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Solitary fibrous tumors (SFTs) are uncommon, with the pleura as a site of predilection. Central nervous system SFTs, particularly intracranial SFTs, are extremely rare. The lesions are generally benign and localized, and surgery is the main therapeutic solution. The current study reports the cases of a patient who presented with right haunch pain, right leg weakness and paresthesias for several months, and a patient with a history of unexpected loss of consciousness. Magnetic resonance imaging revealed the presence of lesions, with a spindle cell morphology evident on pathological examination. The immunohistochemical examination demonstrated a strong immunoreaction for cluster of differentiation 34, which supported the diagnosis of an SFT. Following a near-total resection, the patients had a good neural prognosis. The present study also provides a literature review, discussing the imageological and pathological characteristics of SFT, and the diagnostic methods that aid in distinguishing the entity from other spindle-cell central nervous system tumors.

To construct certain chimeric E3s expression plasmids targetting oncoprotein Ras by harnessing the theory of protein knockdown.We chose the binding domain of Raf-1, PI3K, RalGDS, and the function domain of F-Box as well as the U-Box to construct the plasmids. Then used the double enzyme, PCR, and sequence to test the validity and integrity of the cloned nucleotide fragments. The expression efficiency of the plasmids in eukaryotic cells was detected by Western blot analysis.Five of 6 plasmids in this study expressed the corresponding fusion proteins in HEK293T cells, and (RBD+CRD)(Raf-1)- U-Box-pcDNA3.1 can knocked down the protein level of Ras in PANC-1 cells.We successfully constructed the chimeric E3 expression plasmids, which provides a solid basis for further research on protein knockdown.

To investigate the expression of CXCR3 and its association with clinicopathologic features in breast carcinoma.The expression level of CXCR3 in 18 samples of breast cancer and corresponding normal tissues was investigated using reverse transcriptase-polymerase chain reaction (RT-PCR) and real-time RT-PCR analysis. Immunohistochemistry was carried out to examine the expression of CXCR3 in 80 breast cancers, 20 fibroadenomas and 15 normal breast tissues.(1) RT-PCR and real-time RT-PCR analysis showed a higher level of CXCR3 in breast cancer tissues than that in the corresponding normal breast tissues (P0.05). (2) Immunohistochemistry analysis showed that the positive rate of CXCR3 in breast cancer tissues was significantly higher than that in fibroadenomas and the normal breast tissues (P0.05). The expression level of CXCR3 in the lymph node-positive group was higher than that in the lymph node-negative group (P0.05). The expression of CXCR3 was positively correlated with the number of lymph nodes involved by metastasis, tumor size and pTNM tumor stage (P0.05).Chemokine receptor CXCR3 was up-regulated in breast cancer, and was associated with the progression of breast cancer. CXCR3 might be a novel molecular marker to predict lymph node metastasis and prognosis of breast cancer.

AIM: To elucidate the role of dickkopf3 (Dkk3) in human pancreatic cancer cell growth. METHODS: Dkk3 mRNA and protein expression in human pancreatic cancer cell lines were detected by real-time reverse transcription polymerase chain reaction (real-time RT-PCR), Western blotting and immunofluorescence. Methylation of the Dkk3 promoter sequence was examined by methylation-specific polymerase chain reaction (MSP) and Dkk3 mRNA expression was determined by real-time RT-PCR after 5-aza-2’-deoxycytidine (5-aza-dC) treatment. The effects of Dkk3 on cancer cell proliferation and in vitro sensitivity to gemcitabine were investigated by CellTiter 96® AQueous One Solution Cell Proliferation Assay (MTS) after transfecting the Dkk3 expression plasmid into human pancreatic cancer cells. The expression of β-catenin, phosphorylated extracellular signal-regulated protein kinases (pERK) and extracellular signal-regulated protein kinases (ERK) was also examined by real-time RT-PCR and Western blotting after upregulating Dkk3 expression in human pancreatic cancer cells. RESULTS: The results show that the expression levels of both Dkk3 mRNA and protein were low in all pancreatic cancer cell lines tested. The Dkk3 promoter sequence was methylated in the MIA PaCa-2 and AsPC-1 cell lines, which showed reduced Dkk3 expression. These two cell lines, which initially had a methylated Dkk3 promoter, showed increased Dkk3 mRNA expression that was dependent upon the dosage and timing of the DNA demethylating agent, 5-aza-dC, treatment (P < 0.05 or P < 0.01). When Dkk3 expression was upregulated following the transfection of a Dkk3 expression plasmid into MIA PaCa-2 cells, the ability of cells to proliferate decreased (P < 0.01), and the expression of β-catenin and pERK was downregulated (P < 0.01). Sensitivity to gemcitabine was enhanced in Dkk3 expression plasmid-transfected cells. CONCLUSION: Our findings, for the first time, implicate Dkk3 as a tumor suppressor in human pancreatic cancer, through the downregulation of β-catenin expression via the ERK-mediated pathway.

To investigate the expression of Twist, E-cadherin and N-cadherin in breast carcinoma tissue and to analyse their effects on the breast carcinoma differentiation, size, infiltration and metastasis of the breast carcinoma.The expression of Twist, E-cadherin and N-cadherin in 56 cases of breast invasive ductal carcinoma, 38 cases of invasive lobular carcinoma, 41 cases of carcinoma in situ and 10 cases of normal breast tissue was detected using immunohistochemistry.(1) The expression rate of Twist in three types of breast carcinoma was 46.4% (26/56), 79.0% (30/38) and 26.8% (11/41) respectively, and the expression of Twist in invasive lobular carcinoma was significantly higher than that in invasive ductal carcinoma and carcinoma in situ (P = 0.002, P = 0.000). The expression rate of E-cadherin in three types of breast carcinoma was 78.6% (44/56), 29.0% (11/38) and 80.5% (33/41) respectively, and the expression of E-cadherin in invasive ductal carcinoma and carcinoma in situ was significantly higher than that in invasive lobular carcinoma (P = 0.000, P = 0.000). The expression rate of N-cadherin in three types of breast carcinoma was 53.6% (30/56), 68.4% (26/38) and 31.7% (13/41) respectively, and the expression of N-cadherin in invasive ductal carcinoma and invasive lobular carcinoma was significantly higher than that in carcinoma in situ (P = 0.033, P = 0.001). (2) In all the 135 cases, the expression of Twist was not correlated with that of E-cadherin (P = 0.005, Spearman correlation coefficient = -0.239), however, there was a positive correlation between the expression of Twist and N-cadherin and statistically significant(P = 0.000, Spearman correlation coefficient = 0.319). (3) In the invasive ductal carcinoma, the expression of N-cadherin in poorly-differentiated carcinoma was significantly higher than that of the moderately-or well-differentiated ones (P = 0.004). (4) In the invasive lobular carcinoma, the expression of Twist in cases with lymph node metastasis was significantly higher than that of cases without metastasis (P = 0.037).Twist, E-cadherin and N-cadherin have different expression patterns in the three kinds of breast carcinoma. The positive expression of Twist was correlated to lymph node metastasis in invasive lobular carcinoma and the positive expression of N-cadherin was correlated to cell the tissue differentiation in invasive ductal carcinoma. Detection of the expression of these biomarkers may provide a valuable reference for the study of breast carcinoma progression, metastasis and for the judgment of the biological behavior of the carcinoma.

Ubiquitin-proteasome pathway (UPP) can degrade specific proteins in eukaryotic cells. Targeting specific proteins for ubiquitination and degradation technique, based the theory of UPP and using certain chimeric E3s or protein-targeting chimeric molecules, can specifically knock down the targeted proteins. It is a promising new method for exploring the functions of genes or proteins and, together with gene-silencing technique, may play an important role in basic and clinical research.

Studies have shown that BIRC7, a new member of inhibitor of the apoptosis protein family, is expressed in fetal tissues and most solid tumors in humans. However, there are no reported data concerning BIRC7 expression in lymphomas. We investigated the expression of BIRC7, survivin, Bcl-2, Bax, p53 and p170 proteins in 167 cases of non-Hodgkin's lymphoma (NHL) and 10 cases of non-specific lymphadenitis by tissue microarray-based immunohistochemistry. BIRC7 mRNA in three cell lines and 16 cases of NHL were detected by reverse transcriptase-polymerase chain reaction. BIRC7 protein was exhibited in the cytoplasm of cells in 25 (31%) of 80 cases of B-NHLs, 32 (37%) of 87 cases of T-NHLs, and none in non-specific lymphadenitis. The positive rate of BIRC7 was lower than that of survivin in almost all types of NHL with no significant differences, and similar to that of Bcl-2, Bax or p53. There was no correlation of protein expression between BIRC7 and any other detected markers, except p170 in T-NHL (P0.001). BIRC7 expression did not correlate with clinic pathologic factors such as sex, age, stage and grade, but overexpression of BIRC7 was positively correlated with aggression of NHL cells (P0.05). BIRC7 mRNA expressed in six (38%) of 16 cases of NHLs. BIRC7 mRNA expression was approximately consistent with BIRC7 protein in NHL. Our results indicate that the BIRC7 gene might play a role in the development and aggression of NHL and that the inhibition of BIRC7 expression may be important in NHL treatment.

Survivin is the smallest member of mammalian IAP (inhibitor of apoptosis) family. It is ubiquitous during embryonic development but is not expressed in normal post-natal tissues, except the thymus, colonic epithelial cells and CD34+ hematopoietic stem cells. However, its expression is upregulated during neoplastic transformation in both solid organ and hematological malignancies, including leukemia and lymphoma. In this study, we used RNA interference with short hairpin RNA (shRNA) technique to inhibit survivin expression in a Burkitt's lymphoma cell line Raji and validated its effects on apoptosis and cell proliferation. A survivin-shRNA expression vector were constructed and introduced into Raji cells. Expression of survivin mRNA and protein was assessed by RT-PCR and western blot analysis. Apoptosis index of transfected cells was quantified by flow cytometry and cell proliferation was enumerated by trypan blue exclusion. In Raji cells treated with survivin-shRNA expression vector, survivin mRNA levels were significantly reduced by 67.14% (transient transfection) and 64.28% (stable transfection) respectively, compared with control-shRNA treated group and PBS treated group (p0.05). The levels of survivin protein were significantly reduced by 62.50% (transient transfection) and 60.93% (stable transfection), compared with the two control groups (p0.05). Apoptosis index was significantly increased during transient transfection and stable transfection, respectively 31.20+/-2.45% and 29.40+/-1.72% (p0.05). Survivin-shRNA inhibited the proliferation of Raji cells of stable transfection. In conclusion, the vector-based survivin-shRNA can effectively reduce the expression of survivin gene and induce apoptosis and growth inhibition of transfected Raji cells. We suggest that survivin can be regarded as an ideal target for new anticancer intervention of NHL.

To study the effect of transfecting survivin antisense mRNA on growth and chemotherapy sensitivity of lymphoma cells.Eukaryotic expression plasmid pcDNA3. 1-antisense (As) survivin was constructed and transfected into Jurkat T lymphoblastic lymphoma cell lines with high expression survivin mRNA by use of lipofectmine gene transfer technique. Expression of survivin mRNA and protein were detected by reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemical and Western blot. The effect of transfecting survivin antisense mRNA on the growth of Jurkat cell lines was monitored by population doubling time (PDT) and Apoptotic indexes (AI). The morphologic features were observed in transfected cells by light and electric microscopes. MTT assay was used to analyze the response of transfected cells to CTX and MTX.Compared with the control cells, the expression of survivin mRNA and protein were reduced after transfected pcDNA3. 1-Assurvivin 48 h, 5 w and 6 w, PDT (52 h) was prolonged. Apoptotic indexes were higher in transfected antisense survivin mRNA cells [20.2% (48 h)], 6.2% (5 w) and 6.8% (6 w) than control ones [2.1%, 1.3% (48 h)] and [1.3% (5 w) and 1.0% (6 w)]. The cells grow slowly and the dead cells increase and some swelling and apoptotic cells were observed in transfected pcDNA3. 1-Assurvivin groups by invert, light and electric microscopes. The Jurkat cell line of transfected pcDNA3. 1-Assurvivin had higher sensitivity to CTX and MTX. The rate of inhibition was higher in transfected group. There is a significant difference between the transfected group and untransfected one, P0.05.The result indicated that survivin gene was very important for growth of Jurkat cells. To inhibit the expression of survivin will be significant in therapy of T lymphoblastic lymphoma. Survivin gene might be a target of therapy.

Salvianolic acid B (SalB), a bioactive compound isolated from the plant-derived medicinal herb Danshen, has been shown to exert various anti-oxidative and anti-inflammatory activities in several neurological disorders. In this study, we sought to investigate the potential protective effects and associated molecular mechanisms of SalB in Parkinson's disease (PD) models. To determine the neuroprotective effects of SalB in vitro, MPP+- or lipopolysaccharide (LPS)-induced neuronal injury was achieved using primary cultures with different compositions of neurons, microglia and astrocytes. Our results showed that SalB reduced both LPS- and MPP+-induced toxicity of dopamine neurons in a dose-dependent manner. Additionally, SalB treatment inhibited the release of microglial pro-inflammatory cytokines and resulted in an increase in the expression and release of glial cell line-derived neurotrophic factor (GDNF) from astrocytes. Western blot analysis illustrated that SalB increased the expression and nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). The knockdown of Nrf2 using specific small interfering RNA (siRNA) partially reversed the SalB-induced GDNF expression and anti-inflammatory activity. Moreover, SalB treatment significantly attenuated dopaminergic (DA) neuronal loss, inhibited neuroinflammation, increased GDNF expression and improved the neurological function in MPTP-treated mice. Collectively, these findings demonstrated that SalB protects DA neurons by an Nrf-2 -mediated dual action: reducing microglia activation-mediated neuroinflammation and inducing astrocyte activation-dependent GDNF expression. Importantly the present study also highlights critical roles of glial cells as targets for developing new strategies to alter the progression of neurodegenerative disorders.

—that morbidity from chronic subdural haematoma is lower if a drain is placed postoperatively—will probably change the management of this condition around the world. However, we want to highlight some concerns.Chronic subdural haematomas re-spond strikingly to surgical drainage. Since the difference in 30-day mortality between the drain and non-drain groups was non-signifi cant, the cause of death at 6 months might be unrelated to the recurrence of chronic subdural haematoma. Moreover, after the evacuation of chronic subdural haematomas, death is a rare event, and those that do occur are often not directly related to the complications of chronic subdural haematoma.