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BACKGROUND Gemtuzumab ozogamicin (GO) is an active agent for the treatment of CD33-postive acute myeloid leukemia (AML) and may improve the outcome of specific patient subgroups when combined with conventional chemotherapy. However, to the best of the authors' knowledge, the effects of GO on levels of minimal residual disease (MRD) are unknown. METHODS Pediatric patients with AML who received GO, either alone or in combination with chemotherapy on the AML02 multicenter trial, were analyzed to determine the effects of GO on MRD and outcome. RESULTS Among 17 patients who received GO alone because of persistent leukemia, 14 had a reduction in their MRD level and 13 became MRD negative. Of the 29 who received chemotherapy in combination with GO after responding poorly to chemotherapy, 28 demonstrated reduced MRD and 13 became MRD negative. Treatment with GO effectively reduced MRD before hematopoietic stem cell transplantation and was not found to be associated with increased treatment-related mortality after transplantation. CONCLUSIONS GO is effective in reducing MRD levels in pediatric patients with AML and may improve the outcome of those patients at high risk of disease recurrence. Cancer 2013;119:4036-4043. © 2013 American Cancer Society. [ABSTRACT FROM AUTHOR]

Objective: To assess the ability of an anti-lysozyme antibody to stabilize the plasma pharmacokinetics of lysozyme through a ‘buffering’ effect. Methods: Hen egg lysozyme was radiolabeled with 14C and infused with or without the murine anti-lysozyme antibody D1.3 into the jugular vein of rats. The dosages of antibody and lysozyme were varied, and the antibody and lysozyme were administered either together or in separate infusions. Results: Buffering of lysozyme with an equimolar amount of D1.3 more than doubled the plasma half-life of lysozyme and addition of more antibody buffer prolonged the half-life to an even greater extent. D1.3 bound lysozyme that was infused several minutes after the D1.3 administration, indicating that D1.3 can be charged with drug in vivo. Conclusion: Antibody buffering of monovalent therapeutic enzymes is possible and may have potential for clinical use. [ABSTRACT FROM AUTHOR]