A 47-Year-old Asian female with tracheobronchial space-occupying lesions caused by chronic lymphocytic leukemia.

CASE PRESENTATION: A 47-year-old Asian woman was admitted with worsening chest tightness and dyspnea for 10 days. Computed tomography (CT) showed changes in the trachea and segmental bronchi. Pulmonary function results suggestive of severe obstructive ventilatory dysfunction. Bronchoscopic findings showed the presence of multiple nodular lesions in the patient's trachea and left and right main bronchi. Bronchoscopic biopsy, lymph node biopsy and bone marrow aspiration flow cytometry test results led to a definitive diagnosis of chronic lymphocytic leukemia (CLL), staged as Binet stage B and Rai stage 2.

[Galectin-3 Expression and Its Clinical Significance in Acute Myeloid Leukemia with Positive AML1/ETO Fusion Gene].

OBJECTIVE: To investigate the mRNA expression of galectin-3 and its clinical significance in acute myeloid leukemia (AML) patients carrying AML1/ETOfusion gene. METHODS: RQ-PCR method was used to detect the expression of galectin-3 mRNA in bone marrow mononuclear cells of 53 AML patients with AML1/ETO+, ELISA was used to detect the expression of galectin-3 protein in peripheral blood, and the correlations of galectin-3 expression with clinical and laboratory features and outcomes were analyzed. RESULTS: The mRNA and protein levels of galectin-3 were significantly higher in newly diagnosed AML1/ETO+ AML patients compared with the control ( P<0.001). Galectin-3 mRNA and protein expressions were positively correlated (r=0.732, P<0.001). Galectin-3 protein was significantly decreased during the period of complete remission (CR)( P<0.001). The mRNA expression of galectin-3 was negatively correlated with the count of white blood cells ( P=0.014), and positively correlated with CD34 expression and additional cytogenetic aberrations (ACA) ( P=0.001, P=0.026). There was no significant difference in CR, partial remission (PR), induction death (early mortality) between galectin-3 high-expression group and low-expression group ( P>0.05), but there was significant difference in recurrence rate between the two groups ( P=0.029). The median overall survival (OS) rate and disease-free survival (DFS) rate were shortened in the high-expression group ( P=0.007, P=0.015) and the cumulative incidence of relapse was increased ( P=0.045), but there was no significant difference in the cumulative incidence of CM(155mm]mortality ( P>0.05). Cox regression analysis suggested galectin-3 mRNA level an independent indicator of OS and DFS in AML1/ETO+ AML patients. CONCLUSION: Bone marrow galectin-3 mRNA level may be an important reference index for evaluating the prognosis and guiding the treatment of AML1/ETO+ AML patients.

[Effect of miR-125b on T Cell Activation in Aplastic Anemia by Targetting B7-H4].

OBJECTIVE: To investigate the effect of miR-125b on T cell activation in patients with aplastic anemia (AA) and its molecular mechanism. METHODS: A total of 30 AA patients were enrolled in department of hematology, Binzhou Medical University Hospital from January 2018 to October 2021, as well as 15 healthy individuals as healthy control (HC) group. Peripheral blood mononuclear cells (PBMCs) were isolated, in which the levels of miR-125b and B7-H4 mRNA were detected by RT-qPCR. Immunomagnetic beads were used to separate naive T cells and non-naive T cells from AA patients and healthy people to detect the levels of miR-125b and B7-H4 mRNA. Lentivirus LV-NC inhibitor and LV-miR-125b inhibitor were transfected into cells, and T cell activation was detected by flow cytometry. The dual-luciferase reporter gene assay was used to detect the targetting relationship between miR-125b and B7-H4. RT-qPCR and Western blot were used to detect the levels of miR-125b, CD40L, ICOS, IL-10 mRNA and B7-H4 protein. RESULTS: Compared with HC group, the expression of miR-125b was up-regulated but B7-H4 mRNA was down-regulated in PBMCs of AA patients (P <0.05), and the proportions of CD4+CD69+ T cells and CD8+CD69+ T cells in PBMCs of AA patients were higher (P <0.05). The expression of miR-125b was significantly up-regulated but B7-H4 mRNA was down-regulated in both naive T cells and non-naive T cells of AA patients (P <0.05), and non-naive T cells was more significant than naive T cells (P <0.05). Compared with NC inhibitor group, the expression of miR-125b was significantly decreased, the expression level of CD69 on CD4+ and CD8+ T cells in PBMCs was also significantly decreased, while the luciferase activity was significantly increased after co-transfection of miR-125b inhibitor and B7-H4-3'UTR-WT in the miR-125b inhibitor group (P <0.05). Compared with NC inhibitor group, the mRNA and protein levels of B7-H4 were significantly increased in the miR-125b inhibitor group (P <0.05). Compared with miR-125b inhibitor+shRNA group, the expression levels of CD69 on CD4+ and CD8+ T cells were significantly increased, and the levels of CD40L, ICOS and IL-10 mRNA were also significantly increased in the miR-125b inhibitor+sh-B7-H4 group (P <0.05). CONCLUSION: MiR-125b may promote T cell activation by targetting B7-H4 in AA patients.