ESKM is superior to ESK1 in vivo, and is effective against multiple tumor models. ESKM is superior to ESK1 in vivo, and is effective against multiple tumor.

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ESKM is superior to ESK1 in vivo, and is effective against multiple tumor models. ESKM is superior to ESK1 in vivo, and is effective against multiple tumor models. Tumor burden was determined by luciferase imaging of mice in the supine position (n = 5 per group). Data points are averages of each group, and error bars represent SEM. Arrows indicate treatment with mAb. A, ESKM significantly reduced mean tumor growth of intraperitoneal JMN mesothelioma as assessed by total luminescence (*P < 0.05, multiple T tests on and after day 18), and also significantly improved survival (P = 0.016 vs. isotype, P = 0.095 vs, ESK1), with events representing death or terminal morbidity as assessed on protocol by veterinarians. B, ESKM is effective against SET2 AML (*P < 0.05, multiple T tests). C, ESKM is effective against a disseminated fresh, patient-derived pre-B ALL (*P < 0.05, **P < 0.01, multiple T tests). D, leukemia burden in the bone marrow was quantitated by imaging on day 40, then bone marrow cells were harvested from mice in C and transplanted as subcutaneous tumors into NSG mice. Bone marrow cells from the isotype-treated mice were injected into the right shoulder (viewed from above), whereas an equal number of bone marrow cells from the ESKM-treated mice were injected into the left shoulder. Subcutaneous tumors were then quantitated 28 days after transplantation. In a multicolor flow cytometry analysis of a frozen stock of the same fresh primary ALL sample (before passage in animals), ESK mAb bound the lineagelow/− CD34+ CD38− subset. Nicholas Veomett et al. Clin Cancer Res 2014;20:4036-4046 ©2014 by American Association for Cancer Research