Objective To analyse retrospectively the clinical efficacy and prognostic factors of arterial intervention-al therapy combined with epidermal growth factor receptor (EGFR) and tyrosine kinase inhibitors (TKI) erlotinib (erlotinib) on non-small cell lung cancer (NSCLC) patient with brain metastasis. Methods A total of 45 NSCLC patients with brain metastasis were underwent infusion chemotherapy two-six cycles by selective bronchial artery or intracranial arterial. Erlo-tinib (150 mg, 1/d) was used simultaneously or sequentially with the infusion chemotherapy. The clinical efficacy was as-sessed every two cycles or when the disease got progressed. The progression-free survival (PES) and overall survival (OS) were recorded from the follow up data. Results All the patients received at least two cycles of treatment. The median num-ber of cycles was 3 (range 2-6 cycles). The results were as follows:complete remission (CR) in 7 cases (15.56%), partial re-mission (PR) 12 cases (26.67%), stable (SD) 16 cases (35.56%) and progression (PD) 10 cases (22.22%). The objective re-sponse rate (ORR, CR+PR) and disease control rate (DCR, CR+PR+SD) were 42.22%and 77.78%respectively. Patients in this study were followed up for 19 months (6-45 months), with the median PFS time 11.00 months,the median OS time 17.00 months. The univariate analysis showed that patients with low PS score had longer PFS and OS than those of patients with higher PS score. There were 53 adverse events during the treatment. No serious adverse reactions of drugs were found in patients. Conclusion The arterial interventional therapy combined with erlotinib showed a better short-term effect and pro-longed survival time, and with mild side effects.

Indoleamine 2,3-dioxygenase (IDO) is known as an endogenous immunosuppressive enzyme which plays a significant role in the process of tumor.IDO is not only found in tumor cells but also detected in dendritic cell (DC) in tumor microenvironment,which participates in the formation of tumor immune tolerance through expressing IDO enzyme.Signal transducer and activator of transcription (STAT) is the main signal protein family which participates in the IDO transcriptional regulation of DC.It is necessary to detail the signaling pathway in regulating IDO expression,which will help us develop high specific and more active IDO inhibitors and provide new options for anti-cancer targeted therapy.

Recently, it is reported that regulatory T cells (Tregs) can be reprogrammed into a novel population [interleu?kin (IL)-17+Foxp3+T cells] phenotypically and functionally resembling Th17 cells under complicated cytokine circumstanc?es. IL-17+Foxp3+T cells are characterized by production of IL-17 and expression of retinoic acid receptor related orphan re?ceptor (ROR)γt, demonstrating dual functions in immune response and providing novel insight into the interconnection be?tween Tregs and Th17 cells. In this review, we lay emphasis on the phenotype features, origination, differentiation and the pleiotropic functions of IL-17+Foxp3+T cells. Furthermore, we summarized the functions of IL-17+Foxp3+T cells in inflam?matory disease and tumor microenvironment.

There exists a population of myeloid-origin cells that are associated with tumor immune escape in cancer patients,commonly termed as myeloid derived suppressor cells(MDSCs).M DSCs accumulate in the blood,lymph nodes,bone marrow,and inhibit both adptive and innate immunity.Different suppressive mechanisms are used by MDSCs to block tumor immunity.Reducing the numbers of MDSCs or inhibiting the suppressive pathway conducted by MDSCs will bring new highlight to biotherapy in tumor treatment.

Radiation could induce DNA damage,cell death,and changes of tumor phenotype and tumor microenvironment leading to the regulation of immune response.Immune checkpoint signaling pathways are involved in the immune tolerance of anti-microorganism responses and thus limit tissue damage.In the anti-tumor immune response,these pathways are associated with anti-functional activation of specific cytotoxic T cells and also enhance the inhibition effect of immune response,which always result in immune escape.Blockade of the immune checkpoint signaling pathways benefits to the anti-tumor inmune responses and could delay tumor progress.As a result,the combination treatment of radiotherapy and immune checkpoint biockade has attracted more attentions in clinical application.This paper reviews the recent research progresses in the radiation effect of immune system,the regulation of immune checkpoints and the combination treatment of radiotherapy and immune checkpoint blockade in tumor therapy,trying to arouse some new clues in cancer therapy.

Objective: This study explores the miR-150 expression and its clinical significance in mantle cell lymphoma (MCL). Methods: The miR-150 and c-Myc expression was measured in 29 primary MCL tissue samples and 7 normal donors through quantita-tive real-time polymerase chain reaction. MiR-150 expression was detected in Mino and HBL-2 cells after c-Myc was knocked down by small interfering RNAs. MiR-150 was analyzed in tet-treated P493-6 cells with Myc turned off. The number of tumor colonies in the BL-2 cells transfected with pre-miR-150 was determined through colony formation assay, and c-Myb was detected through Western blot. Results: Compared with the normal donors, miR-150 expression was significantly downregulated and c-Myc was considerably overexpressed in MCL. Moreover, MCLs with high Myc expression had a significantly low miR-29 expression. MiR-150 was upregu-lated in the Mino and HBL-2 cells with c-Myc knockdown. MiR-150 was evidently upregulated in P493-6 cells after c-Myc was turned off. MiR-150 overexpression suppressed colony formation and c-Myb expression of HBL-2. Conclusion: MiR-150 is downregulated in MCL, which may be related to c-Myc overexpression. The recovery of miR-150 suppresses MCL cell survival. These results indicate that miR-150 may be a potential therapeutic target of MCL.

Objective: This study aims to investigate the correlation between the expression of FoxP3, TGF-β1, and epitheli-al-mesenchymal transition (EMT) in breast cancer and to determine the clinical significance of FoxP3. Methods: The expression of FoxP3, TGF-β1, E-Cadherin, N-Cadherin, Vimentin, and Fibronectin protein were detected in the cancer cells of 74 cases with breast carcinoma via immunohistochemistry. The correlation of FoxP3 protein with clinico-pathologic features of breast carcinoma and the re-lationships among the expressions of FoxP3, TGF-β1, and epithelial-mesenchymal transition (EMT) were analyzed. Results:The ex-pression rates of FoxP3, TGF-β1, and EMT are 36.5%(27/74), 39.2%(29/74), and 40.5%(30/74), respectively. The FoxP3 protein ex-pression in breast cancer is correlated with lymph node metastasis (P<0.05) but not with other clinico-pathological features (P>0.05). The expression of FoxP3 is also correlated with the expression of TGF-β1. Furthermore, TGF-β1 can induce EMT (P<0.05). Conclu-sion:The expression of FoxP3 is correlated with lymph node metastasis and EMT in breast cancer. Therefore, FoxP3 may be a marker for predicting metastasis.

Aurora-A is a mitotic serine/threonine kinase that is evolutionally conserved and localized at the centrosome. Aurora-A activation is required for mitotic entry, centrosome maturation, and centrosome separation. Aurora-A is frequently amplified and/or over-expressed in breast, ovarian, esophageal, colon, lung, and bladder cancers. Aurora-A has recently become a new target of malignant tumors. The Aurora-A inhibitor can be combined with other chemotherapeutic drugs to provide a new way for cancer treatment. In this study, we review the function and inhibitor of Aurora-A kinase.

Objective:This study aims to investigate the correlation and significance between the expression of P53 and epitheli-al-mesenchymal transition (EMT) in breast cancer. Methods:The expression patterns of P53, Twist, Snail, E-cadherin, N-cadherin, Vi-mentin, and Fibronectin protein were detected via immunohistochemistry in 63 cases with breast carcinoma. The correlation of P53 pro-tein with clinicopathologic features and survival of breast carcinoma, as well as the relationship between the expression of P53 and EMT, was analyzed. Results:The expression rates of P53, Twist, Snail, and EMT are 44.4%(28/63), 54.0%(34/63), 68.3%(43/63), and 41.3%(26/63), respectively. The P53 protein expression is correlated with tumor grade (P<0.05) but not with other clinicopatholog-ic features (P>0.05). The expression of P53 is also correlated with the expression of Twist and Snail, which are associated with EMT (P<0.05). Multivariate survival analysis reveals that lymph node metastasis, P53, and EMT are independent prognostic factors. Conclu-sion:The expression of P53 is correlated with tumor grade and EMT in breast cancer, which can be used as an independent prognostic factor. Therefore, P53 may be an effective target for breast cancer therapy.

Objective:To study the role of FDCs-miR-548m-CDK6 axis on clonogenicity in mantle cell lymphoma. Methods:RT-qPCR and Western blot were used respectively to test the expression of miR-548m and CDK6. Bioinformatics assay was applied to predict the targets of miR-548m, and Western Blot was used to test the expression level of CDK6 after miR-548m overexpression or in-hibition. Luciferase report assay was performed to test whether CDK6 was a direct target of miR-548m. Colony forming assay was used to test the colony forming activity in MCL after overexpression of miR-548m or knockdown of CDK6. Results:Cell adhesion to FDCs induced downregulation of miR-548m and CDK6 expression in MCL. Bioinformatics assay revealed that miR-548m could target the 3'-UTR of CDK6 and that a negative correlation exists between the level of miR-548m and the CDK6 expression. Luciferase report as-say confirmed that miR-548m directly targeted 3'-UTR of CDK6. Colony forming assay showed that overexpression of miR-548m or knockdown of CDK6 significantly suppressed MCL colony formation. Conclusion:This study reveals that FDC-enhanced mantle cell lymphoma clonogenicity is mediated by the miR-548m/CDK6 axis.