), andBCR-ABL–induced CML-like disease (panels P-T). A Balb/c mouse killed 5 weeks after transplantation with untransduced bone marrow was used as the control (panels A-E). Magnifications are ×750 for PB, ×100 for small bowel, and ×200 for liver and spleen. Although mice with TEL-ABL–induced CML-like disease occasionally had infiltration of the bowel submucosa with neutrophils (panel M, ×500 insert), neutrophil infiltration of villi was found only in mice with SBS (panel H, ×500 insert).

Comparative histopathological findings in TEL-ABL–induced andBCR-ABL–induced hematologic diseases.

Photomicrographs of Wright-Giemsa–stained PB (panels A, F, K, and P); hematoxylin-eosin–stained spleen (panels B, G, L, and Q), small bowel (panels C, H, M, and R), and hematoxylin-eosin–stained liver (panels D, I, N, and S); and ORO-stained liver (panels E, J, O, and T) from mice with TEL-ABL–induced SBS (panels F-J),TEL-ABL–induced CML-like disease (panels K-O), andBCR-ABL–induced CML-like disease (panels P-T). A Balb/c mouse killed 5 weeks after transplantation with untransduced bone marrow was used as the control (panels A-E). Magnifications are ×750 for PB, ×100 for small bowel, and ×200 for liver and spleen. Although mice with TEL-ABL–induced CML-like disease occasionally had infiltration of the bowel submucosa with neutrophils (panel M, ×500 insert), neutrophil infiltration of villi was found only in mice with SBS (panel H, ×500 insert).

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