Advances in research on extracapsular lymph node invasion and its prognostic significance in lung cancer / 中华胸心血管外科杂志

The status of lymph node metastasis is an important prognostic factor for many malignant tumors, including lung cancer. In the 8th edition of the TNM staging system for lung cancer, the T staging had obvious changes and refinements, but the N staging had little changes. Recently, several studies have found that the prognosis of patients with the same N stage can vary greatly, suggesting that a more detailed subgroup of patients with the same N stage should be subdivided, including the inclusion of extra-capsular lymph node metastases (ENE). In this review, we reviewed the definition, classification/grading, imaging diagnosis, pathological diagnosis, related molecular markers and their relationship with the prognosis of lung cancer patients.

TRIM56 Suppresses Multiple Myeloma Progression by Activating TLR3/TRIF Signaling

PURPOSE: Tripartite-motif-containing protein 56 (TRIM56) has been found to exhibit a broad antiviral activity, depending upon E3 ligase activity. Here, we attempted to evaluate the function of TRIM56 in multiple myeloma (MM) and its underlying molecular basis. MATERIALS AND METHODS: TRIM56 expression at the mRNA and protein level was measured by qRT PCR and western blot analysis. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry analysis was performed to investigate the effect of TRIM56 on MM cell proliferation and apoptosis. The concentrations of interferon (IFN)-β, interleukin (IL)-6, and tumor necrosis factor-α in MM cell culture supernatants were detected with respective commercial ELISA kits. Western blot was employed to determine the effect of TRIM56 on toll-like receptor 3 (TLR3)/toll-IL-1 receptor (TIR) domain-containing adaptor inducing IFN-β (TRIF) signaling pathway. RESULTS: TRIM56 expression was prominently decreased in MM cells. Poly (dA:dT)-induced TRIM56 overexpression in U266 cells suppressed proliferation, induced apoptosis, and enhanced inflammatory cytokine production, while TRIM56 knockdown improved growth, diminished apoptosis, and inhibited inflammatory cytokine secretion in RPMI8226 cells. Moreover, TRIM56 knockdown blocked TLR3 signaling pathway. Furthermore, poly (I:C), a TLR3 agonist, markedly abolished TRIM56 depletion-induced increase of proliferation, decrease of apoptosis, and reduction of inflammatory factor in MM cells. CONCLUSION: TRIM56 may act as a tumor suppressor in MM through activation of TLR3/TRIF signaling pathway, contributing to a better understanding of the molecular mechanism of TRIM56 involvement in MM pathogenesis and providing a promising therapy strategy for patients with MM.

Clinical observation of 21 cases of unrelated donor hematopoietic stem cell transplantation for leukemia / 西安交通大学学报(医学版)

non-myeloablative BuCy+fludarabine conditioning regimen,and another one was treated with TBI+VP-1 6 +CTX+CCNU conditioning regimen.Only one case received short-term MTX,cyclosporin A and ATG regimen for prevention of graft-versus-host disease (GVHD).The GVHD prevention regimens of the other patients were based on short-term MTX,cyclosporin A,ATG and mycophenolate mofetil regimen.The hematopoietic reconstitution, complications and prognosis were observed.Results One patient died of intracranial hemorrhage,and hematopoi-etic reconstitution was achieved in the other 20 patients.The median time for hematopoietic reconstitution shortened by one day in large-dose group compared with that in low-dose group.Adverse reactions included high fever, shivering,gastrointestinal tract adverse reaction,liver injury,oral mucositis and other rare side effects.GVHD occurred more frequently in patients with HLA mismatched transplantation.Nine patients with aGVHD and 9 patients with cGVHD recovered after effective treatment.Within 100 days after transplantation,18 patients had bacterial or fungal infection,mainly upper respiratory tract infection;7 patients had cytomegalovirus infection;2 had EB viremia,and one had urinary BK virus infection.Only one patient died of VOD.Hemorrhagic cystitis occurred in 5 patients and improved after treatment.The median survival time was 24 months (ranging from 136 days to 9 years).One-year and 3-year overall survival rates were 85.2% and 63.9%,the disease free survival rates were 81% and 23.8%,recurrence free survival rates were 71.4% and 14.3%,respectively.Conclusion URD-HSCT was an effective method to treat leukemia.Conditioning regimen of BuCy and modified BuCy2 were safe and effective,the adverse reactions were reversible and well tolerated.Hematopoietic reconstitution time shortened in large-dose MNC and CD34 + cell number groups compared with that in low-dose group.The occurrence rate of GVHD with HLA mismatched transplantation was more than that of HLA matched transplantation.Low-dose heparin,prostaglandin E1 and Danshen injection can effectively prevent VOD.

Increased expression of the 20S proteasome in peripheral blood mononuclear cells of type 2 diabetic patients / 药物分析学报

Objective To investigate the dynamic expression of the 20S proteasome in peripheral blood mononuclear cells (PBMCs) of type 2 diabetic patients without vascular complications. Methods PBMCs were prepared from 30 type 2 diabetic patients and 30 nondiabetic controls. The general indexes including weight, height and blood pressure were recorded. Fasting plasma glucose, fasting plasma insulin and glycosylated hemoglobin were measured. The protein level of the 20S proteasome was measured by Western blotting. The mRNA expression levels of the 20S proteasome β1, β2 and β5 subunits were detected by real-time PCR. Results Compared with that in the nondiabetic controls, the protein level of the 20S proteasome was significantly increased in the diabetic patients and was positively associated with glycosylated hemoglobin. Conclusion Type 2 diabetic patients without vascular complications have an increased 20S proteasome expression, the significance of which needs to be explored by further study.

TAD regimen with melphalan to treat 18 cases of multiple myeloma / 白血病·淋巴瘤

Objective To observe the clinical results of combination therapy for multiple myeloma by arsenic trioxide,melphalan,vitamin C and dexamethasone.Methods 18 cases with multiple myeloma,12 males and 6 females were given the treatment including arsenic trioxide,melphalan,vitamin C and dexamethasone combination therapy;the dosage of arsenic trioxide 10 mg,d1～5,d8～12;vitamin C 1.0 g,d1～5,d8～12;dexamethasone 20 mg,d1～4,d8～11;melphalan 2 mg,tid,d1～12.Complete response(CR),partial response(PR),minimal response(MR),no ehange(NC)were observed.Results The CR werel6.7%(3/18),PR were 77.7%(14/t8),MR were 5.6%(1/18).Conclusion Combinational arsenic trioxide,melphalan,vitamin C and dexamethasone is an effective therapy with less side effects,which can be considered for treating the initial or relapsed or refractory MM.

VEGF antisense oligodeoxynucleotides in enhancing the apoptosis-inducing effect of Cinobufotalin on K562 cells / 西安交通大学学报(医学版)

Objective To study the vascular endothelium growth factor(VEGF) antisense oligonucleotide(ASON) Cinobufotalin in enhancing apoptosis induced by human chronic myeloid leukemia K562 cell line.Methods The synthesis of VEGF ASON was transfected into the K562 cells;Cinobufotalin of four concentrations(1,3,5 and 7mg/L) acted on the K562 cell line for 24h,48h and 72h.Western blot was used to detect VEGF protein expression,while in situ apoptosis(TUNEL) and flow cytometry method(FCM method) were employed to detect the apoptosis.Results The different doses of Cinobufotalin all inhibited K562 cell line in time-and dose-dependent manners.K562 cell line transfected by VEGF ASON had a more pronounced induction of apoptosis.Conclusion The in vitro Cinobufotalin at a certain range of concentration can induce apoptosis in K562 cell line,and VEGF ASON enhances Cinobufotalin's effect in inducing apoptosis of K562 cells.

Gene expression profile changes in NB4 cells induced by realgar / 中华医学杂志(英文版)

<p><b>OBJECTIVES</b>To compare the gene expression profiles of acute promyelocytic leukemia cell line NB(4) before and after 12 hours of realgar treatment using cDNA microarray.</p><p><b>METHODS</b>Two cDNA probes were prepared through reverse transcription from mRNA of both untreated and realgar treated NB(4) cells. The probes were labeled with Cy3 and Cy5 fluorescence dyes individually, hybridized with cDNA microarray representing 1003 different human genes, and scanned for fluorescent intensity. The genes were screened through the analysis of the difference in two gene expression profiles.</p><p><b>RESULTS</b>The analysis of gene expression profiles indicates that 9 genes were up-regulated and 37 genes were down-regulated. Among the 9 up-regulated genes, 2 genes were involved in a proteasome degradation pathway. Some genes related to protein synthesis, signal transduction and cell receptors were down-regulated.</p><p><b>CONCLUSION</b>PSMC2 and PSMD1 genes may play an important role in the apoptosis and partial differentiation of NB(4) cells.</p>

The expression and clinical significance of multi-genes in breast cancer / 中国普通外科杂志

0.05). Expression of MDR1 had a positive ~correlation with mutant p53 accumulation and HER2 expression(P0.05 ).In univariate analyses,TNM staging, axillary lymph node metastasis, mutant p53 accumulation, and HER2 over-expression were negatively correlated with DFS and OS, and MDR1 over-expression significantly reduced OS but not DFS. In multivariate analysis, axillary lymph node metastasis, over-expression of MDR1 and HER2 were independent risk factors for prognosis. Conclusions ~Induction of multidrug resistance and poor response to chemotherapy and endocrinotherapy may be the chief reasons for poor prognosis of breast cancer with mutant p53 accumulation, and HER2 and MDR1 over-expression. ~Determination of the above genes′expression in breast cancer tissue can be of use in deciding the degree of ~malignancy , metastasis phenotype and prognosis of brest cancer. Increasing anthracycline dose may increase the ~overall response rate to chemotherapy and improve prognosis in patients with mutant p53 accumulation, HER2 and MDR1 over-expression, especially HER2 over-expression.