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Titlebook: Chemotherapy for Leukemia; Novel Drugs and Trea Takanori Ueda Book 2017 Springer Nature Singapore Pte Ltd. 2017 Acute promyelocytic leukemi

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樓主: FETID
31#
發(fā)表于 2025-3-26 22:51:20 | 只看該作者
Nelarabineethoxylated to ara-G by adenosine deaminase in the blood. The ara-G is subsequently transported into cancer cells via nucleoside transporters. Inside the cells, ara-G is phosphorylated by either deoxycytidine kinase to cytosolic ara-G monophosphate or by deoxyguanosine kinase to mitochondrial ara-G
32#
發(fā)表于 2025-3-27 03:44:06 | 只看該作者
33#
發(fā)表于 2025-3-27 07:27:49 | 只看該作者
34#
發(fā)表于 2025-3-27 09:42:24 | 只看該作者
35#
發(fā)表于 2025-3-27 15:36:55 | 只看該作者
36#
發(fā)表于 2025-3-27 21:51:09 | 只看該作者
Rituximab and Alemtuzumab for Chronic Lymphocytic Leukemia: Clinical Pharmacology and Therapeutic Remended for unfit patients with relevant comorbidities without . defects. Alemtuzumab has proven efficacy in patients with . defects and has become a therapeutic option for these patients, but its role in the management of B-CLL patients is hampered by its substantial toxicity.
37#
發(fā)表于 2025-3-28 01:04:17 | 只看該作者
The Molecular Basis of Arsenic Trioxide Treatment for Acute Promyelocytic Leukemia (APL)promyelocytic differentiation, leading ultimately to cell death of APL cells. Recent studies have shown that the combination of ATRA and ATO has synergistic effects in vitro and in vivo, and these findings have translated successfully to the clinic with great improved outcome for APL patients.
38#
發(fā)表于 2025-3-28 03:53:25 | 只看該作者
39#
發(fā)表于 2025-3-28 10:05:23 | 只看該作者
Two-Step Double Photoionization of MoleculesTherefore, a third-generation ABL TKI, ponatinib, was developed and shows good clinical efficacy against CML cells harboring the T315I mutation. Thus, treatments for CML are progressing rapidly, and further evolution is expected.
40#
發(fā)表于 2025-3-28 11:32:31 | 只看該作者
Dasatinib, Nilotinib, Bosutinib, Ponatinib, and Other TKIsTherefore, a third-generation ABL TKI, ponatinib, was developed and shows good clinical efficacy against CML cells harboring the T315I mutation. Thus, treatments for CML are progressing rapidly, and further evolution is expected.
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