博爱家 发表于 2025-3-23 10:42:52
http://reply.papertrans.cn/23/2264/226398/226398_11.pngCardiac-Output 发表于 2025-3-23 17:43:03
https://doi.org/10.1007/978-3-531-91124-3 be long-term effective because of CML stem cells’ insensitivity to tyrosine kinase inhibitors. Therefore, studying more about CML stem cells is essential to understand the pathways of CML stem cell development and proliferation and finally lead to effective treatments to eliminate CML stem cells anOptimum 发表于 2025-3-23 21:48:54
http://reply.papertrans.cn/23/2264/226398/226398_13.pngbotany 发表于 2025-3-23 23:15:07
https://doi.org/10.1007/978-3-531-91124-3-phase CML patients are treated with impressive efficacy with TK inhibitors (TKi) such as imatinib mesylate (IM). However, rather than definitively curing CML, TKi induces a state of minimal residual disease, due to the persistence of leukemia stem cells (LSC) which are insensitive to this class ofGum-Disease 发表于 2025-3-24 04:45:59
http://reply.papertrans.cn/23/2264/226398/226398_15.pngBiomarker 发表于 2025-3-24 06:56:50
http://reply.papertrans.cn/23/2264/226398/226398_16.png情感脆弱 发表于 2025-3-24 11:55:12
https://doi.org/10.1007/978-3-531-91124-3s the genome. The method creates specific signatures at unmethylated and methylated CpG sites by sequential digests of genomic DNA with restriction endonucleases .I and .I, respectively. Both enzymes have the same CCCGGG recognition site; however, they differ in their sensitivity to CpG methylationPopcorn 发表于 2025-3-24 18:41:37
https://doi.org/10.1007/978-3-531-91124-3ng Chronic Myeloid Leukemia (CML). This leads to deregulation of transcription that is often causally linked to the tumorigenic state. Chromatin-immunoprecipitation coupled with massively parallel DNA sequencing (ChIP-.) is the key technology to study transcription as it allows in vivo whole-genome不利 发表于 2025-3-24 22:06:26
http://reply.papertrans.cn/23/2264/226398/226398_19.pngchalice 发表于 2025-3-25 02:58:06
https://doi.org/10.1007/978-1-4612-3878-2patient relapse remains a challenge. Acquisition of BCR-ABL mutations is crucial in the resistance but the underlying molecular mechanisms are poorly understood. Here we describe a cell culture model for CML acquired resistance in which blast crisis CML cells undergo initial apoptosis upon treatment