A clone system designated SAC was established from a SRS-82 mouse ascitic turnout cell line by using limited dilution method. Clones SAC-ⅡB_2, SAC-ⅡB_3 of this system were found to be different in their morphology, growth pattern, karyotypes and tumorigenicity from their parent cell line. Both the two clones and their parent cell line were X-C assay positive, and type A and type C virus particles were found in the cytoplasm and cell surface of these cells electronmicroscopically. Cell surface markers(ALS, Thy, SmIg G) of these two clones and their parent cell line were investigated by ABC immunohistochemical method and immunofluorescent staining technique, the results of which indicate that all of them belong to T cell origin.

Objective To investigate the effects of combined treatment of suberoylanilide hydroxamic acid(SAHA)and TNF?related apoptosis inducing ligand(TRAIL)on proliferation and morphology change of triple?negative breast cancer cell MDA?MB?231. Methods The effects of combination treatment of SAHA and TRAIL on proliferation and morphology change of MDA?MB?231 cells were monitored by RTCA. Morphology changes of MDA?MB?231 cells by different treatment factors were observed through time?lapse live cell imaging acquisition. Results Real?time cell proliferation assays showed that a synergistic effect were found when MDA?MB?231 cells were treated with combination of SAHA and TRAIL , and reached the best effect with 5μmol/L SAHA and 50 ng/mL TRAIL. The results of time?lapse live cell imaging acquisition showed that the growth inhibition of MDA?MB?231 cells with combined treatment of SAHA and TRAIL were more obvious than that with treatment of SAHA or TRAIL alone. Conclusion The combined treatment of SAHA and TRAIL induces a synergistic effect on growth inhibition in triple?negative breast cancer cell line MDA?MB?231.

Histone deacetylases (HDACs) catalyze the deacetylation of histone and nonhistone proteins. They play important roles in regulating chromatin remodeling and gene transcription,and that aberrant chromatin remodeling and transcriptional dysregulation are associated with many neurodegenerative diseases. Preclinical studies have suggested that histone deacetylases inhibitors (HDACIs) can target diverse pathophysiologies of ischemic stroke,not only reduce neuronal damage and infarct volume,but also promote the neuronal plasticity and functional recovery after ischemia. This article mainly reviews the neuroprotective mechanisms of HDACIs in ischemic stroke.

Belief in and rejection of a relationship of occlusion and temporomandibular joint (TMJ)condyle-fossa position with normal and abnormal function are still contentious issues.Clinical opinions can be strong,but support in most published data (mostly univariate)is problematic.Distribution overlap,low sensitivity and specificity are a common basis to reject any useful prediction value.Notwithstanding,a relationship of form with function is a basic tenet of biology.These are multifactor problems,but the questions mostly have not been analysed as such.This review moves the question forward by focusing on TMjoint anatomic organisation as the multifactor system it is expected to be in a closed system like a synovial joint.Multifactor analysis allows the data to speak for itself and reduces bias.Classification tree analysis revealed useful prediction values and usable clinical models which are illustrated,backed up by stepwise logistic regression.Explained vari-ance,R2 ,predicting normals from pooled TMJ patients was 32.6%,sensitivity 67.9%,specificity 85.7%;37% versus disc displacement with reduction;and 28.8% versus disc displacement without reduction.Significant osseous organisational differences between TMjoints with clicking and locking suggest that this is not necessarily a single disease continuum.However,a subset of joints with clicking contained char-acteristics of joints with locking that might contribute to symptom progression versus resistance.Moderately strong models confirm there is a relationship between TMJ osseous organisation and function,but it should not be overstated.More than one model of normals and of TMde-rangement organisation is revealed.The implications to clinical decision-making are discussed.

Mounting evidences suggest that the ATRX (α-thalassaemia/mental retardation syndrome X-linked) and DAXX (death-domain associated protein) which encode 2 subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres,and multiple endocrine neoplasia type 1 (MEN-1) genes are significantly mutated in most patients with pancreatic neuroendocrine tumors (pNETs),as are genes encoding key molecules of the mammalian target of rapamycin (mTOR) signaling pathway.These mutated genes promote deregulation of epigenetic processes such as chromatin remodeling,histone modification and activation of alternative lengthening of telomeres,and thus combined alteration of these genes may contribute to drive tumorigenesis and metastasis of pNETs which are characterized by complex patterns of phenotypes.These findings may have great significance in the diagnosis and treatment of pNETs and predicting the prognosis,as well as providing clinical implications for targeted cancer therapy.

Invasion and migration are distinctive features of the malignant tumors.Studies showed that epithelial-mesenchymal transition ( EMT) , a conversion process with the loss of epithelial cell features and the gain of mesenchymal phenotype has been recog-nized as a key element of invasion and migration of malignancy.When EMT occurs, the downregulation of E-cadherins and the loss of adhesion in extracellular matrix play a critical role which are regarded as important indicators in the assessment of EMT.The latest re-searches indicated that integrin, one of the cell adhesion molecules family, was involved in EMT directly or indirectly through mediating either adhesion among cells, extracellular matrix or signal pathways by activating multiple kinases tyrosine phosphorylation cascade. The relationship between EMT and integrin is summarized in this article.

Objective:To investigate the clinical and pathological factors of metastasis in patients with oral squamous cell carcinoma (OSCC)and clinical lymph node-negative(cN0).Methods:85 patients of OSCC with cN0 treated in 2008-07 -2013-07 were inves-tigated retrospectively.Results:In the 85 patients 24(28.34%)showed occult metastasis.Patient's gender,lesion location had no im-pact to metastasis(P >0.05),the patient's age,tumor size,growth pattern and histopathologic grade showed significant influence on the metastasis of OSCC(P <0.05).Conclusion:The greater tumor volume,lower differentiation degree and young age are the factors of higher occult lymph node metastasis.Selective neck dissection treatments of OSCC is recommended.

Objective To study role of bone marrow mesenehyme stem cells in tumor formation.Methods Nude mice (n = 18) were randomly divided into two groups.Mice in the control group were subcutaneously injected with human embryonic MSCs, and F6 cells were injected into the nine mice of the experimental group.Three mice were sacrificed to remove tumor tissue, which was then prepared for real-time BT-PCR detection at 4 (F6-4), 6 (F6-6) and 7 (F6-7) weeks, respectively.Human lung cancer tissue samples and adjacent non-malignant lung tissue samples were collected from 4 lung cancer patients.The difference between gene expression of F6 cells and MSCs was distinguished by fluorescent differential display (FDD) and verificated by PCR and the western blot analysis. Real-time fluorescent quantitative reverse transcription polymerase chain reaction (FQ-BT-PCR) was used to detect gene expression in tumor tissues after tumorigenesis in nude mice.A new tumor cell line, denominated F6, was established from mutated human embryonic bone marrow mesenchymal stem cells (MSCs) which were induced by the GMCSF and IL-4 in vitro.Results FDD analysis confirmed that cyelin Ⅰ was positively up-regulated in F6 cells compared with MSCs. Similar results were obtained by PCR and western blot.The cyclin Ⅰ gene expression levels in MSCs, F6, F6-4, F6-6 and 176-7 were significantly different(F=12.29 ,P ＜ 0.01).The cyclin Ⅰ gene expression level in F6(4.49±0.40) was 112 folds higher than those of MSCs(0.04±0.02,P＜0.01).Expression levels in F6-4 , F6-6 and F6-7 tissue were 1.82±0.80,3.30±0.43,3.68±1.67 which were significantly higher than that in MSCs (P＜0.05 or ＜0.01).The expression of cyclin Ⅰ increased significantly alone with the accreting volume of tumor.The expression levels of cyelin Ⅰ in human lung cancer tissues in four patients were 0.15±0.02, 0.58±0.23, 4.82±1.12, 1.21±0.60,respectively, and were significantly higher than that in adjacent non-malignant lung tissues (0.04±0.02,0.09±0.04,0.94±0.74,0.15±0.08) (F=12.39,P＜0.01).The protein expression level of cyclin Ⅰ in F6 cells was 0.32±0.08, which was 3.6-fold higher than that in MSCs (0.09±0.06, t=3.86,P＜0.05).Conclusions The expression level of cyclin Ⅰ in tumor tissue is higher during the entire course of tumorigenesis.Cyclin Ⅰ might be one of the factors playing important roles during tumorigenesis,especially in MSCs mutation.

Objective To investigate the expressions of tenascin(TN)and microvessel density(MVD) in esophageal squamors cell carcinoma.Methods The experessions of TN and MVD were observed by immunohistochemiccal methods in 91 cases of esophageal carcinoma and 47 cases of ono-esophageal carcinoma.Results ①The expression of tenascin in esophageal cancer was much high than that in t he normal tissue(t=12.331,P＜0.01).②Over expression of TN was related to th length(F=12.373,P＜0.01),the invasion(F=11.039,P＜0.01),the lymphatic metastasis(F=6.882,P=0.01)and the pathologic trade(F=5.060,P=0.003)of cancer.③The expression fo MVD in the esophageal carcinoma tissues was stonger than that in the nonesophageal carcinoma tissues(t=6.023,P＜0.01).④Over expression of NVD wsa related to the length(F=9.033,P＜0.01),the lymphatic metastasis(F=12.429,P＜0.01)and the pathologic grade(F=5.717,P＜0.01)of cancer.⑤The positive expressions of TN and MVD were associated(P=0.001).Conclusion TN;s voerexpressions may be a biological marker in esophageal squamous cell carcinoma..It was associated with the expression of MVD.The levels of TN and NVD were useful molecular markers for evaluating malignancy degree and lymph node metastasis of esopageal carcinoma.

Objective To improve the understanding of small cell carcinoma of the urinary bladder. Methods The pathological and clinical data of 6 small cell carcinoma cases (4 men and 6 women, mean age of 51 years) were analyzed.Of them 2 cases had components of transitional cell carcinoma or adenocarcinoma.Two cases underwent partial cystectomy,and 4 cases,cystectomy.After operation,5 of them underwent 2～6 courses of chemotherapy. Results All the 6 cases were followed-up for 12～60 months,and they all died of tumor relapse.Their average survival time was 28 months. Conclusions Small cell carcinoma of urinary bladder accounts for 0.44% of the primary malignant tumor of urinary bladder.It has high malignancy and easily metastasizes to lymph nodes,liver and bones,thus the prognosis is bad.Radical cystectomy in combination with systemic chemotherapy has better efficacy.