Retinoic Acid and Arsenic for Treating Acute Promyelocytic Leukemia 英文参考文献.docVIP

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Retinoic Acid and Arsenic for Treating Acute Promyelocytic Leukemia 英文参考文献.doc

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Retinoic Acid and Arsenic for Treating Acute Promyelocytic Leukemia 英文参考文献

Open access, freely available online Research in Translation Retinoic Acid and Arsenic for Treating Acute Promyelocytic Leukemia Guang-Biao Zhou, Wei-Li Zhao, Zhen-Yi Wang, Sai-Juan Chen, Zhu Chen* A cute promyelocytic leukemia (APL) was ?rst identi?ed as a distinct subtype of acute myeloid leukemia in 1957 by Leif Hillestad. It is called M3 in the French–American–British classi?cation, with a variant type referred to as microgranular (M3v in the French– American–British nomenclature) [1]. APL is characterized by three features: (1) the presence of an accumulation of abnormal promyelocytes (see Glossary) that do not differentiate into mature granulocytes, (2) the occurrence of ?brinogenopenia and disseminated intravascular An important discovery of the early 1970s was that myeloid leukemic cells could be reprogrammed to resume normal differentiation and to become non-dividing mature granulocytes or macrophages as a result of stimulation by various cytokines [3,4]. Based on this discovery, Leo Sachs at the Weizmann Institute of Science, Rehovot, Israel, hypothesized in 1978 that treatment with agents that induce cancer cells to complete differentiation could be a potential therapeutic option for patients with cancer [5]. In the early 1980s, Breitman and colleagues showed that retinoic acid (RA; Figure 2), a derivative of vitamin A, could induce terminal differentiation of human promyelocytic leukemic cells in vitro [6,7]. But the ?rst clinical reports of using RA showed con?icting results. Some case reports showed bene?cial effects of 13-cis RA in people with refractory or relapsed APL [8,9,10], but other reports showed that 13-cis RA was ineffective in treating APL [11]. Beginning in the early 1980s, the Shanghai Institute of Hematology conducted a series of experiments on differentiation therapy for APL. These experiments showed that all-trans RA (ATRA) could induce terminal differentiation of HL-60, a cell line with promyelocytic features, and fresh leukem