| Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia (AML) distinguished by the morphology of blast cells, by coagulopathy and by the presence of the t(15;17). this balanced t(15;17) translocation results in a reciprocal fusion between the RAR a , a member of the super family of nuclear hormone receptors, located on chromosome 17q21 and PML ,a putative transcription factor, located on chromosome 15q22. The fusion product, PML-RAR a ,which is found in approximately 100% of patient-derived promyelocytic leukemia cells, is a molecular marker of APL. As suggested recently, this anomalous protein may have a critical role in promyelocytic leukemo-genesis. PML-RAR a , which contains the amino-terminal part of PML including its dimerization and DNA-binding domains and the DNA and hormone binding domains of RAR a , displays altered transactivating properties compared with RAR a in response to all-trans retinoic acid(ATRA) treatment. It is postulated that PML-RAR a functions as a dominant negative mutation, its product may contribute to outgrowth of the APL blasts andmydoid differentiation blockage at the promyelocyte stage.The vitamin A derivative all-trans retinoic acid is one of the most potent and extensively studied differentiating agents. It inhibits proliferation and induces differentiation of malignant cells in vitro. Since it was first introduced in Shanghai in 1986 that ATRA has been successfully used in treatment of the APL patients with a high rate of complete remission (CR), APL was the first example of neoplastic disease that can be treated by differentiation agents. However, ATRA therapy has a major drawback, which is retinoic acid syndrome (RAS) and the quick development of resistance to ATRA, so the remission durations were found to be relatively short with ATRA alone after achievement of CR. It is necessary to look for other new antineoplastic strategy for treating APL. In 1992, reported by Harbin medical university from the Northeast of China, arsenic compounds including arsenic trioxide (As2O3) and arsenic disulfide, two compounds used in some traditional Chinese remedies, are very effective in APL treatment. It has been shown that As2O3 induced clinical completed remission in about 70% of APL patients. More interestingly, arsenicals can overcome drug resistance of all-trans retinoic acid, which raise hope for gravely ill patients resistant to ATRA and chemotherapy. The journal of science reported this therapy to the world titled as "Cancer Research: Ancient Remedy Performs New Tricks". That As2O3 induces APL cell apoptosis, first shown by Chen Z., with downregulation of Bcl-2expression and modulation of PML-RAR a /PML protein may be the possible mechanism of arsenic trioxide in the treatment of APL. Arsenic trioxide, an old potion named PiSuang in Chinese medicine, is toxic and has severely adverse effects in clinic, including fever, skin rash, proteinuria, vomiting, spastic abdominalgia and fetal brain disease which lead Some patients to death. All in all, for hematologist, it is always of interest and significance in looking for new drug inducer in leukemia treatment.Antimonials, as an effective anti-parasite drug, can, like arsenicals, inactivate some important enzymes by binding to the sulfhydryl groups, which can be explained by the chemical similarity of both substances. Antimony and arsenic are elements from group V of the periodic table, classified as metalloids, which suggests that Antimonials can be an alternative new drug in treatment of APL. This study shows that antimonials can induce APL cell apoptosis effectively. Using animproved subtractive hybridization (ISH), we batch cloned the differentially expressed gene of NB4 associated apoptosis induced by antimonials, of which the known gene give a counterevidence of above results and 74 novel gene have been accepted by NCBI Genbank. Our experiment results make it possible that antimonials can be alternative therapy in APL treatment. All of experimental results showed as follows:1 , An...
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