The PIWI family members are defined as conserved PAZ and PIWI domains and play important roles in stem-cell self-renewal,spermatogenesis,RNA interference and translational regulation.Recent researches have showen that some PIWI are specifically expressed in tumors and associated with tumor development and growth.PIWI is likely to be a new significante index for tumor diagnose and prognosis,the feasibility of PIWI acting in tumor gene theropy could be in vestigated by studying the mechanism of PIWI expression and regulation.

Endothelial progenitor cells(EPC),which have the capacity to differentiate into mature endothelial cells,have been found to home to and incorporate into the angiogenic vasculature of growing tumors with high specificity once mobilized into the circulation.Yet the mechanism still remains unclear.EPC have potential as spatial-specific delivery vehicles.Thus,further studies on the mechanisms of tumor neovascularization and tumor therapy in glioma using genetically engineered EPC as angiogenesis-selective vectors will be of help to explore the potential in the basic and clinical application of EPC in(glioma.)

Objective To evaluate the endoscopic findings and clinicopathologic characteristics of ischemic colitis and risk factors in older to avoid misdiagnosis. Methods 101 cases with ischemic colitis underwent endosopy within 14 days of onset of symptom in center of our hospital were retrospectively reviewed for their endosopic findings , clinicopathologic characteristics and risk factors. Results The common features of 101 cases included abdominal pain,diarrhea,or bloody diarrhea and hematochezia. Endoscopic visualization of mild ischemic colitis included pete-chial hemorrhages,edematous and fragile mucosa,segmental erythema,scattered erosion,longitudinal ulcerations,and sharply defined segment of involvement. Stricture ischemic colitis was characterised by full-thickness mucosa, lumens stricture and haustrations disappeared. Clinicpathological examination revealed mucosal inflammation accompanied by erosion,granulation tissue hyperplasis and gland atrophy,lamina propria hemorrhage,especially macrophages with he-mosiderin pigmentation in submucosa. Hypertension pressure, diabetes, atrial fibrilation were risk factors for ischemic colitis ( P < 0.05 ). Conclusion Although there was on specific changes on endoscopic findings and pathologic characteristics , but combined with history, was helpfu in diagnosis of ischemic colitis and reducing the misdiagnosis.

Objective To explore the hematology adverse reactions of imatinib mesylate (IM) in the treatment of chronic phase (CP) of chronic myeloid leukemia (CML).Methods The clinical data of 435 CML-CP patients treated with IM were analyzed respectively in the Affiliated Cancer Hospital of Zhengzhou University from Jan 2013 to Jan 2015.The hematology adverse reactions were followed up regularly and the incidences in different groups with various factors were compared.Results Until the end of follow-up,74 (17.0 ％) patients had hematology adverse reactions.61 (14.02 ％) patients had neutropenia,including 9 (14.75 ％) patients who had level Ⅲ-Ⅳ neutropenia.60 (13.79 ％) cases had thrombocytopenia including 11 (18.33 ％) patients with level Ⅲ-Ⅳ thrombocytopenia.Anemia occurred in 50 (11.49 ％) patients,of whom 5 (10.00 ％) cases were grade Ⅲ-Ⅳ anemia.33 (7.59 ％) cases experienced pancytopenia.The incidence of hematology adverse reactions was influenced by nine factors,including the course before treatment,the size of spleen,Sokal scores,the use of interferon,fusion genes,chromosomes,complete cytogenetic response,main molecular reaction and Karnofsky scores (all P ＜ 0.05),while it was not influenced by age,gender,BMI,smoking and drinking (all P ＞ 0.05).Conclusions During the initial treatment of CML-CP,if patients experienced level Ⅰ-Ⅱ hematology adverse reactions,they can continue to taking IM.However,when level Ⅲ-Ⅳ hematology adverse reactions happened,they need to reduce the dose or stop taking,and one month later,hemocyte will get well.In the long-term treatment of CML,once level Ⅲ-Ⅳ hematology adverse reactions occur,the patients need to receive some related inspections,such as bone marrow morphology and molecular biology detection,to clear the disease stage.When it is necessary,the patients can take the second generation of tyrosine kinase inhibitors.

Aclarubicin ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cytarabine ; therapeutic use ; Granulocyte Colony-Stimulating Factor ; therapeutic use ; Humans ; Interferons ; therapeutic use ; Interleukin-2 ; therapeutic use ; Leukemia, Myeloid, Acute ; drug therapy ; Recurrence ; Remission Induction ; Thalidomide ; therapeutic use

OBJECTIVETo investigate the characteristics and clinical outcome of T315I mutation in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) and chronic myeloid leukemia (CML).

METHODSThe clinical data of 118 tyrosine kinase inhibitors (TKIs) resistant Ph(+) ALL and CML cases who were detected ABL kinase domain mutation in Affiliated Tumor Hospital of Zhengzhou University from March 2014 to June 2015 were collected. Karyotypes and BCR-ABL fusion gene were analyzed respectively by R-banding, real-time quantitative polymerase chain reaction (PCR). Total RNA was extracted by TRIzol reagent and ABL kinase domain mutation was detected by direct sequencing.

RESULTSIn 23 TKIs resistant Ph(+) ALL and 95 CML cases, the rate of ABL kinase domain mutation was 60.9% (14/23) and 41.1% (39/95), respectively, and the rate of T315I mutation was respectively 34. 8% vs 5.3%, the difference was significant (χ(2)=13.586, P<0.01). The rate of mutations in chronic phase/accelerate phase /blast crisis CML patients was 38.8% (19/49), 47.1% (8/17) and 41.4% (12/29), respectively, and there was no significant difference (χ(2)=0.360, P=0.835). In Ph (+) ALL and CML patients, the median time from the beginning of TKI therapy to appearance of T315I mutation was 10 months and 19 months, the median time from the appearance of T315I to death/deadline was 2 months and 3 months, the median time of persistent hematologic response was 10 months and 16 months and the median time of overall survival (OS) was 13 months and 42 months.

CONCLUSIONT315I mutation was more easily occurred in Ph(+) ALL than CML, but two diseases are similar in the median time from the beginning of TKI therapy to appearance of T315I, the median time of persistent hematologic response and OS.

Acute Disease ; Blast Crisis ; Drug Resistance, Neoplasm ; Fusion Proteins, bcr-abl ; genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; genetics ; Mutation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; genetics ; Protein Kinase Inhibitors ; therapeutic use

Objective To evaluate the biological effect of a kind of protective cover against inhalation of depleted uranium (DU) dust particles. Methods At 1 and 3 d after inhalation of DU dust particles, uranium concentrations in the blood, lung, bronchia, kidney, and liver of the rats in the protected group and non protected group were measured and the efficiency of protection was calculated. Results Uranium levels in all tissues and fluids of the rats in the protected group decreased significantly to 71.2%-96.1% as compared with those in non protected group. Conclusion The protective cover is effective to reduce the harm due to inhalation of DU dust particles.

Objective:To evaluate risk factors and available treatments of extramedullary relapse (EMR) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with myeloid leukemia.Methods:A total of 280 patients were retrospectively analyzed from January 2008 to December 2018 in Affiliated Cancer Hospital of Zhengzhou University. Clinical data were collected including disease patterns, pre-transplantation status, chromosome karyotype, conditioning regimen, types of donor, extramedullary disease before transplantation and graft-versus-host disease (GVHD). The log-rank test and Cox proportional hazard model were uesd for univariate analysis and multivariate analysis, respectively.Results:Twenty patients developed EMR (7.14%). The median time of EMR was 7.5 (1-123) months after allo-HSCT. The mortality of EMR was 80% (16/20). Univariate analysis identified disease patterns, second complete remission (CR2) or progressive disease before transplantation, extramedullary disease, abnormal karyotype and conditioning regimen without total body radiation as significant factors correlated to EMR ( P<0.05). Multi-variable analysis revealed that CR2 or progressive disease ( RR=3.468,95% CI 2.189-7.786), abnormal karyotype ( RR=1.494,95% CI 1.020-2.189) and extramedullary disease before transplantation ( RR=8.627,95% CI 3.921-18.452) were independent risk factors of EMR. Conclusions:The clinical outcome of EMR after allo-HSCT is poor.It is crucial to comprehensively assess and identify EMR as early as possible.

OBJECTIVETo investigate the mechanism of U87 cell apoptosis induced by inhibiting miR-21 expression.

METHODSAntisense oligonucleotides of miR-21 were chemically synthesized and transfected into U87 cells. The apoptosis, proliferation, and invasion of the cells were evaluated. The relationship between miR-21 and PTEN or caspase was identified by bioinformatics and Western blot.

RESULTSInhibiting miR-21 expression led to U87 cell growth suppression, apoptosis induction, invasion reduction, caspase-3 activity elevation and caspase-9 activation, but did not affect PTEN and caspase-8 expression.

CONCLUSIONmiR-21 may function as an antiapoptotic miRNA in U87 cells. Inhibiting miR-21 expression could induce U87 cell apoptosis via caspase-9 and 3 activation, but not PTEN activation.

Animals ; Apoptosis ; drug effects ; genetics ; Caspases ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Enzyme Activation ; genetics ; Gene Expression Regulation, Neoplastic ; Glioma ; genetics ; pathology ; Humans ; MicroRNAs ; antagonists & inhibitors ; genetics ; Oligoribonucleotides, Antisense ; genetics ; pharmacology ; PTEN Phosphohydrolase ; metabolism ; Transfection

Objective: To investigate the influence of additional clonal chromosome abnormalities in Ph negative cells (CCA/Ph^-) on the efficacy of chronic myeloid leukemia (CML) after tyrosine kinase inhibitors (TKI) treatment. Methods: The clinical data of 28 CML patients with CCA/Ph^- treated in Henan Cancer Hospital from July 2014 to December 2017 were analyzed retrospectively. The univariate analysis was carried out by Kaplan-Meier method. Multivariate analysis was done by Cox proportional risk model. Results: A total of 28 CCA/Ph^-patients were recruited including 17 males and 11 females with median age of 42.5 years old. The most common CCA/Ph^-were trisomy 8 (60.7%), monosomy 7 (14.3%). 64.3% CCA/Ph^-were transient and 35.7% recurrent (more than 2 times). Cytopenia in two or three lineages of peripheral blood was seen in 42.9% patients. As to the efficacy, 89.3% patients achieved major cytogenetic response (MCyR), 25% with major molecular response (MMR). The median follow-up time was 26.5 months. Treatment failure (TF) of TKI occurred in 32.1% patients with median duration of response 8 (1-41) months. Univariate analysis showed that TF rate was significantly correlated with the frequency of CCA/Ph^-and cytopenia (all P<0.05). The MMR rate was also significantly correlated with cytopenia (P<0.05). Cytopenia of two lineages or pancytopenia was an independent risk factor related to MMR rate (RR=3.868, 95%CI 1.216-12.298, P=0.022) . Conclusions Cytopenia in CCA/Ph^-appears to be an independent risk factor of MMR in CML patients with TKI treatment. The recurrent CCA/Ph^-may link to higher treatment failure rate. Drug withdrawal or alternative strategy should be considered according to response and the ABL kinase mutations.