Objective : To explore the relationship between single nucleotide polymorphisms ( SNPs) in D-loop region of mitochondrial DNA ( mtDNA) and mtDNA copy number and the risk of dermatomyositis ( DM) ，and its in- fluencing factors． Methods : 74 patients with DM and 92 healthy controls were included in the study． Genomic DNA was extracted from peripheral blood and the target fragment of mtDNA D-loop region was amplified by PCR technique，and the products were subsequently sequenced．Serum levels of ROS were assessed using a high-sensi- tivity reactive oxygen species detection kit．The expression levels of cytokines，interleukin ( IL) -5，IL-13，inter- feron-γ ( IFN-γ) ，IL-2，IL-6，IL-10，tumor necrosis factor-α ( TNF-α) and IL-4 were measured using Flow Fluo- rescence Immunmicrobeads Assay．Wilcoxon rank-sum test was used to assess the potential correlation between cy- tokines and SNPs associated with DM risk．The relative copy number of mtDNA was measured using quantitative re- al-time polymerase chain reaction ( qPCR) analysis． Results : Two SNPs ( 16304T / C，16519T / C) were found to be associated with the risk of developing DM，and alleles 16304C ( χ2 = 4. 937，P = 0. 026) and 16519C ( χ2 = 4. 405，P = 0. 036) in the mitochondrial D-loop region were confirmed to be associated with DM development risk． The DM risk-associated allele 16304C was significantly associated with lower IL-4 expression ( P = 0. 016) ．The mtDNA copy number was significantly higher in DM patients than in controls ( P ＜0. 001) ． Conclusion Mitochondrial D-loop SNPs can be potential biomarkers for DM risk，and SNPs may be involved in DM by influencing cytokines．DM shows high expression of mtDNA copy number，and the increase in mtDNA copy number may lead to mitochondrial dysfunction，which triggers the pathogenesis of DM．

In the tyrosine kinase inhibitor (TKI) therapy era, patients with chronic myeloid leukemia (CML) have embarked on the trend of "chronic disease management". With the advent of 4 generations TKI drugs, there remain unmet needs for optimal CML treatment, such as treatment-free remission and disease recurrence after discontinuation. This article reviews the research progress of CML at the 63rd American Society of Hematology annual meeting.

As the driver gene of lung cancer, Kirsten rat sarcoma viral oncogene (KRAS) mutation often occurs in lung adenocarcinoma resistant to treatment with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), which has attracted attention due to its poor prognosis and lack of targeted drugs. Recent studies have found that KRAS mutation can promote tumor progression and affect treatment and prognosis by affecting the expressions of signal transducer and activator of transcription 3 (STAT3), G-protein-coupled receptor (GPCR) and programmed death receptor-ligand 1 (PD-L1), mammalian target of rapamycin (mTOR) signaling pathway activation and co-mutation of multiple genes. A phase Ⅰ clinical trial shows that AMG 510, a novel small molecule KRAS G12C inhibitor, is hopeful in treatment. Summarizing the pathogenesis, prognostic factors, targeted therapy and immunotherapy of KRAS mutation in lung adenocarcinoma is helpful to improve the understanding of KRAS mutation and can provide ideas and basis for subsequent studies.

Objective:To investigate the induction of tanshinoneⅡA (TanⅡA) on the differentiation of human placenta-derived mesenchymal stem cells (hPDMSCs) into cardiomyocytes, and to provide an experimental basis for TanⅡA as a cardiomyocyte differentiation inducer.Methods:The hPDMSCs were treated with different concentrations of TanⅡA (0.1, 0.2, 0.4, 0.6, 0.8, 1.0, 2.0, 4.0, 6.0, 8.0, and 10.0mg·L-1) , and the nontoxic dose of TanⅡA (0.1mg·L-1) was screened by MTT assay for experiment.The hPDMSCs were divided into control group, 5-aza induction (10μmol·L-1) group, and TanⅡA induction (0.1mg·L-1) group.After culture for 20d, the expressions ofα-sarcomeric actin (α-SCA) in the cells in various groups were detected with immunohistochemistry;the positive expression rates of cardiac troponin I (cTnI) in the cells in various groups were detected with immunofluorescence, and the differentation rates of cardiomyocytes were calculated.The expression levels of GATA-binding protein 4 (GATA4) , atrial natriuretic factor (ANF) , cTnI, glycogen synthase kinase-3β (GSK-3β) andβ-catenin in the cells were detected with Western blotting method.Results:The biological characteristics of hPDMSCs accorded with the mesenchymal stem cells.The MTT results showed that when the concentration of TanⅡA was more than 0.1mg·L-1, the cell survival rates were decreased with the increase of concentration;the cells in control group showed a rapid growth trend before 12d, and the proliferation activities of the cells began to decrease on the 12th day.Compared with control group, the cell activities in 5-aza induction group and TanⅡA induction group were significantly decreased (P＜0.05) .The immunohistochemistry staining results showed that the cells in control group didn't expressα-SCA, and the cells in 5-aza induction group and TanⅡA induction group expressedα-SCA, especially in TanⅡA induction group.Compared with control group, the expression levels of GATA4 (t5-aza=2.937, P5-aza＜0.05;tTanⅡA=4.769, PTanⅡA＜0.05) , ANF (t5-aza=3.728, P5-aza＜0.05;tTanⅡA=5.912, PTanⅡA＜0.05) , cTnI (t5-aza=3.623, P5-aza＜0.05;tTanⅡA=7.153, PTanⅡA＜0.05) and GSK-3β (t5-aza=2.995, P5-aza＜0.05;tTanⅡA=5.420, PTanⅡA＜0.05) proteins in the cells in 5-aza induction group and TanⅡA induction group were significantly increased, and the expression levels ofβ-catenin (t5-aza=2.985, P5-aza＜0.05;tTanⅡA=6.951, PTanⅡA＜0.05) protein were significantly decreased;compared with 5-aza induction group, the expression levels of GATA4, ANF, and GSK-3βproteins in TanⅡA induction group were increased (P＜0.05) .Conclusion:TanⅡA can induce the differentiation of hPDMSCs into cardiomyocytes, which has better effect than 5-aza, and its mechanism may be related to inhibiting the Wnt/β-catenin signaling pathway.