Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
Cancer Res. 2010 Oct 1;70(19):7347-52. doi: 10.1158/0008-5472.CAN-10-1528. Epub 2010 Aug 31.
Expression of cytokine receptor-like factor 2 (CRLF2) has recently been shown to be upregulated as well as mutated in populations of B-progenitor acute lymphoblastic leukemia (B-ALL), including Down syndrome (DS-ALL) patients, lacking recurring chromosomal translocations. Increased CRLF2 expression associates with JAK2 mutation, a combination that transforms hematopoietic cells, suggesting that mutant JAK2 and CRLF2 may cooperate to contribute to B-ALL formation. Importantly, elevated CRLF2 expression correlates with poor outcome in high-risk B-ALL patients. Therefore, CRLF2 may provide a new prognostic marker for high-risk B-ALL, and inhibition of CRLF2/JAK2 signaling may represent a therapeutic approach for this population of ALL patients.
细胞因子受体样因子 2(CRLF2)的表达最近被证明在 B 祖细胞急性淋巴细胞白血病(B-ALL)人群中上调和突变,包括缺乏复发性染色体易位的唐氏综合征(DS-ALL)患者。CRLF2 表达增加与 JAK2 突变相关,这种组合可转化造血细胞,表明突变 JAK2 和 CRLF2 可能合作促进 B-ALL 的形成。重要的是,CRLF2 的高表达与高危 B-ALL 患者的不良预后相关。因此,CRLF2 可能为高危 B-ALL 提供新的预后标志物,抑制 CRLF2/JAK2 信号可能代表 ALL 患者这一人群的治疗方法。