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1.
Journal of Experimental Hematology ; (6): 126-130, 2022.
Artigo em Chinês | WPRIM | ID: wpr-928680

RESUMO

OBJECTIVE@#To analyze the clinical characteristics and long-term prognosis of patients with primary bone lymphoma (PBL).@*METHODS@#The clinical data of 21 patients with PBL treated in our center from 2005 to 2018 were analyzed retrospectively, the clinical characteristics and the factors affecting prognosis of the patients were analyzed.@*RESULTS@#The median age of all the 21 newly diagnosed PBL patients was 40(12-71) years old. Ostealgia was the initial symptom in most of the patients (19/21,90.5%). 42.9%(9/21) of the patients showed single bone lesion only. 571% (12/21) of the patients showed diffuse large B cell lymphoma. 28.6% (6/21) of the patients showed anaplastic large cell lymphoma and 9.5% (2/21) of the patients showed T cell lymphoblastic lymphoma. All the patients received chemotherapy (CHOP or CHOP like regimen, 33.3% plus rituximab) with or without radiotherapy and/or autologous hematopoietic stem cell transplantation (ASCT). 18 patients achieved clinical remission (including 15 for CR and 3 for PR). The median follow-up time was 48 months. The 5-year overall survival rate and progression-free survival rate of the patients were was 67.5% and 63.7%, respectively. The single factors analysis showed that ASCT was the important prognostic factor of PFS, while the single or multiple bone lesion was the factors affecting OS of the patients. There were no statistical differences with the effects of age, sex, stage, ECOG score, LDH level, B symptoms and radiotherapy for the prognosis of patients.@*CONCLUSION@#Diffuse large B cell lymphoma is the most common pathological type of PBL. Chemotherapy is the main treatment, which can be combined with radiotherapy and/or ASCT. The ASCT and the number of bone lesion are the factors for long time survival of the patients.


Assuntos
Adulto , Idoso , Humanos , Pessoa de Meia-Idade , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Ciclofosfamida , Intervalo Livre de Doença , Doxorrubicina , Linfoma Difuso de Grandes Células B/tratamento farmacológico , Prednisona , Prognóstico , Estudos Retrospectivos , Rituximab/uso terapêutico , Transplante Autólogo , Vincristina
2.
Journal of Experimental Hematology ; (6): 1627-1632, 2019.
Artigo em Chinês | WPRIM | ID: wpr-775673

RESUMO

OBJECTIVE@#To study the regulatory effect of deubiquitinase MYSM1 on differentiation of B cells to plasma cells.@*METHODS@#The interfering and overexpression plasmids of MYSM1 were constructed and then the corresponding lentiviruses were packaged. Human CD19 B cells were isolated from human peripheral blood with Miltenyi B cell isolation kit. Purified CD19 B cells were transduced with lentiviruses and then treated with LPS, the CD138 expression was detected by flow cytometry. The expression of transcription factor was determined by quantitative PCR.@*RESULTS@#The differentiation of B cells to plasma cells was enhanced after interfering in MYSM1 expression. Quantitative PCR showed that mRNA levels of Pax5 and Bach2 in cells with interfering in MYSM1 were much lower than their counterpart (P<0.01), and mRNA levels of Prdm1 and Xbp1 in cells with interfering in MYSM1 were much higher than their counterpart (P<0.01). On the contrary, the differentiation of B cells to plasma cells was inhibited after the overexpression of MYSM1. Quantitative PCR showed that mRNA levels of Pax5 and Bach2 in cells with MYSM1 overexpression were higher than those in control cells (P<0.01), and mRNA levels of Prdm1 and Xbp1 in cells with MYSM1 overexpression were much lower than those in their counterpart (P<0.01).@*CONCLUSION@#MYSM1 negatively regulates differentiation of human B cells to plasma cells.


Assuntos
Humanos , Linfócitos B , Diferenciação Celular , Proteínas de Ligação a DNA , Genética , Enzimas Desubiquitinantes , Plasmócitos , Fatores de Transcrição , Genética
3.
Chinese Journal of Oncology ; (12): 143-147, 2010.
Artigo em Chinês | WPRIM | ID: wpr-260450

RESUMO

<p><b>OBJECTIVE</b>Erlotinib is a small-molecule inhibitor of EGFR tyrosine kinase, showing a significant improvement of survival in non-small-cell lung cancer (NSCLC) after the failure of front-line chemotherapy. The aim of this study was to evaluate the antitumor efficacy and toxicity of Erlotinib in the treatment of advanced NSCLC patients.</p><p><b>METHODS</b>A total of 104 patients with advanced NSCLC admitted in our department during December 2006 to November 2008 were enrolled in this study. Eligible patients received oral Erlotinib 150 mg/d until disease progression or intolerable toxicity. Best clinical response was determined using RECIST criteria, the adverse events were evaluated according to the NCI criteria.</p><p><b>RESULTS</b>The total effective rate was 27.9% (29/104) and the clinical benefit was 76.0% (79/104). The median progression-free survival was 5.1 months (95%CI 4.0 - 8.0). The median survival time was 13.1 months (95%CI 10.0 - 15.7). The 1-year survival rate was 61.5%. Significant survival benefit from erlobinib therapy was observed for patients with good personal status (HR 0.56, P = 0.006), adenocarcinoma (HR 0.43, P = 0.004) and skin rash (HR 0.46, P = 0.005). But patients with smoking (HR 2.75, P < 0.001) and liver metastasis (HR 2.91, P = 0.002) add the risk of death. The adverse events were mild (grade < or = 2), most common toxicities were skin rash in 73.1% (76/104) and diarrhea in 41.3% (43/104). Only 6.7% (7/104) patients got adverse events of grade > or = 3.</p><p><b>CONCLUSION</b>Erlotinib is an effective and well-tolerated treatment option for advanced NSCLC and could offer an alternative for patients after the failure of first-line chemotherapy, unsuitable for or not wishing to receive chemotherapy.</p>


Assuntos
Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adenocarcinoma , Tratamento Farmacológico , Patologia , Neoplasias Encefálicas , Tratamento Farmacológico , Carcinoma Pulmonar de Células não Pequenas , Tratamento Farmacológico , Patologia , Diarreia , Intervalo Livre de Doença , Cloridrato de Erlotinib , Exantema , Seguimentos , Neoplasias Hepáticas , Tratamento Farmacológico , Neoplasias Pulmonares , Tratamento Farmacológico , Patologia , Estadiamento de Neoplasias , Modelos de Riscos Proporcionais , Inibidores de Proteínas Quinases , Usos Terapêuticos , Quinazolinas , Usos Terapêuticos , Receptores ErbB , Usos Terapêuticos , Indução de Remissão , Fumar , Taxa de Sobrevida
4.
Chinese Journal of Oncology ; (12): 17-21, 2010.
Artigo em Chinês | WPRIM | ID: wpr-295192

RESUMO

<p><b>OBJECTIVE</b>To assay the expression of cytidine deaminase (CDA), ribonucleotide reductase subunit 1 (RRM1), phosphatase and tensin homologue deleted from chromosome 10 (PTEN), excision repair cross-complementation group 1 (ERCC1), deoxycytidine kinase (dCK) and RRM1(-)37A/C polymorphism, which have been shown relevant to gemcitabine resistance in two human gemcitabine-resistant non-small cell lung cancer cell lines A549/Gem and NCI-H460/Gem, so as to make clear how do they vary during the course of acquiring resistance to gemcitabine.</p><p><b>METHODS</b>The human gemcitabine-resistant non-small cell lung cancer cell lines A549/Gem and NCI-H460/Gem were established in our Department by repeated clinical serum peak concentration and gradually increasing doses. Real-time fluorescent quantitative PCR was used to examine the expression of CDA, RRM1, PTEN, ERCC1, dCK and RRM1(-)37A/C polymorphism in those cell lines at different time points during their induction process.</p><p><b>RESULTS</b>The resistance indexes of A549/Gem and NCI-H460/Gem cells reached 163.228 and 181.684, and then remained stable at 115.297 and 129.783, respectively. The expression of CDA, RRM1, PTEN and ERCC1 varied along with the changing gemcitabine resistance indexes, but expression of dCK did not change apparently. The wild type promoter was able to amplify the genomic DNA in different induction stages of A549/Gem and NCI-H460/Gem cells, but allelotype did not, indicating that the gene type of A549/Gem, NCI-H460/Gem and their parental cells remaining still wild type.</p><p><b>CONCLUSION</b>Compared with their parental cells, the expressions of CDA, RRM1, PTEN and ERCC1 in human gemcitabine-resistant non-small cell lung cancer cell lines A549/Gem and NCI-H460/Gem rise, the expression of dCK changes inapparently, therefore, their gene type are remaining wild type.</p>


Assuntos
Humanos , Antimetabólitos Antineoplásicos , Farmacologia , Carcinoma de Células Grandes , Genética , Metabolismo , Patologia , Carcinoma Pulmonar de Células não Pequenas , Genética , Metabolismo , Patologia , Linhagem Celular Tumoral , Citidina Desaminase , Genética , Metabolismo , Proteínas de Ligação a DNA , Genética , Metabolismo , Desoxicitidina , Farmacologia , Desoxicitidina Quinase , Genética , Metabolismo , Resistencia a Medicamentos Antineoplásicos , Endonucleases , Genética , Metabolismo , Neoplasias Pulmonares , Genética , Metabolismo , Patologia , PTEN Fosfo-Hidrolase , Genética , Metabolismo , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas , RNA Mensageiro , Metabolismo , Proteínas Supressoras de Tumor , Genética , Metabolismo
5.
Chinese Journal of Integrated Traditional and Western Medicine ; (12): 89-93, 2005.
Artigo em Chinês | WPRIM | ID: wpr-284506

RESUMO

Progress of studies concerning the protective effect of ginsenoside on central nerve system (CNS) in animals and its mechanism published in recent decade were reviewed in this paper. It showed that ginsenosides could improve the learning capacity and memory in normal, aged animals, as well as in model animals with impaired memory. The mechanism of the protective effect on CNS involves the effects on calcium channel blockade, glutamate and gamma-aminobutyric acid, antiperoxidation, estrogen-like action, nitric oxide and its synthase, also the inhibition on cerebral nerve cell apoptosis and amelioration on mitochondrial dysfunction, etc.


Assuntos
Animais , Envelhecimento , Aprendizagem da Esquiva , Ginsenosídeos , Farmacologia , Memória , Transtornos da Memória , Tratamento Farmacológico , Fármacos Neuroprotetores , Farmacologia , Usos Terapêuticos , Óxido Nítrico Sintase , Metabolismo
6.
China Journal of Chinese Materia Medica ; (24): 132-135, 2002.
Artigo em Chinês | WPRIM | ID: wpr-274995

RESUMO

<p><b>OBJECTIVE</b>To set the measuring method of tyrosine hydroxylase activity in the brain of conscious rats.</p><p><b>METHOD</b>By using microdialysis and High Performance Liquid Chromatography-Electrochemical Detector system, the 3, 4-dihydrioxphenylalanine (DOPA) formation in the striatum of 6-hydroxdopamine-pretreated rats during infusion of an L-aromatic amino-acid decarboxylase inhibitor (NSD1015) was monitored.</p><p><b>RESULT</b>The absence of DOPA in dialysates of 6-hydroxdopamine-pretreated rats, the measurable DOPA and the steady decreasing of 3,4-dihydroxyphenylacetic acid(DOPAC) during infusion of NSD1015 and the disappearance of DOPA after administration of alpha-methyl-rho-tyrosine indicated that the dialyzed DOPA was derived from dopaminergic nerve terminals. After intraperitoneal administration of dopamine receptor agonist apomorphine the DOPA output was deseased. After intraperitoneal administration of dopamine recepter antagonist haloperidol, the DOPA output was increased. The study showed that twenty-four hours ofter implantation of the probe with infusion of 0.01 mmol.L-1 NSD1015, the DOPA level in the striatum of 6-hydroxdopamine-pretreated rats was 0.39 +/- 0.12 pmol/min (X +/- S, n = 5).</p><p><b>CONCLUSION</b>The DOPA concentration in striatal dialysates could be considered as an index of tyrosion hydroxlase activity during infusion of 0.01 mM NSD1015. The method in vivo to monitor tyrosine hydroxlase activity in the brain is reliable.</p>


Assuntos
Animais , Feminino , Masculino , Ratos , Apomorfina , Farmacologia , Encéfalo , Di-Hidroxifenilalanina , Metabolismo , Agonistas de Dopamina , Farmacologia , Antagonistas de Dopamina , Farmacologia , Haloperidol , Farmacologia , Microdiálise , Ratos Sprague-Dawley , Tirosina 3-Mono-Oxigenase , Metabolismo
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