Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài:Isolation of specific and biologically active peptides that bind cells from patients with acute myeloid leukemia (AML) | BioMed Central Journal of Hematology Oncology Research Isolation of specific and biologically active peptides that bind cells from patients with acute myeloid leukemia AML Naomi Galili 11 Emmanuelle Devemyt2 and Azra Raza1 Open Access Address Saint Vincent s Comprehensive Cancer Center New York NY USA and 2McGill University Montreal Canada Email Naomi Galili - ngalili@ Emmanuelle Devemy - Azra Raza - araza@ Corresponding author tEqual contributors Published 10 July 2008 Received 19 May 2008 Journal of Hematology Oncology 2008 1 8 doi 1756-8722-1 -8 Accepted 10 July 2008 This article is available from http content 1 1 8 2008 Galili et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Purpose In a departure from conventional strategies to improve treatment outcome for myeloid malignancies we report the isolation of leukemia-specific peptides using a phage display library screened with freshly obtained human myeloid leukemia cells. Results A phage display library was screened by 5 rounds of biopanning with freshly isolated human AML cells. Individual colonies were randomly picked and after purification biologic activity growth and differentiation on fresh AML cells was profiled. Ten peptides were synthesized for further biological studies. Multiple peptides were found to selectively bind to acute myeloid leukemia AML cells. The peptides bound to leukemia cells were internalized and could induce proliferation and or differentiation in the target patient cells. Two of the peptides HP-A2 and HP-G7 appeared to have a novel mechanism of inducing differentiation since they did not cause G1 arrest in cycling cells even as the .
