Objective: To investigate the clinical and prognostic characteristics of newly diagnosed multiple myeloma (NDMM) patients with myelofibrosis (MF). Methods: The clinical data of 160 NDMM patients admitted to Henan Provincial People's Hospital from January 2012 to July 2022 were analyzed retrospectively. They were divided into MF group(n=74) and non-MF group(n=86) according to whether combined with MF. Patients in MF group were further splited into MF-1 group (n=47) and MF-2/3 group (n=27). All patients were treated with bortezomib and immunomodulatory-based combination therapy. The efficacy was evaluated after 4 courses, and the clinical features and prognosis between the two groups were compared. The deadline for follow-up was December 30, 2022 and the median follow-up period [M (Q1, Q3)] was 23.5 (14.4, 40.5) months. Kaplan-Meier method was used for survival analysis, and Cox regression model was used to analyze the influencing factors of survival. Results: Among 160 patients with NDMM, 91 were males and 69 were females, with a median age [M (Q1, Q3)] of 59 (54, 69) years. In MF group, the bone marrow immature plasma cell percentage, total plasma cell percentage were 9.6% (3.2%, 28.5%) and 36.4% (18.5%, 51.1%), respectively, which were higher than 6.0% (1.2%, 17.2%) and 24.0% (12.0%, 46.0%) of the non-MF group (both P<0.05). Hb level was 84.0(74.5, 100.5)g/L and PLT was (151.99±90.68) ×109/L in the MF group, which were lower than 96.0 (81.0, 112.0)g/L and (180.38±85.32) ×109/L of non-MF group (both P<0.05). But there were no significant differences in ISS stage, karyotypic and fluorescence in situ hybridization (FISH) high-risk genetic abnormalities between the two groups (all P>0.05). Objective response rate (ORR), overall survival (OS) and progression-free survival (PFS) were not significantly different between the two groups (all P>0.05). The rate of 17p- was 25.9% (7/27) in MF-2/3 group, which was higher than 8.1% (7/86) of non-MF group (P=0.049). The median OS of the MF-2/3 group was 25.0 (95%CI: 23.6-26.4) months, which was shorter than that of the non-MF group (54.0 months, P=0.031). Multivariate Cox regression analysis showed that grade MF-2/3 was not a risk factor for OS in NDMM patients (HR=1.507, 95%CI: 0.624-3.993, P=0.425). Conclusions: The ratio of bone marrow immature plasma cells and total plasma cells in NDMM patients with MF are higher than that in patients without MF, and the Hb and PLT are lower than that in patients without MF. NDMM patients with grade 2/3 MF have shorter survival than those without MF.

To investigate the clinical characteristics of metastatic tumors in small intestine. The clinical manifestations, imaging and endoscopic findings, treatment methods and follow-up of patients with small bowel metastatic tumors admitted to the First Affiliated Hospital of Zhengzhou University from January 1, 2018 to December 31, 2022 were retrospectively analyzed. A total of 10 patients were included, including 7 males and 3 females, aged 33-77 (56.4±12.6) years. The main clinical manifestations were intestinal obstruction (8 cases), such as abdominal pain, abdominal distension, nausea, vomiting, and reduced defecation. Some patients had intussusception (abdominal pain, vomiting, black stool and other symptoms, 1 case) or gastrointestinal bleeding (1 case) with early symptoms imperceptible. The primary tumors include gastric cancer (3 cases), malignant melanoma (2 cases), ovarian cancer (2 cases), colon cancer (1 case), rectal cancer (1 case), and lung cancer (1 case). Most of the primary tumors were poorly differentiated (6 cases) or moderately to poorly differentiated (2 cases). The median time from primary tumor surgery to detection of small bowel metastasis [M (Q1, Q3)] was 22 (18, 28) months.The metastatic lesions were single (6 cases) or multiple (4 cases), in both jejunum and ileum. Positron emission tomography-computed tomography (PET-CT, 3 cases) and endoscopy (2 cases) were helpful for detection of small intestinal metastases. The main treatment methods were surgical resection (9 cases), supplemented by radiotherapy, targeted drugs, immunotherapy, etc. Postoperative recurrence and metastasis occurred in some patients (5 cases). Most patients died within 4 to 29 months after diagnosis. Metastatic tumors in small intestine are rare in clinical practice with atypical early symptoms. The patients often present with complications such as intestinal obstruction, which is prone to delayed diagnosis and poor prognosis.

Variant acute promyelocytic leukemia with IRF2BP2-RARA fusion gene: a case report and literature review Wu Chengye, Yang Shiwei, Li Yulong, Dong Xiaoyan, Yu Runhong, Zhang Lin, Shang Baojun, Shi Pingling, Zhu Zunmin Institute of Hematology of Henan Provincial People's Hospital, Henan Key Laboratory of Hematopathology, Henan Provincial Engineering Research Center of CART Cell Treatment and Transformation, Henan Key Laboratory of Stem Cell Differentiation and Modification, Zhengzhou 450003, China; Henan Eye Institute, Henan Provincial People's Hospital, Zhengzhou 450003, China Corresponding author: Zhu Zunmin, Email: zhuzm1964@163.com

Objective: To explore the characteristics, clinical features and prognostic effects of NOTCH1/FBXW7 gene mutations in T-cell acute lymphoblastic leukemia (T-ALL) patients. Methods: The clinical data of 61 T-ALL patients who underwent second-generation gene sequencing in Henan Provincial People's Hospital from March 2016 to March 2021 were retrospectively analyzed. There were 46 males and 15 females, with a median age [M (Q1, Q3)] of 18 (11, 30) years. The relationship between NOTCH1/FBXW7 gene mutation characteristics, clinical and laboratory parameters and their impact on event free survival (EFS) and overall survival (OS) were analyzed. Results: NOTCH1 gene mutations were found in 34 cases (55.7%, 34/61), including 22 cases of heterodimer domain (HD) mutations (64.7%), 7 cases of proline/glutamate/serine/threonine (PEST) mutations (20.6%), and 5 cases of both HD and PEST mutations (14.7%). FBXW7 gene mutations were detected in 9 cases (14.8%, 9/61), of which 5 cases had both NOTCH1 and FBXW7 gene mutations. Twenty-three (37.7%, 23/61) cases were wild type. The median white blood cell count of patients in NOTCH1/FBXW7 gene mutations group and wild-type group was 76.4×109/L (8.3×109/L, 149.2×109/L), 54.1×109/L (5.3×109/L, 156.6×109/L), respectively. Moreover, the hemoglobin was (89.1±27.1) g/L and (99.5±23.1) g/L, respectively, and the median proportion of bone marrow primordial cells was 84.5% (69.0%, 91.3%) and 60.0%(35.0%, 80.0%), respectively. The gene expression rate of SIL-TAL1, Hox11 and Hox11L2 was 7.9% (3/38) vs 17.4% (4/23), 18.4% (7/38) vs 4.3% (1/23), 5.3% (2/38) vs 13.0% (3/23), respectively (all P>0.05). However, the median platelet level in the NOTCH1/FBXW7 gene mutations group was 60.5×109/L (36.8×109/L, 100.3×109/L), which was lower than that in the wild-type group [116.0×109/L (63.0×109/L, 178.0×109/L)] (P=0.018). The median number of gene mutations in the group with NOTCH1/FBXW7 gene mutations group was 2.5 (1.8, 4.0), which was more than that in the group without NOTCH1/FBXW7 gene mutations group [0 (0, 1.0)] (P<0.001). The median EFS and OS of adult NOTCH1/FBXW7 gene mutations group were 28.0 (95%CI: 7.3-48.7) months and 30.0 (95%CI: 8.9-51.1) months, respectively, which were better than those of adult wild-type group [4.5 (95%CI: 0-11.6) months and 9.0 (95%CI: 0-19.1) months] (P=0.008 and 0.014).The median EFS and OS of children NOTCH1/FBXW7 gene mutations group were 12.0 (95%CI: 10.4-13.6) months and 19.0 (95%CI: 13.6-24.4) months, respectively, and those of wild-type group were 10.0 (95%CI: 8.9-11.1) months and 21.0 (95%CI: 0-51.4) months, respectively (P=0.673 and 0.434). Conclusions: The mutation rate of NOTCH1/FBXW7 gene is higher in T-ALL patients. Patients with NOTCH1/FBXW7 gene mutations group have lower platelet count and better EFS and OS. NOTCH1/FBXW7 gene mutation may be used as a hierarchical basis for individualized treatment of adult T-ALL patients.

The significance of bone marrow immature plasma cell burden in the prognosis of newly diagnosed multiple myeloma patients Li Yulong, Shi Jie, Liu Fengzhen, Dong Xiaoyan, Wu Chengye, Cheng Wei, Huang Zhoufeng, Zhu Zunmin Hematological Institute of Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, People’s Hospital of Henan University, Zhengzhou 450003, China; Laboratory of Henan Provincial People’s Hospital, Zhengzhou 450003, China Corresponding author: Zhu Zunmin, Email: zhzm1964@163.com

Objective: To investigate the effects of additional chromosomal abnormalities (ACA) in Philadelphia chromosome-positive (Ph(+)) cells on biological characteristics, therapy efficacy, and prognosis of patients with primary chronic myeloid leukemia (CML) -chronic phase (CP) and those who developed CML-accelerated phase/blast phase (AP/BP) during therapy. Methods: The clinical data of 410 patients with Ph(+) CML, including 348 patients with primary CML-CP and 62 patients who progressed to CML-AP/BP during treatment, who were admitted to Henan People's Hospital from January 2013 to June 2020 were retrospectively analyzed to categorize into high-risk, non-high-risk, and non-ACA groups according to the ELN2020 criteria. The effects of high- and non-high-risk ACA on biological characteristics, therapy efficacy, and prognosis were compared. Results: ①Among the 348 patients with primary CML-CP, 20 patients (5.75% ) had ACA, including 3 and 17 patients with high-risk and non-high-risk ACA, respectively, whereas the remaining 328 patients did not have ACA. There were no significant differences in baseline clinical characteristics between those with and without ACA (P>0.05 for all) . The rates of complete hematological response, complete cytogenetic response, major molecular remission, and 5-year overall survival (OS) were not significantly different between the non-high-risk ACA and non-ACA groups (P>0.05 for all) ; however, the 5-year progression-free survival of the non-high-risk ACA group (42.0% ) was significantly lower than that of the non-ACA group (74.5% ) (χ(2)=4.766, P=0.029) .②Of the 62 patients who progressed to CML-AP/BP during treatment, 41 patients (66.13% ) had ACA, including 28 and 13 patients with high-risk and non-high-risk ACA, respectively, whereas the remaining 21 patients did not have ACA. Platelet counts of the high-risk ACA group (42.5×10(9)/L) were lower than those of the non-high-risk (141×10(9)/L) and non-ACA groups (109×10(9)/L) (χ(2)=4.968, P=0.083) . There was no significant difference in the incidence of point mutations in ABL kinase among the three groups (P=0.652) . The complete cytogenetic response of the high-risk ACA group (5.3% ) was significantly lower than that of the non-ACA group (46.7% ) (χ(2)=5.851, P=0.016) . The 5-year OS of the high-risk ACA group was lower than that of the non-ACA group (46.2% vs 77.8% , χ(2)=3.878, P=0.049) . Subgroup analysis revealed that the 5-year OS rate of the high-risk group Ⅱ, which included -7/7q-, i (17q) , and complex karyotype comprising ≥2 high-risk ACA, was significantly lower than that of the non-ACA group (28.6% vs 77.8% , χ(2)=8.035, P=0.005) whereas the 5-year OS rate was not significantly different between high-risk group Ⅰ, which included +8,+Ph, and complex ACA with +8/+Ph, and the non-ACA group (54.5% vs 77.8% , χ(2) =1.514, P=0.219) . Conclusion: Due to different disease stages and ACA/Ph(+) types, treatment response and prognosis vary among patients with CML harboring ACA/Ph(+). The emergence of high-risk ACA during therapy suggests worse therapy efficacy and prognosis. Strict and standardized cytogenetic monitoring is critical for early detection, precise diagnosis, and treatment of these patients.

[13] Cheson BD, Fisher RI, Barrington SF, et al. Recommendations for initial evaluation, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: the Lugano classification[J]. J Clin Oncol, 2014, 32(27): 30593068. DOI: 10.1200/JCO. 2013.54.8800. [14] Lok AS, Liang RH, Chiu EK, et al. Reactivation of hepatitis B virus replication in patients receiving cytotoxic therapy. Report of a prospective study[J]. Gastroenterology, 1991, 100(1):182188. DOI: 10.1016/0016-5085(91)90599-g. [15] Chen J, Wang J, Yang J, et al. Concurrent infection of hepatitis B virus negatively affects the clinical outcome and prognosis of patients with non-Hodgkin's lymphoma after chemotherapy[J]. PLoS One, 2013, 8(7): e69400. DOI: 10.1371/journal.pone. 0069400. [16] Deng L, Song Y, Young KH, et al. Hepatitis B virus-associated diffuse large Bcell lymphoma: unique clinical features, poor outcome, and hepatitis B surface antigendriven origin[J]. Oncotarget, 2015, 6(28): 2506125073. DOI: 10.18632/ oncotarget.4677. [17] Dong HJ, Ni LN, Sheng GF, et al. Risk of hepatitis B virus (HBV)reactivation in non-Hodgkin lymphoma patients receiving rituximabchemotherapy: a metaanalysis[J]. J Clin Virol, 2013, 57(3): 209-214. DOI: 10.1016/j.jcv.2013.03.010. [18] Koutsianas C, Thomas K, Vassilopoulos D. Prevention of HBV reactivation in patients treated with biologic agents[J]. Expert Rev Clin Pharmacol, 2016, 9(4): 579589. DOI: 10.1586/ 17512433.2016.1143773. [19]张令, 袁晓莉, 姜丽, 等. 非霍奇金淋巴瘤合并HBV感染患者 的临床特征及预后相关因素分析[J]. 中华血液学杂志, 2018, 39(7): 563568. DOI: 10.3760/cma.j.issn.02532727.2018. 07.007. [20] Su WP, Wen CC, Hsiung CA, et al. Longterm hepatic consequences of chemotherapyrelated HBV reactivation in lymphoma patients[J]. World J Gastroenterol, 2005, 11(34): 52835288. DOI: 10.3748/wjg.v11.i34.5283. (收稿日期:2021-01-26) (本文编辑:律琦)

Acute promyelocytic leukemia with PML cryptic breakpoint t (15; 17) (q22; q21) negative: a case report and literatures review Wu Chengye, Li Yulong, Dong Xiaoyan, Zhang Lin, Shang Baojun, Cheng Wei, Huang Zhoufeng, Zhu Zunmin Institute of Hematology, Henan Provincial People's Hospital; Henan Key Laboratory for Hematopathology; Henan Key Laboratory of Stem Cell Differentiation and Modification; Zhengzhou University People's Hospital, Henan University People's Hospital, Zhengzhou, Henan 450003, China Corresponding author: Zhu Zunmin, Email: zhuzm1964@163.com

Clinical and biological characteristics and prognosis of patients with biclonal multiple myeloma Cheng Wei, Li Yulong, Huang Zhoufeng, Li Zhaobo, Dong Xiaoyan, Shang Baojun, Zhang Lin, Shi Jie, Zhu Zunmin Department of Hematology, Zhengzhou University People's Hospital, Institute of Hematology, Henan Province People's Hospital, Henan Key Laboratory of Stem Cell Regulation and Differentiation, Zhengzhou 450003, China Corresponding author: Zhu Zunmin, Email:zhuzm1964@163.com

Objective:This study aims to investigate the characteristics of gene mutation and clinical prognosis in de novo acute myeloid leukemia (AML) patients with myelofibrosis (MF) .Methods:From January 1, 2016, to February 1, 2020, 103 newly diagnosed AML patients in Henan Provincial People’s Hospital who simultaneously underwent bone marrow biopsy examination were included. They were divided into the AML-MF group (MF grades 1-3) and the AML without MF group (MF grade 0) , and the clinical features, gene alterations, chemotherapy efficacy, and prognosis were compared between the two groups retrospectively.Results:①MF was confirmed in 44.7% of AML patients (46/103) , of which 84.8% (39/46) were MF-1 and 15.2% (7/46) were MF-2/3, while MF was not confirmed in 55.3% (57/103) of AML patients. The median of WBC in the AML-MF group was significantly higher than in the AML without MF group [11.205 (0.69-191.82) ×10 9/L vs 4.64 (0.18-95.10) ×10 9/L, P=0.024]. More patients in the AML-MF group had nucleated erythrocytes in the peripheral blood (43.5% vs 24.6% , χ2=4.119, P=0.042) . All four AML-M 0 patients were in the AML-MF group, while AML without MF group had a higher proportion of AML-M 2 ( P=0.014) . ②FLT3-ITD and NPM1 mutations were more frequent in the AML-MF group ( P=0.021 and 0.039) , while CEBPA mutation was more frequent in the AML without MF group ( P=0.029) . ③The CR rate in the AML-MF group was significantly lower than in the AML without MF group (69.7% vs 93.2% ) ( χ2 =7.412, P=0.006) . Multivariate analysis showed that MF, especially the grade of fibrosis, was an independent risk factor for CR in de novo AML. ④The 3-year OS of patients in the AML-MF group was significantly lower than in the AML without MF group (20.5% vs 72.2% , χ2=4.032, P=0.045) . Subgroup analysis showed that OS and PFS of AML-MF1 and AML-MF 2/3 groups were also significantly worse than those of the AML without MF group ( P=0.001) and MF, especially MF ≥2, was an independent marker for inferior OS and PFS in de novo AML ( P=0.021 and 0.044) . Conclusion:AML-MF has unique laboratory and clinical characteristics. MF is an independent risk factor for CR, OS, and PFS in AML. Evaluation of MF is very significant for therapy efficacy and prognosis judgment in de novo AML.

Objective: To reveal the related factors of inhibitors and differences ofhemorrhage and joint disease before and after the production of inhibitors in children with hemophilia A (HA) . Methods: Retrospective analyses of the clinical data of 381 children with HA under the age of 16 registered in the Registration Management Center of Hemophilia in Henan Provincial from January 2015 to August 2018. Results: A total of the 381 children were enrolled with 116 (30.4%) mild, 196 (51.4%) moderate, and 69 (18.1%) severe cases; 54 patients (14.2%) had inhibitors, including 22 high and 32 low titer inhibitors. Positive family history was positively associated with inhibitors[P<0.001, OR=3.299 (95%CI 1.743-5.983) ], and high-intensity exposure was associated with inhibitors[P=0.002, OR=2.587 (95%CI 1.414-4.731) ]. High-intensity exposure was associated with high titer inhibitor production[P=0.001, OR=8.689 (95%CI 2.464-30.638) ], and high-intensity exposure increased the risk of high titer inhibitors in HA patients. After inhibitors occurred in 54 patients with HA, the rates of overall joint annual bleeding (z=-3.440, P=0.001) and traumatic annual bleeding (z=-2.232, P=0.026) increased, but the rates of the annual joint bleeding (z=-1.342, P=0.180) and spontaneous annual bleeding (z=-1.414, P=0.157) remained to be not statistically significant. The joint ultrasound score did not change significantly after the inhibitor information (z=-0.632, P=0.527) . Conclusions: Positive family history and high-intensity exposure could increase the risk of F Ⅷ inhibitors in HA patients, and high-intensity exposure increased the risk of high titer inhibitors. The rates of the overall joint annual bleeding and traumatic annual bleeding increased after the inhibitor information.

OBJECTIVE:This study aimed to explore the possible role and mechanism of lncRNA ZEB2-AS1 in the pathogenesis of colon cancer (CCa).PATIENTS AND METHODS:The expression level of ZEB2-AS1 in 41 colon cancer tissue samples and 25 normal tissues was detected by qRT-PCR, and appropriate colon cancer cell lines were screened for in vitro experiments. Subcellular localization of ZEB2-AS1 was examined. After ZEB2-AS1 was transfected into colon cancer cells by liposome method, the cell proliferation, migration ability, and cell apoptosis percentage were evaluated by CCK-8 test, transwell assay, and flow cytometry, respectively. In addition, bioinformatics was applied to detect the target genes of microRNA-188. The Luciferase gene reporter assay was then performed to analyze the relative activity of Luciferase between microRNA-188 and TAB3 or ZEB2-AS1. At the same time, the control sequence, microRNA-188 mimics, microRNA-188 mimics+ ZEB2-AS1, si-TAB3, and microRNA-188 inhibitor+ si-TAB3 were respectively transfected into cells to further verify the interaction between TAB3 and microRNA-188 or ZEB2-AS1. Besides, the glucose and lactate levels were measured to explore their roles in glycolysis.RESULTS:The expression of ZEB2-AS1 in colon cancer tissues and cells was significantly higher than that in normal ones, and ZEB2-AS1 was confirmed to be mostly located in the cytoplasm. In addition, ZEB2-AS1 overexpression could enhance the cell proliferation rate and migration ability as well as reduce the cell apoptosis, which could be reversed by microRNA-188 overexpression. In addition, bioinformatics prediction and Dual-Luciferase reporter assays revealed that ZEB2-AS1 could bind to microRNA-188, which could directly target TAB3. At the same time, it was found that the overexpression of ZEB2-AS1 and low expression of microRNA-188 promoted glycolysis, while the opposite result was observed after overexpression of microRNA-188 and low expression of TAB3.CONCLUSIONS:The expression of ZEB2-AS1 is significantly increased in colon cancer tissues and cells, which can promote the proliferation, migration, and promote apoptosis of colon cancer cells. It may be involved in the development of this cancer through the process of glycolysis regulated by microRNA-188/TAB3.

患者,男性,46岁,入院前1个月受凉后出现发热.外院查血常规:WBC 44.05×109/L,RBC 3.68×1012/L,HGB 101 g/L, PLT 34×109/L,嗜碱性粒细胞1.84×109/L,外周血涂片发现原幼细胞占 0.12,为进一步诊治至我院就诊.入院查体,脾脏肋缘下8 cm,浅表淋巴结未触及.彩超显示颈部双侧、双侧腋窝及腹股沟区淋巴结肿大.外周血涂片:原幼细胞占0.07,嗜碱性粒细胞占 0.45,未见早、中、晚幼粒细胞.骨髓象:原幼细胞占0.116,嗜碱性粒细胞占0.440,以成熟阶段为主;粒细胞可见核浆发育失衡;可见单圆核双圆核巨核,血小板少见.

Objective: To analyze the percentage of myeloperoxidase (MPO)-positive acute myeloid leukemia (AML) blast cells, and to explore the correlation of MPO expression with the clinical features, gene alterations, therapeutic response and prognosis of AML. Methods: The expressions of MPO in BM blasts cells of 233 newly diagnosed AML were retrospectived analyzed, they were divided into two groups using the percentage of MPO-positive blast [low (≤70%) and high (>70%)], clinical features, gene alterations, chemotherapy efficacy and prognosis were compared between the two groups. Results: ①Of the 233 patients, 121(51.9%) were in the low MPO group, and the rest 112(48.1%) in the high MPO group. Favorable-risk group according NCCN guidelines of AML was always MPO-high (χ(2)=32.773, P<0.001), while MPO-low was closely related to poor-risk (χ(2)=7.078, P=0.008); ②DNMT3A mutation (χ(2)=6.905, P=0.009), spliceosome genes mutation (SF3B1/SRSF2/U2AF1) (χ(2)=5.246, P=0.022), RUNX1 mutation (χ(2)=4.577, P=0.032), ASXL1 mutation (χ(2)=7.951, P=0.005) and TP53 mutation (P=0.004) were more likely to be seen in the low MPO group, while C-KIT mutation (χ(2)=8.936, P=0.003) and CEBPA mutation (χ(2)=12.340, P<0.001) were more frequent in the high MPO group, especially CEBPA double mutation; ③The rates of first complete remission in the low MPO group were significantly lower than that in the high MPO group (38.8% vs 68.1%, χ(2)=15.197, P<0.001). Multivariate analysis showed that low MPO positivity significantly affected the CR(1) unfavourably. ④The overall survival (OS) and the progression-free survival (PFS) were significantly worse in the low MPO group (18.0% vs 89.4% for OS, and 11.5% vs 56.7% for PFS, P<0.001). Multivariate analysis disclosed that the low number of MPO was significantly unfavourable prognostic factor. ⑤The low MPO group still showed a worse survival even when restricted to the patients with normal karyotype, the OS and the PFS were 31.1% and 18.8% respectively. Conclusions: AML with different MPO expression percentage had a unique gene mutation spectrum. Low expression of MPO was an independent risk factor for CR(1), OS and PFS in AML patients, which may be a simple and highly significant factor for AML patients when evaluating the therapeutic efficacy and prognosis.

混合表型急性白血病(MPAL)是一种少见类型的白血病,表达一种以上系列特异性抗原.根据WHO 2016分类标准,MPAL 分为五种亚型:MPAL 伴 t(9;22)(q34;q11.2);MPAL 伴 MLL 重 排 ;MPAL,B/髓 系 ,非 特 指 型(NOS);MPAL,T/髓系,NOS;MPAL 罕见型,NOS.我们收集了 25例成人 MPAL 患者临床资料,对其细胞遗传学及基因学特征、治疗及预后进行了回顾性分析,报道如下.

Asthma is a respiratory disease that affects people of all walks of life, and is a hotspot of continuous research, with significant manpower and resources invested in its study. Airway remodeling is an important associated pathological change, and a mark of the irreversible damage produced by asthma. It involves compositional and functional changes in the cells of the airway walls, leading to reversible structural changes, and complicating treatment. Airway remodeling is mediated by different inflammatory pathways which have been targeted for treatment, with good results. However, given its complexity, systematic study of the pathogenesis of airway remodeling is still needed, and additional targeted therapies are necessary. Macrolide drugs, such as erythromycin, azithromycin, and clarithromycin, have antibacterial effects and also influence the cytokine secretion of macrophages and T-lymphocytes. They have direct effects on a variety of cytokines, inhibiting inflammation and reducing airway reactivity. In this study, we investigated the protective effect of azithromycin on airway remodeling through the phosphoinositol-3 kinase/Akt/mechanistic target of rapamycin kinase/hypoxia-inducible factor 1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway. We observed that a long course of azithromycin could significantly reduce airway reactivity and ovalbulmin-induced pathological alterations in asthmatic mice. Gene expression analysis confirmed that HIF-1α and VEGF were significantly down-regulated following a long course of azithromycin administration.

OBJECTIVEThis study aims to investigate the miR-26a effects on H2O2-induced apoptosis of Type II alveolar epithelial cells (AEC-II) and the potential mechanism.MATERIALS AND METHODSAEC-II cells were treated with 0.5 mmol/L H2O2 to mimic cellular model of acute lung injury. Transmitting electron microscopy (TEM) was employed to observe the change of morphological structures. After infecting with miR-26a mimics, flow cytometry was performed to detect cell apoptosis. Western blot was also done to explore mitochondrial apoptosis-related markers: Caspase-3, B-cell lymphoma-2 (Bcl-2) and Bax. AEC-II cells treated with 0.5 mmol/L H2O2 exhibited significant cell apoptosis. Overexpression using miR-26a mimics partially reversed the effects of H2O2-induced apoptosis in AEC-II cells, evidenced by flow cytometry results.RESULTSFurther Western blot results revealed increased levels of Caspase-3 and Bax, and the decreased Bcl-2 level after infecting with miR-26a mimics, indicating miR-26a has protective effects against mitochondrial apoptosis in AEC-II cells.CONCLUSIONSMiR-26a protected AEC-II cells against apoptosis via mitochondrial pathway. Thus, miR-26a promises to be a potential therapy in treatment of Acute Respiratory Distress Syndrome (ARDS).