Background: B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive hematological malignancy. Long non-coding RNAs (lncRNAs) play important roles in hematological diseases; nevertheless, their mechanistic contributions to B-ALL are still poorly defined.Purpose: This study aimed to investigate the oncogenic role of HOTAIR and the regulatory mechanism underlying the progression of B-ALL via the HOTAIR/miR-326/IGF-1R axis.Methods: The expression levels of HOTAIR and miR-326 were quantified by RT-qPCR in peripheral blood mononuclear cells (PBMCs) from B-ALL patients. CCK-8, EdU, and TUNEL assays were employed to evaluate cell viability, proliferation, and apoptosis, respectively. Dual-luciferase reporter assays were performed to verify molecular interactions, and Western blotting was performed to detect the activation of the PI3K/AKT signaling pathway.Results: HOTAIR was prominently upregulated in patient-derived PBMCs, correlating with enhanced proliferation and suppressed apoptosis. Mechanistically, HOTAIR directly targeted miR-326 binding sites and regulated the expression of IGF-1R. Experiments affirmed that overexpression of miR-326 or knockdown of IGF-1R reversed the oncogenic effects induced by HOTAIR. Furthermore, silencing of HOTAIR decreased PI3K/AKT phosphorylation, indicating pathway dependence.Conclusion: HOTAIR promotes the progression of B-ALL via the miR-326/IGF-1R axis and PI3K/AKT activation, suggesting its potential as a therapeutic target.

Background Imatinib (IM) is the primary treatment for patients with chronic-phase CML (CML-CP). However, an increasing number of CML-CP patients have developed resistance to IM. Our study aims to explore the expression of miR-629-5p in extracellular vesicles (EVs) from both IM-sensitive (K562) and resistant (K562-Re) CML cell lines and to investigate the impact of regulating miR-629-5p expression on the biological characteristics of K562 and K562-Re cells.Methods Assess miR-629-5p expression levels in IM-sensitive and resistant CML cell lines. Separate EVs and verify it. EVs from K562-Re cells were co-cultured with K562 cells to detect the expression level of miR-629-5p. Target genes of miR-629-5p were determined and validated through luciferase experiments. Examined by manipulating miR-629-5p expression in cells using transfection techniques. The expression level of phosphorylated proteins in the PI3K/AKT/mTOR signaling pathway after IM was detected in CML cell lines. In K562-Re cells, the expression level of phosphorylated protein in the PI3K/AKT/mTOR signaling pathway was detected after single transfection of miR-629-5p inhibitor and cotransfection of miR-629-5p inhibitor and siSENP2.Results Increasing concentrations of EVs from K562-Re cells elevated miR-629-5p expression levels. The expression levels of miR-629-5p in CML cells varied with IM concentration and influenced the biological characteristics of cells. SENP2 was identified as a target gene of miR-629-5p. Furthermore, miR-629-5p was found to modulate the SENP2/PI3K/AKT/mTOR pathway, impacting IM resistance in CML cells.Conclusion EVs from IM-resistant CML cells alter the expression of miR-629-5p in sensitive cells, activating the SENP2/PI3K/AKT/mTOR pathway and leading to IM resistance.

目的 探究miR-424 靶向张力蛋白同源第10 号染色体缺失的磷酸酶基因(PTEN)调控白细胞介素(IL)-6/信号转导与转录因子(STAT)3 信号通路影响骨髓瘤(MM)细胞增殖和凋亡的机制.方法 靶基因预测、双荧光素酶报告实验验证miR-424 对PTEN的靶向调控作用;采用实时荧光定量-聚合酶链反应(qRT-PCR)检测骨髓瘤患者骨髓标本及骨髓瘤细胞株中miR-424、PTEN的表达,并分析miR-424 表达与患者临床病理参数的关系;采用脂质体瞬时转染法将mimic NC、miR-424 mimic、anti-miR-424 mimic、si-control、si-PTEN转染H929、U266 细胞并分为对照组、miR-NC组、miR-424 组、anti-miR-424 组、an-ti-miR-424+si-NC组和anti-miR-424+si-PTEN组;噻唑蓝(MTT)法及单克隆染色检测细胞增殖情况,流式细胞仪检测细胞凋亡水平,Western印迹检测PTEN、IL-6、STAT3、B细胞淋巴瘤(Bcl)-2、Bcl-2相关X蛋白(Bax)、原癌基因(c-Myc)水平.结果 双荧光素酶实验及Western印迹验证了miR-424 对PTEN的靶向调控作用.MM患者骨髓标本及MM细胞株中miR-424 水平明显高于正常骨髓标本及浆细胞,PTEN水平明显低于正常骨髓标本及浆细胞,且miR-424 水平与PTEN水平呈负相关,与ISS分期、危险分层、轻链类型呈正相关关系.与miR-NC组相比,miR-424 组细胞增殖能力、IL-6、STAT3、Bcl-2、c-Myc水平明显升高,凋亡率、PTEN、Bax水平明显降低;anti-miR-424 组细胞增殖能力、IL-6、STAT3、Bcl-2、c-Myc水平明显降低,凋亡率、PTEN、Bax水平明显升高(P<0.05).与anti-miR-424+si-NC组相比,anti-miR+424-si-PTEN组细胞增殖能力、IL-6、STAT3、Bcl-2、c-Myc水平明显升高,凋亡能力、PTEN、Bax水平明显降低(P<0.05).结论 MM细胞的增殖、凋亡受miR-424 及PTEN的双重调控,miR-424 可靶向PTEN调控IL-6/STAT3 信号通路影响MM细胞的增殖和凋亡.

Objective: B lymphocyte miR-150-targeting c-Myb is involved in the occurrence and development of autoimmune haemolytic anaemia (AIHA). Methods: Our sample included 20 patients with AIHA haemolytic attacks treated in the Haematology Department of our hospital between January 2020 and January 2021, defined as the attack group, as well as 10 healthy controls. Peripheral blood mononuclear cells were extracted from the two groups. CD19(+)B lymphocytes in the peripheral blood of the two groups were sorted and purified using magnetic attraction. Total RNA was extracted using the TRIzol method. The number of CD5(+)B cells before transfection of peripheral blood CD19(+)B lymphocytes was detected using flow cytometry. The hsa-miR-150 high expression plasmid was transfected into cells using the Lipofectamine (TM) 2000 liposome transfection reagent. The expression of IL-10 on the cell surface was measured using an enzyme-linked immunosorbent assay. Real-time fluorescent PCR was used to detect the expression of miR-1 and 50c-Myb. A luciferase kit was used to detect relative luciferase activity and analyse the transcription activity of the target gene. Results: The expression of miR-150 in the attack group before transfection was significantly lower than in the control group (p< 0.05). There was no significant difference in the proportion of peripheral blood CD5(+)CD19(+)B cells in the attack group compared with before transfection (p> 0.05). There was a significant difference between the attack group and the control group (P< 0.05). The proportion of peripheral blood CD5(+)CD19(+)B cells in IL-10 cells in the attack group was significantly lower than before transfection (p< 0.05); There was a significant difference between the attack group and the control group (p< 0.05). After transfection, the expression level of miR-150 in peripheral blood CD19+B lymphocytes was significantly lower than in the control group (p< 0.05). The expression level of the c-Myb gene was significantly higher than in the control group (p< 0.05). The double luciferase experiment showed that the has-miR-150 high expression plasmid in B lymphocytes can significantly inhibit the luciferase activity of c-Myb (i. e. the transcriptional activity of c-Myb), proving that the c-Myb group in B lymphocytes is the target of miR-150. Conclusion: The up-regulated expression of miR-150 in B lymphocytes of AIHA patients can inhibit the expression of the c-Myb gene, which may be involved in the occurrence and development of the disease.

OBJECTIVE:To observe the curative efficacy of tyrosine kinase inhibitors (TKIs) in the treatment of e19a2 transcript (P230) CML chronic phase (CML-CP) patients.METHODS:The clinical data of 11 P230 CML-CP patients were collected from July 2008 to December 2019. Blood routine examination, bone marrow cytology, chromosome, and BCR-ABL qualitative and quantitative tests were performed at initial diagnosis. After TKIs treatment, BCR-ABL (P230)/ABL in peripheral blood was regularly detected to evaluate molecular response by real-time quantitative PCR.RESULTS:There were 11 patients (7 males and 4 females) in chronic phase from 6 domestic hospitals enrolled, their median age was 46 years old (range from 19 to 56 years old). Among 4 patients treated with imatinib (400 mg, qd) firstly, 3 cases switched to nilotinib (400 mg, bid) and 1 case switched to dasatinib (100 mg, qd) due to failure to achieve best molecular response at the landmark time or mutation of ABL kinase. Then major molecular response (MMR) was obtained within 1 year. In addition, 5 patients were treated with nilotinib (300 mg, bid) and 2 patients with dasatinib (100 mg, qd) as first-line treatment, all of them got MMR within 6 months.CONCLUSION:For intolerance or resistance to imatinib, second-generation TKIs can enable P230 CML patients to achieve deeper molecular response, and MMR in a short time.

Background It has been reported that lncRNA SNHG10 (SNHG10) promotes the progression of liver cancer and osteosarcoma; however, the role of SNHG10 in acute myeloid leukemia (AML) remains unknown. This study was to explore the role of SNHG10 in AML. Methods The expression of SNHG10 and miR-621 in BM mononuclear cells (BMMNCs) isolated from 60 AML patients and 60 healthy controls were determined by RT-qPCR. Correlation between SNHG10 and miR-621 was analyzed by Pearson correlation coefficient. The overexpression of SNHG10 and miR-621 in transfected AML cells was detected by RT-qPCR, and the regulatory relationship between them was explored. Methylation-specific PCR (MSP) was applied to detect the methylation of miR-621 induced by the overexpression of SNHG10. CCK-8 assay was conducted to evaluate cell proliferation. Results In this study, we found that the expression of SNHG10 was upregulated and the expression of miR-621 was downregulated in AML samples. Moreover, SNHG10 and miR-621 were inversely correlated across AML samples, and a high level of SNHG10 predicted poor survival of AML patients. Bioinformatics analysis showed that SNHG10 could be targeted by miR-621. In AML cells, miR-621 overexpression downregulated the expression of SNHG10, while SNHG10 overexpression could not affect the expression of miR-621. However, it was found that the reduction of miR-621 caused by SNHG10 overexpression might be due to the increase of miR-621 methylation. In addition, SNHG10 overexpression significantly promoted BMMNC proliferation, whereas miR-621 overexpression inhibited BMMNC proliferation and abolished the effect of SNHG10 overexpression on BMMNC proliferation. Conclusion miR-621 targets SNHG10 to suppress cell proliferation in AML.

目的 探讨氟马替尼二线治疗慢性髓系白血病慢性期(CML-CP)患者的疗效.方法 回顾性分析2例CML-CP患者临床资料,并复习相关文献.结果 1例患者伊马替尼400 mg/d治疗后出现全身皮疹,不耐受,并检测出集落刺激因子3受体(CSF3R)exon17(p.P733T)突变,转换氟马替尼治疗3个月后复查ISBCR-ABL1(P210)/ABL1达到主要分子学缓解(MMR);另1例患者伊马替尼治疗2年一直未达到MMR,转换氟马替尼治疗3个月后复查ISBCR-ABL1(P210)/ABL1达到MR4.结论 对于伊马替尼不耐受或效果不佳的CML-CP患者,氟马替尼具有良好的疗效.

OBJECTIVE:To explore the effect of regulating A20 expression on NF-κB and biological characteristics of Jurkat cells with glucocorticoid (GC) resistance.METHODS:CCRF CEM and Jurkat cells were treated with dexamethasone (DEX) at concentrations of 100、10、1、0.1、0.01 and 0.001 μmol/L, and cultured for 24、48 and 72 h. The proliferation inhibition rate of Jurkat cell was detected by CCK-8. A20 plasmid was constructed, A20-siRNA was designed and synthesized, and transfected into Jurkat cells by liposome. CCK-8 was used to detect the proliferation rates of Jurkat cells in different concentrations of DEX group, DEX combined with A20 plasmid group and A20-siRNA group. The mRNA expression level of NF-κB was detected by RT-qPCR, the protein expression level of NF-κB was detected by Western blot, and the apoptosis of Jurkat cells was examined by flow cytometry.RESULTS:The inhibitory effects of DEX at different concentrations on the growth of CCRF CEM cells were time-dependent (r=0.984, P＜0.05) and concentration-dependent (r=0.966, P＜0.05). At the point of 24 hour, the IC50 approached 1 μmol/L in CCRF CEM cells. Great large differences began to appear between 1 and 10 μmol/L, the proliferation rate of Jurkat cells treated with 1 μmol/L DEX did not show a significant change. Therefore, 1 μmol/L was selected as control group. The cell proliferation rate of A20 plasmid transfection combined with different concentrations of DEX group was lower than that of DEX group and A20-siRNA combined with DEX group. After transfection of A20 plasmid, the expression level of NF-κB was significantly lower than that of control group (P＜0.05), and the apoptotic rate was significantly higher than that of control group (P＜0.05). After transfection of Jurkat cells with A20-siRNA, the expression level of NF-κB was significantly higher than that of control group (P＜0.05). The apoptotic rate of cells in A20-siRNA group was not significantly changed (P＞0.05).CONCLUSION:Jurkat cells are resistant to DEX. A20 overexpression combined with DEX can increase sensitivity of Jurkat cells with GC resistance and decrease the proliferation rate of Jurkat cells, down-regulate the expression level of NF-κB and promote the apoptosis of Jurkat cells.

目的:探讨套细胞淋巴瘤(MCL)的临床特征、并发症及治疗措施.方法:回顾性分析伊布替尼联合利妥昔单抗(IR)方案治疗1例初发MCL的临床资料,并复习相关文献.结果:本病例于2018年2月经淋巴结病理活检及影像学检查等确诊为MCL,予IR方案治疗后达完全缓解后,伊布替尼维持治疗.11月出现发热,肝区低密度影逐渐增大,病理活检考虑肝结核可能性大,加用抗结核治疗后肝区病灶消失,病情稳定,目前仍在定期随访之中.结论:伊布替尼治疗初发MCL疗效显著,该类患者免疫力低下,易并发感染,本报道可为MCL临床诊疗提供一定的经验借鉴.

Alterations in messenger RNAs (mRNAs) of protein-coding genes can influence the malignant behaviors of acute lymphoblastic leukemia (ALL) cells. According to the prediction from The Cancer Genome Atlas (TCGA) database, we discovered that glutathione peroxidase 1 (GPX1) was up-regulated in acute myeloid leukemia (LAML) tissues, which pushed us to explore the feasible role and its related modulatory mechanism of GPX1 in ALL. In this research, we first proved the high expression of GPX1 in ALL cells compared with normal cells. Functional assays further revealed that the proliferation was obstructed and the apoptosis was facilitated in ALL cells with silenced GPX1. Then, both miR-491-5p and miR-214-3p that were down-regulated in ALL cells were affirmed to target GPX1. Subsequently, VPS9D1 antisense RNA 1 (VPS9D1-AS1) was recognized as the upstream regulator of miR-491-5p-miR-214-3p/GPX1 axis in a competing endogenous RNA (ceRNA) model. Importantly, we proved that VPS9D1-AS1 served as a tumor promoter in ALL through elevating GPX1. In conclusion, VPS9D1-AS1 contributed to ALL cell proliferation through miR-491-5p-miR-214-3p/GPX1 axis, hinting an optional choice for the treatment of ALL.

BACKGROUND Leukemia cells have strong proliferation and anti-apoptosis capabilities. The purpose of this study was to investigate the effect of silencing the leucine-rich alpha-2-glycoprotein1 (LRG1) gene, which was found to regulate tumor proliferation and apoptosis in acute myeloid leukemia (AML) cell lines. MATERIAL AND METHODS Plasmid interference technique was used to silence the LRG1 gene in the KASUMI-1 cell line. The cell counting kit-8 (CCK-8) assay was used to test the effect of transduction on cell viability. Cell cycle and apoptosis were detected by flow cytometry. Western blot and quantitative real-time polymerase chain reaction (RT-qPCR) were applied to detect the expression levels of proteins and mRNA, respectively. RESULTS KASUMI-1 cells with the CD34⁺CD38⁻ phenotype were sorted by flow cytometry. After transfection of the siLRG1 plasmid, the level of LRG1 expression was downregulated and cell viability was reduced. Silencing of LRG1 gene blocked KASUMI-1 cells in G0/G1 phase and promoted apoptosis. Further experiments found that LRG1 gene silencing significantly downregulated cell cycle-associated proteins and anti-apoptotic proteins, while upregulating pro-apoptotic proteins. Downregulation of LRG1 gene expression also inhibits signal transduction of the JAK-STAT pathway. CONCLUSIONS LRG1 gene silencing regulates the expression of cyclin and apoptosis-related proteins to reduce cell viability and promote apoptosis, probably through inhibition of the JAK-STAT pathway.

目的 探讨驱动突变对贵州地区BCR-ABL阴性骨髓增殖性肿瘤(myeloproliferative neoplasms,MPNs)患者临床特征的影响及血栓栓塞事件的危险因素.方法 回顾性分析贵州地区124例BCR-ABL阴性MPNs患者的临床资料;使用Lo-gistic回归分析血栓栓塞事件的危险因素.将患者的血清铁蛋白(serum ferritin,SF)与年龄、外周血细胞成分、乳酸脱氢酶(lactate dehydrogenase,LDH)进行相关性分析.结果 ①伴JAK2V617F突变的真性红细胞增多症(polyeythemia vera,PV)患者白细胞计数(white blood cell,WBC)与血小板计数(platelet,PLT)高于未突变者,其危险分层更高;伴JAK2V617F突变的原发性血小板增多症(essential thrombocythemia,ET)患者WBC、血红蛋白(hemoglobin,Hb)、红细胞比容(hematocrit,HCT)高于CALR突变者,且Hb、HCT、血栓栓塞事件发生率也高于3种基因均阴性者;CALR突变ET患者PLT明显高于JAK2V617F突变者及3种基因突变均阴性者.②单因素分析提示,ET患者年龄≥60岁、有心血管危险因素、伴JAK2V617F突变者更易发生血栓栓塞事件;多因素分析发现年龄≥60岁是导致血栓栓塞事件发生的独立危险因素.③MPNs患者的SF平均水平高于健康人群(原发性骨髓纤维化(primary myelofibrosis,PMF)患者表现尤为明显).④LDH升高的ET患者WBC、PLT显著高于LDH正常组,且危险度分层较高.结论 ①驱动突变对MPNs患者临床特征、预后评估的影响存在差异;②高龄是MPNs患者发生血栓栓塞的独立危险因素;③MPNs患者SF升高和ET患者LDH升高可能与疾病预后不良有关,尚待深入研究.

[目的]评估不同剂量双环醇预防非M3型急性髓系白血病(AML)患者大剂量阿糖胞苷化疗相关性肝损伤的临床疗效.[方法]收集初治非M3型AML患者150例,将患者随机分为BI75(双环醇75 mg口服,n=50)、BI150(双环醇150mg口服,n=50)及阿托莫兰组(2 g/d,n=50).分别于中剂量阿糖胞苷化疗前、化疗后7、14 d对肝功能指标进行监测,共监测3个疗程.[结果]阿托莫兰组在3个疗程中,其预防药物性肝损伤(DILI)发生的疗效均低于BI150及BI75组;此外,从第2疗程起,BI75的DILI发生率即明显高于BI150组,且随疗程次数的递增,这种差异性有逐渐增高的趋势.此外,大剂量阿糖胞苷相关性DILI患者年龄较大(约半数为50～59岁)、且多发生于接受2～3次大剂量阿糖胞苷者(83.86％).[结论]双环醇可有效预防大剂量阿糖胞苷所致的DILI,而150mg/d较75 mg/d疗效更为显著.

OBJECTIVE:To investigate the role of lncRNA ZEB1-AS1 in B-lineage acute lymphoblastic leukemia (B-ALL).RESULTS:ZEB1-AS1 levels were aberrantly up-regulated in B-ALL. All correlated with STAT3 activation and IL-11 production. Moreover, a high level of ZEB1-AS1 predicted poor prognosis of B-ALL patients. Mechanistically, ZEB1-AS1 could bind to IL-11 and promote IL-11 stability. Down-regulation of ZEB1-AS1 decreased IL-11 production of human bone marrow stromal cells (BMSCs), which led to suppressed proliferation and inhibited IL-11/STAT3 pathway in BALL-1 cells.CONCLUSIONS:ZEB1-AS1 promotes the activation of IL-11/STAT3 signaling pathway by associating with IL-11 in B-ALL.

Objective: To explore correlations between CD7, CD34, CD56 and HLA-DR expressions and its prognosis among patients with acute myeloid leukemia. Methods: 225 patients with Acute Myeloid Leukemia (AML) with initial treatment and complete data in our hospital from Jan 2013 to Dec 2016 were selected as study objects. 30 healthy volunteers who took part in the marrow test but were not detected for leukemia in the same period were selected as control patients. Fresh bone marrow of all patients was abstracted, from which single cell was separated. Flow cytometer detection was given after using monoclonal antibody of living cells immunofluorescent. CD7, CD34, CD56 and HLA-DR expressions of bone marrow among patients were detected. Fluorescent antibody staining positive cells were equal or greater than 20%, they were positive; equal or greater than 50%, they were high expression. Various immunophenotypes distribution in AML patients with different types was given statistics. Complete Remission (CR) rate of different immunophenotype positive and negative patients were given statistics. Mean survival of different immunophenotype positive and negative patients were given statistics. Results: There was no significant difference of leukemia patient and healthy volunteer in the aspects of age, sex, past medical history with relevant comparability (p>0.05). Antigen expression rate, from the high level to low were HLA-DR (58.22%), CD349 (50.67%), CD56 (30.67%), CD (723.11%). CR rate of patients in CD7, CD34, CD56 and HLA-DR positive groups were lower than negative group significantly, there were statistical differences between two groups (P<0.05). MST among patients in CD7, CD34, CD56 and HLA-DR positive group were lower than negative group significantly, there were statistical differences between two groups (P<0.01). Conclusion: Complete remission rate of CD7, CD34, CD56 and HLA-DR antigen expression positive among patients with Acute Myeloid Leukemia (AML) is low, mean survival is short and prognosis is poor.

Malignant tumor patients are often complicated with depressive disorder, which may affect tumor progression and threatens life quality or span. This study aimed to investigate the effect of depression on immune function and survival quality of acute leukemia patients. A total of 200 acute leukemia patients were recruited. Those had depression based on scale. Other non-depressive patients were recruited in the control group. Clinical information of patients was collected, and depressive condition was evaluated by Hamilton depression scale (24) and self-evaluative depression scale. General survey of health status (SF-36) was used to evaluate life quality. Count and ratio of regulatory T (Treg) cells and Th17 cells in peripheral blood were quantified by flow cytometry. ELISA was used to measure serum secretion level of IL-6, IL-17, IL-10 and TGF-beta 1. Correlation analysis was performed between two groups. Among 200 acute leukemia patients, 46 fitted diagnostic criteria of depressive disorder. 46 patients were randomly collected from non-depressive patients, and education level was significantly different between two groups (p<0.05). Compared to control group, depressive patients had significantly elevated peripheral Treg and Th17 levels, with decreased Treg/Th17 ratio (p<0.05). Depression was significantly correlated with Treg (r=0.533, p=0.013), Th17 (r=0.316, p=0.028) and Th17/Treg (r=0.397, p=0.010). Depression patents had higher serum IL-6, IL-17, IL-10 and TGF-beta 1 levels, and lower score in SF-36 scale (p<0.05). Depression significantly suppressed immune function of acute leukemia, and decreased life quality of patients.

AIM To study the clinical efficacy and adverse reactions of VcR-CAP protocol (bortezomib + rituximab + cyclophosphamide + doxorubicin + prednisone) in the treatmnent of previously untreated mantle cell lymphoma (MCL).METHODS One hundred and thirty-eight patients with previously untreated MCL were divided into low risk group,middle risk group and high risk group according to mantle cell lymphoma international prognostic index (MIPI) score.Patients were treated with VcR-CAP protocol and each treatment course was 21 days.The specific course were as follows:rituximab 375 mg·m-2 (day 1);cyclophosphamide 750 mg·m-2 (day 1);doxorubicin 50 mg·m-2 (day 1);prednisone 100 mg·m-2 (day 1 to 5);bortezomib 1.3 mg· m-2 (day 1,4,8,11).There were totally 6 courses of treatment.The clinical efficacy,clinical features and survival analysis were evaluated.Meanwhile the adverse reactions were observed.RESULTS The total effective rate of the low risk group,the middle risk group and the high risk group was 70％ (47/67),50％(21/42) and 34％ (10/29),respectively.The progression free survival and overall survival of the patients,age ≥ 60 years old,Ann Arbor stage Ⅲ-V,invasion and with increased lactate dehydrogenase,were shorter than the patients,age ＜ 60 years,Ann Arbor stage Ⅰ-Ⅱ stage,non invasion and with normal lactate dehydrogenase (P ＜ 0.05).There were significant differences in survival time among the low risk group,the middle risk group and the high risk group (P ＜ 0.05).The main adverse reactions of chemotherapy including anemia,thrombocytopenia,neutrophil depletion,nausea/vomiting,the extent of which was mainly 1-2 grade,and didn't affect the progress of treatment.CONCLUSION VcR-CAP protocol is safe and effective in the treatment of previously untreated MCL patients.

Regulatory T cells (Treg) are a subgroup of T cells with immunosuppressive function that play critical roles in antitumor immune response and immune escape. This study investigated Treg cells expression in Non-Hodgkin's Lymphoma (NHL) to discuss its relationship with clinical characteristics, curative effect, and prognosis. B lymphocyte NHL patients diagnosed in our hospital between Jan 2014 and May 2015 were selected. Flow cytometry was used to test CD4(+)CD25(+)Foxp3(+) T/CD4(+) T cell ratio in peripheral blood before and after chemotherapy to analyze its relationship with clinical features. The patients were divided into two groups upon the median of Treg cell percentage to compare the chemotherapy effect and survival rate. Peripheral CD4(+)CD25(+)Foxp3(+) T/CD4(+) T cell ratio in NHL patients (8.35 +/- 1.43%) was significantly higher than normal control (1.98 +/- 0.44%) before chemotherapy. It obviously declined after chemotherapy (4.56 +/- 1.11%) but was still higher than healthy control. Peripheral Treg cell ratio in NHL patients was significantly correlated with clinical stage (r = 0.745, P = 0.041) and IPI score (r = 0.798, P = 0.030). Treg cell proportion in patients with elevated lactic dehydrogenase (LDH) was markedly higher than the normal LDH group (t = 2.488, P = 0.007). The survival rate of high Treg group was apparently lower than the low Treg group (X-2 = 4.719, P = 0.029). Peripheral Treg ratio significantly increased NHL patients and was related to clinical stage and IPI. Treg elevation patients presented worse chemotherapy response, survival rate, and prognosis.

Objective To compare the effect of DA and IA regimen in the treatment of adult patients with acute my-elogenous leukemia. Methods From February 2013 to March 2015 in the People's Hospital of Guizhou Province 100 patients diagnosis for early treatment acute myelogenous leukemia were selected,they were randomly divided into 50 cases of study group and 50 cases of control group,the study group received to idarubicin plus cytarabine consolidation therapy,the control group re-ceived daunorubicin and cytarabine consolidation therapy. Neutrophil recovery time, the minimum value of white blood cell, effect,after treatment for 1 years disease-free survival rate between the two groups were compared. Results There were sig-nificant differences in the neutrophil recovery time and the lowest value of leukocyte between the study group and the control group ( P〈0. 05). The total effetive rate,after treatment for 1 years disease-free survival rate of the study group were higher than the control group( P〈0. 05). Conclusion The effect of IA regimen in the treatment of adult patients with acute myelogenous leukemia is better than the DA regimen,patients with bone marrow suppression during the induction period of light,have long lifetime.

目的探讨延长给药周期小剂量利妥昔单抗治疗成人温抗体型自身免疫性溶血性贫血的临床疗效。方法收集我科2012年7月~2014年7月4年间初诊温抗体型AIHA患者78例，根据治疗不同，将患者分为小剂量利妥昔组(n=34)及常规治疗组(n=44)。并比较两组缓解率及血细胞计数变化趋势。结果治疗后6月及12月，小剂量利妥昔组血红蛋白均明显高于常规治疗组(91.33±11.72 vs 69.00±17.58，=0.021；90.33±16.77 vs 71.67±12.90，=0.029)。治疗后12月，小剂量利妥昔组完全缓解率为76.47%(27/34),常规治疗组为38.63%(17/44),小剂量利妥昔组明显高于常规治疗组。结论100mg利妥昔d7,21给药方案可有效提高AIHA缓解率，临床值得推广。