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. 2014 Jan 1;28(1):58–70. doi: 10.1101/gad.232009.113

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© 2014 Kelly et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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Figure 2. — Loss of Mcl-1, even loss of a single allele, greatly impairs the sustained growth of Eμ-Myc lymphomas within the whole animal. (A) Survival curves of C57BL/6-Ly5.1⁺ recipient mice transplanted with Eμ-Myc;CreERT2;Mcl-1^fl/+ (red line), Eμ-Myc;CreERT2;Mcl-1^fl/fl (blue line), or control (Eμ-Myc;CreERT2; black line) lymphoma cells and treated with tamoxifen to inactivate Mcl-1 where applicable. (n) Total number of recipient mice analyzed; (N) number of independent lymphomas tested. Heterozygous and homozygous deletion of Mcl-1 significantly delayed lymphoma growth. (****) P < 0.0001. For the mice transplanted with the control Eμ-Myc;CreERT2 lymphomas, 3% regressed, and the overall median survival was 19 d. For the mice transplanted with the Eμ-Myc;CreERT2;Mcl-1^fl/+ lymphomas, 20% regressed, and the overall median survival was 23 d. For the mice transplanted with the Eμ-Myc;CreERT2;Mcl-1^fl/fl lymphomas, 30% regressed, and the overall median survival was 35 d. (B) Bioluminescence imaging of the tumor burden in C57BL/6-albino recipient mice injected with primary Eμ-Myc;CreERT2;Mcl-1^fl/fl lymphoma cells. At 10 d post-transplant, a cohort of these mice was treated with tamoxifen. These mice were subsequently imaged for bioluminescence.