Fig. 3.
Fig. 3. Lymphomas that develop in MCL1 transgenic mice exhibit alterations in the B-cell compartment. / (A-C) Cell surface marker expression was assayed on cells from a normal nontransgenic lymph node (left column) and from diseased lymph nodes from transgenic animals with diffuse large-cell lymphoma (either localized [middle column] or disseminated [right column] disease). Similar results were obtained when CD19 was used instead of B220. The numbers on the graphs represent the percentage of cells in each quadrant, where those in parentheses were obtained on gating of the population of cells with increased forward scatter. (D) Cells from lymph nodes of MCL1 transgenic mice with disseminated disease (░), or nontransgenic controls (■), were assayed for cell surface markers characterizing lymphoid (B220, IgM, CD3, CD5), myeloid (CD11b), and immature (Sca1, CD34, c-kit) cells. The values shown represent the mean ± SE, where 4 animals per group were tested for the lymphoid and myeloid markers (the animals in the left and right columns along with 3 additional pairs in which the transgenic animals had polymorphic lymphoma) and 3 transgenic and 2 nontransgenic animals were tested for immature cell markers. IgM−B220+ cells represented 64% of the total B220+ population in the diseased transgenic lymph nodes (± 4% SE; n = 4), as compared with a control value of 13% (± 2%). This difference was significant (P < .02; analysis of variance with Sheffee testing), whereas comparisons with the other markers were not.

Lymphomas that develop in MCL1 transgenic mice exhibit alterations in the B-cell compartment.

(A-C) Cell surface marker expression was assayed on cells from a normal nontransgenic lymph node (left column) and from diseased lymph nodes from transgenic animals with diffuse large-cell lymphoma (either localized [middle column] or disseminated [right column] disease). Similar results were obtained when CD19 was used instead of B220. The numbers on the graphs represent the percentage of cells in each quadrant, where those in parentheses were obtained on gating of the population of cells with increased forward scatter. (D) Cells from lymph nodes of MCL1 transgenic mice with disseminated disease (░), or nontransgenic controls (■), were assayed for cell surface markers characterizing lymphoid (B220, IgM, CD3, CD5), myeloid (CD11b), and immature (Sca1, CD34, c-kit) cells. The values shown represent the mean ± SE, where 4 animals per group were tested for the lymphoid and myeloid markers (the animals in the left and right columns along with 3 additional pairs in which the transgenic animals had polymorphic lymphoma) and 3 transgenic and 2 nontransgenic animals were tested for immature cell markers. IgMB220+ cells represented 64% of the total B220+ population in the diseased transgenic lymph nodes (± 4% SE; n = 4), as compared with a control value of 13% (± 2%). This difference was significant (P < .02; analysis of variance with Sheffee testing), whereas comparisons with the other markers were not.

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