Figure 1.
Figure 1. Clinical, pathological, and molecular characterization of Bcr/Abl-induced CNS leukemia. (A) A mouse with CML-like myeloproliferative disorder with right forelimb paresis and right ptosis that developed on imatinib mesylate therapy, and a timeline illustrating the onset of neurologic signs (•; N=11). (B) H&E–stained section of a parenchymal lesion in the cerebral cortex (i-ii) and a meningeal infiltrate in the Virchow Robin space (iii-iv; the associated blood vessel is shown at the large arrow) composed of cells with abundant cytoplasm and punctate nucleoli. Note occasional binucleated forms (ii, small arrow). Anti–Mac-3 IHC of the brain lesion (v) or a control section from the liver of a mouse with Bcr/Abl-induced macrophage leukemia (vi)1,2 confirms the cells are of the macrophage lineage. Scale bars are 50 μM. (C) A massive infiltration of the pyriform sinus (i-ii) and spinal cord meninges (iii-iv) by a homogeneous population of medium-sized cells with scant cytoplasm and indistinct nucleoli. Anti–B-lymphoid cell antibody (CD45R/B220) staining of the pyriform mass (v) and control normal mouse spleen (vi) confirms the B-lymphoid cell lineage. Scale bars are 50 μM. (D) A laser-dissected brain lesion (right photomicrograph; lane 4) and an adjacent area of normal brain (acumbens) composed of small neurons (left photomicrograph; lane 3) were analyzed by PCR using primers specific for the P210BCR/ABL cDNA junction (B/A, top blot). For comparison, a section from the liver of a mouse with macrophage leukemia (lane 6) or normal liver (lane 5) was processed in the same fashion. 32D cells expressing P210 Bcr/Abl (lane 2) or neomycin alone (lane 1), or water only (–), were amplified using the same primers. To control for equivalent specimen quality, samples were also analyzed using primers detecting expression of the ribosomal-associated gene L7. Sizes of the PCR products are shown at right. The results depicted were confirmed in 3 additional PCR experiments from 2 independent sets of tissue dissections. Original magnification, × 10.

Clinical, pathological, and molecular characterization of Bcr/Abl-induced CNS leukemia. (A) A mouse with CML-like myeloproliferative disorder with right forelimb paresis and right ptosis that developed on imatinib mesylate therapy, and a timeline illustrating the onset of neurologic signs (•; N=11). (B) H&E–stained section of a parenchymal lesion in the cerebral cortex (i-ii) and a meningeal infiltrate in the Virchow Robin space (iii-iv; the associated blood vessel is shown at the large arrow) composed of cells with abundant cytoplasm and punctate nucleoli. Note occasional binucleated forms (ii, small arrow). Anti–Mac-3 IHC of the brain lesion (v) or a control section from the liver of a mouse with Bcr/Abl-induced macrophage leukemia (vi)1,2 confirms the cells are of the macrophage lineage. Scale bars are 50 μM. (C) A massive infiltration of the pyriform sinus (i-ii) and spinal cord meninges (iii-iv) by a homogeneous population of medium-sized cells with scant cytoplasm and indistinct nucleoli. Anti–B-lymphoid cell antibody (CD45R/B220) staining of the pyriform mass (v) and control normal mouse spleen (vi) confirms the B-lymphoid cell lineage. Scale bars are 50 μM. (D) A laser-dissected brain lesion (right photomicrograph; lane 4) and an adjacent area of normal brain (acumbens) composed of small neurons (left photomicrograph; lane 3) were analyzed by PCR using primers specific for the P210BCR/ABL cDNA junction (B/A, top blot). For comparison, a section from the liver of a mouse with macrophage leukemia (lane 6) or normal liver (lane 5) was processed in the same fashion. 32D cells expressing P210 Bcr/Abl (lane 2) or neomycin alone (lane 1), or water only (–), were amplified using the same primers. To control for equivalent specimen quality, samples were also analyzed using primers detecting expression of the ribosomal-associated gene L7. Sizes of the PCR products are shown at right. The results depicted were confirmed in 3 additional PCR experiments from 2 independent sets of tissue dissections. Original magnification, × 10.

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