Comparative study between the free radicals and tumor markers in patients with gastrointestinal tumors

The tumorous processes, increased level of tumor markers and the change of free radical status are associated in patents with gastrointestinal tumors. The aim of this study was to examine free radical status and tumor markers in patients with gastrointestinal tumors. Two hundered and thirteen patients with gastrointestinal tumor were examined. In the control group 44 non-tumorous patients were examined. The tumor markers (CEA, CA 19-9, CA 72-4, AFP, TPA, AGP) and free radical status (total scavenger capacity) were diagnosed using venal blood (obtained by LIA-kits and chemiluminescent methods, LIA-mAT and the Lumat Berthold instrument). It has been found that: (1) The results showed that the tumor markers, TPA and AGP are the best indicators for the tumorous process; (2) The AGP serum level was in the operable case 91.56+/-38.29 mg/dl meanwhile its value was, 128.46+/-47.62 mg/dl (P<0.001) in the inoperable case; and (3) The TPA value was 118.37+/-155.47 mg/dl in the operable case, (P<0.001) while its value was 227.32+/-244.39 mg/dl in inoperable cases. The significantly high levels of the plasma Chemiluminescent Light Intensity (CLI)=28.12+/-25.96; was obtained in patients with rectal tumors vs. in the control cases CLI= 4.27+/-5.12 RLU% (Relative Light Unit; mean+S.D.; P<0.005). In six of these cases, the free radical status examination indicated the presence of the tumor, even though the level of tumor markers was normal. It has been concluded that the testing of both regular tumor markers and free radical status has an important role in the diagnosis and monitoring of the patients with gastrointestinal tumors.     

Structural Basis for Auto-Inhibition of the NDR1 Kinase Domain by an Atypically Long Activation Segment

1. Download high-res image (197KB)
2. Download full-size image

     

P53，Rb和c－myc基因在人脑原发性肿瘤中的转录表达

采用RNA斑点杂交分析,对21例人脑原发性胶质瘤和11例人脑膜瘤中p53,Rb和c-myc基因转录水平的表达进行研究.发现48.4%的肿瘤中p53基因表达减弱,21.9%的肿瘤中Rb基因表达减弱;71.9%的肿瘤中c-myc基因表达增强.在p53基因表达减弱的15例病例中有13例(80%)c-myc基因表达增强.结果表明,p53基因表达减弱和c-myc基因表达增强与人脑原发性肿瘤的发生有关.     

Association study between of Tie2/Angiopoietin-2 and VEGF/KDR pathway gene polymorphisms and vascular malformations

Vascular malformations (VMs) are common congenital and neonatal dysmorphogenesis. VMs mostly occur sporadically with a few exceptions of inheritability. Tie2/angiopoietins-2 (Ang-2) and VEGF/KDR pathways are known to be involved in normal and pathogenic angiogenesis. Our study was aimed to test the contribution of these pathway gene variants to VMs. A total of 8 variants were found among 103 VM patients and 142 healthy controls. These variants comprised rs638203, rs639225, rs80338908 and rs80338909 in Tie2 gene, rs1870377 and rs2305949 in KDR gene, rs79337921 and rs34590960 in ANTXR1 gene. Our results indicated that rs638203 (p = 0.029) and rs639225 (p = 0.018) in Tie2 gene were associated with VM. A further bioinformatics analysis suggested the rs638203-G and rs639225-G might cause an abnormal splicing of Tie2 gene into to a defective protein. Our results identified two novel Tie2 gene polymorphisms with genetic susceptibility to VMs, although future functional validation of the two polymorphisms is warranted in the future.     

原肌球蛋白相关激酶B在肿瘤中的研究进展

原肌球蛋白相关激酶B(tropomyosin-related kinase B,TrkB)是一种神经营养性酪氨酸受体激酶,通过介导丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)、磷脂酶C-γ(phospholipase C-γ,PLC-γ)、磷脂酰肌醇3-激酶(pho...     

Giant locally advanced and metastatic squamous cell skin carcinoma of head and neck region: case report

IntroductionAt the present time, the skin tumors are among the most common cancers. Optimal therapy is based on the extent of the disease and the age of the patient. The need for radiotherapy occurs for inoperable locally advanced tumors and in the event of failure, salvage surgery is applied.Materials and methodsWe provided a case report of an older patient with giant squamous cell skin carcinoma and a review of published articles.ResultsWe present a rare case of giant squamous cell skin carcinoma with metastatic satellite tumors that was primarily treated with curative radiotherapy. Five months after radiotherapy, a recurrent tumor was detected at the site of origin and the treatment was completed by salvage surgery. Full remission was achieved for four years.ConclusionDespite the seemingly incurable finding it is always necessary to consider radical treatment regardless of the patient´s age. Curative treatment could achieve long term remission in the group of older patients.     

Mechanisms of metastasis: epithelial-to-mesenchymal transition and contribution of tumor microenvironment

Every year about 500,000 people in the United States die as a result of cancer. Among them, 90% exhibit systemic disease with metastasis. Considering this high rate of incidence and mortality, it is critical to understand the mechanisms behind metastasis and identify new targets for therapy. In recent years, two broad mechanisms for metastasis have received significant attention: epithelial-to-mesenchymal transition (EMT) and tumor microenvironment interactions. EMT is believed to be a major mechanism by which cancer cells become migratory and invasive. Various cancer cells--both in vivo and in vitro--demonstrate features of epithelial-to-mesenchymal-like transition. In addition, many steps of metastasis are influenced by host contributions from the tumor microenvironment, which help determine the course and severity of metastasis. Here we evaluate the diverse mechanisms of EMT and tumor microenvironment interactions in the progression of cancer, and construct a rational argument for targeting these pathways to control metastasis.     

Requirement of c-Jun NH2-terminal kinase activation in interferon-alpha-induced apoptosis through upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in Daudi B lymphoma cells

Interferon alpha (IFN-alpha) inhibits growth, at least in part, through induction of apoptosis. However, the molecular mechanisms underlying IFN-alpha-induced apoptosis are not completely understood. In the present study, we found that IFN-alpha induced a sustained activation of c-Jun N-terminal kinase 1 (JNK1), but not extracellular kinases (ERKs), in Daudi B lymphoma cells, as assessed by Western blotting using phospho-specific antibodies. Several lines of evidence support the notion that the IFN-alpha-induced activation of JNK is responsible for IFN-alpha-induced apoptosis, at least in part, through upregulation of TNF-related apoptosis-inducing ligand (TRAIL). First, pretreatment of Daudi cells with a JNK inhibitor reduced IFN-alpha-induced upregulation of TRAIL and loss of mitochondrial membrane potential (DeltaPsim) and annexin-positive cells, which was assessed by flow cytometry. Second, a dominant-negative form of JNK1 (dnJNK1) also reduced these apoptotic events, while a constitutively active form of JNK1, MKK7-JNK1beta, enhanced them. Finally, treatment with IFN-alpha enhanced the promoter activity of the TRAIL gene, which was partially abrogated by either JNK inhibitor or dnJNK1, while it was moderately enhanced by MKK7-JNK1beta. These findings are useful for understanding molecular mechanisms of IFN-alpha-induced apoptosis and also for development of treatment modalities of some tumors with IFN-alpha.     

乳腺癌易感蛋白2的结构和功能

乳腺癌易感蛋白2是由乳腺癌易感基因2编码的一种在维持哺乳动物细胞染色体的稳定及DNA损伤生物应答中发挥重要作用的蛋白质。文章通过介绍近几年来对乳腺癌易感蛋白2的结构研究,阐述其在双链DNA损伤修复中的作用模型及其在肿瘤抑制中的功能。