Correlation Between Matrix Metalloproteinases With Coronary Artery Lesion Caused by Kawasaki Disease.

This study was designed to clarify the role of matrix metalloproteinases (MMPs) in coronary artery lesions (CAL). Serum samples were acquired from healthy, febrile, and Kawasaki disease (KD) children with or without CAL. Standard blood parameters were examined and enzyme-linked immunosorbent assay (ELISA) was used to assess the levels of MMP-2 and MMP-9. Intravenous immunoglobulin (IVIG) therapy was conducted on the KD patients and the changes of MMPs before and after treatment were compared. The correlations between MMP levels and clinical parameters were also evaluated. Compared to febrile and healthy controls, KD patients demonstrated clinical signs characteristic of abnormal immunoregulation. However, the clinical parameters of KD patients with or without CAL were not significantly different. MMP-2 and MMP-9 levels, however, were significantly higher in KD patients with CAL than those without CAL. IVIG treatment effectively downregulated the levels of MMPs in KD patients, which was more prominent in those with CAL. Significant correlations were found between MMP levels and some clinical parameters of KD, such as fever time, white blood cell count, etc. The upregulation of MMPs significantly correlates with coronary artery aneurysms (CAAs) in KD patients, making it important biomarkers of CAL in KD patients.

[Research Progress on Pathogenic Genes of Ph-like Acute Lymphoblastic Leukemia--Review].

Abstract　　Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL or BCR-ABL1-like ALL) is a kind of acute leukemia which has the similar gene expression profiles and manifests the biological behavior same to Ph-positive ALL, but lacks the BCR-ABL1 fusion gene. Ph-like ALL was involved in multiple abnormal changes of genomes, activating kinase and cytokine receptor signaling. This review focuses on the progress of classical genetic abnormalities of PH-like ALL in the JAK-STAT signaling, ABL kinase activation, TKI resistance in Ph-like ALL, SH2B3 gene inactivating mutation and IKZF1 gene abnormality. Besides, also summarizes the frontier progress of novel gene mutation (ATF7IP exon 9 fused with PDGFRB exon 11, PDGFRBC843G mutation caused by fusion of exon 11-23 of PDGFRB with exon 1-6 of AGGF1 gene) in recent years.