Relation of MBL ExonI 54 and NFκB1-94ins/del ATTG Polymorphism with Fever during Neutropenia in Patients with Acute Leukaemia after Chemotherapy / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To explore the correlation between MBL ExonI 54 and NFκB1-94ins/del ATTG polymorphism and fever during neutropenia in patients with acute leukaemia (AL) (except M3) after first chemotherapy in Chinese Han population.</p><p><b>METHODS</b>Blood samples obtained from 76 fever patients with AL during neutropenia episodes were detected to analyse single nucleotide polymorphism (SNP) in the MBL ExonI 54 and NFκB1-94ins/del ATTG gene, and analyse the correlation between above-mentioned 2 polymorphisms and fever during neutropenia of AL patients after chemotherapy.</p><p><b>RESULTS</b>In 76 patients, no correlation were found between MBL ExonI 54 and NFκB1-94ins/del ATTG polymorphism and fever during neutropenia in patients with acute leukaemia after chemotherapy (P > 0.05). No significant relation were found in sex, age, underlying disease, disease status or degrees of neutropenia in febrile neutropenia between MBL ExonI 54 and NFκB1-94ins/del ATTG polymorphism (P > 0.05). However, patients with MBL ExonI 54 mutation presented longer febrile duration with a median of 5 days compared to 3 days of patients with wildtype MBL ExonI 54 genotype (P < 0.05).</p><p><b>CONCLUSIONS</b>There is no clear correlation between MBL ExonI 54 and NFκB1-94ins/del ATTG polymorphism and fever during neutropenia in patients with acute leukaemia after chemotherapy. However, the patients with MBL ExonI 54 mutation have been observed to present a longer febrile duration.</p>

Roles of CEBPA mutation and expression abnormality in acute myeloid leukemia - review / 中国实验血液学杂志

CCAAT enhancer binding protein A (CEBPA) and its product transcription factor CCAAT enhancer binding protein α (C/EBPα) play pivotal roles in early granulocyte development. C/EBPα induces the transition and keeps the balance of differentiation and proliferation of myeloid progenitors. The mutation and dysregulation of CEBPA at transcription, translation or post-translation level lead to differentiation block and over proliferation of immature hematopoietic cells, which are important mechanisms of acute myeloid leukemia (AML). The mutation and dysregulation of CEBPA also provide clues for evaluating the outcome of AML patients and potential targets for differentiation-inducing therapies. This review focus on CEBPA mutation and AML, dysregulation of C/EBPα protein expression and AML, as well as C/EBPα protein and targeting therapy.