CALM-AF10白血病多见于中青年患者，常伴纵膈浸润，约占成人急性髓系白血病的2%，儿童急性T淋巴细胞白血病的14%，预后极差。t(10;11)(p13;q14-21)染色体倒位致CALM与AF10基因融合从而导致白血病转化，但其致病机制并未明确。BioTAP-XL交联及串联亲和纯化技术可有效降低非特异性结合，并能同时纯化出相互作用蛋白及染色质成分。申请人在前期工作中克隆并鉴定了CALM-AF10融合基因，并成功构建了CALM-AF10-BioTAP高亲和力表达载体。本课题拟采用BioTAP-XL交联技术，并通过小鼠骨髓造血前体细胞基因转染、移植模型、串联亲和纯化、蛋白质组学及第二代深度测序技术，深入分析白血病细胞中CALM-AF10相互作用的蛋白质及染色质，揭示CALM-AF10致病分子机制，为寻找新的治疗靶点、实现个体化治疗提供理论依据。

CALM-AF10 leukemia appear to be most frequently associated with young patients, often accomplished with mediastinal invasion. CALM-AF10 accounts for approximately 2% of adult acute myeloid leukemia and 14% of childhood acute T lymphoblastic leukemia, associated with poor prognosis. The t(10;11)(p13;q14-21) translocation cause CALM gene fusion to AF10, driving leukemia transformation. The mechanism is not fully understood. BioTAP-XL cross linking methodology can not only reduce non-specific binding but also purified protein composition of chromatin associated complexes. We have cloned and characterized the CALM-AF10 fusion gene in previous work, and successfully constructed CALM-AF10-BioTAP high affinity expression vector. By using BioTAP-XL cross linking approach, as well as mouse bone marrow progenitor cell transfection, transplantation model, tandem affinity purification, mass spectrometry and next-generation sequencing technology, we try to deeply identify CALM-AF10 interacting protein and chromatin in leukemia cells, revealing its pathogenic molecular mechanism, finding new therapeutic targets, and developing individualized treatment plan.