开花期女 发表于 2025-3-26 22:51:20
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奖牌 发表于 2025-3-27 03:44:06
http://reply.papertrans.cn/23/2250/224970/224970_32.pngAbsenteeism 发表于 2025-3-27 07:27:49
http://reply.papertrans.cn/23/2250/224970/224970_33.png真实的人 发表于 2025-3-27 09:42:24
http://reply.papertrans.cn/23/2250/224970/224970_34.png晚间 发表于 2025-3-27 15:36:55
http://reply.papertrans.cn/23/2250/224970/224970_35.pngaverse 发表于 2025-3-27 21:51:09
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.arthroscopy 发表于 2025-3-28 01:04:17
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.Exploit 发表于 2025-3-28 03:53:25
http://reply.papertrans.cn/23/2250/224970/224970_38.png柔美流畅 发表于 2025-3-28 10:05:23
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.费解 发表于 2025-3-28 11:32:31
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.