BackgroundEphA5 is a member of the Eph/ephrin family and plays a critical role in the regulation of carcinogenesis. A significant reduction of EphA5 transcripts in high-grade prostate cancer tissue was shown using a transcriptomic analysis, compared to the low-grade prostate cancer tissue. As less is known about the mechanism of EphA5 downregulation and the function of EphA5, here we investigated the expression and an epigenetic change of EphA5 in prostate cancer and determined if these findings were correlated with clinicopathologic characteristics of prostate cancer.MethodsSeven prostate cell lines (RWPE-1, LNCap, LNCap-LN3, CWR22rv-1, PC-3, PC-3M-LN4, and DU145), thirty-nine BPH, twenty-two primary prostate carcinomas, twenty-three paired noncancerous and cancerous prostate tissues were examined via qRT-PCR, methylation-specific PCR, bisulfite sequencing, immunohistochemistry and western blotting. The role of EphA5 in prostate cancer cell migration and invasion was examined by wound healing and transwell assay.ResultsDownregulation or loss of EphA5 mRNA or protein expression was detected in 28 of 45 (62.2%) prostate carcinomas, 2 of 39 (5.1%) hyperplasias, and all 6 prostate cancer cell lines. Methylation of the EphA5 promoter region was present in 32 of 45 (71.1%) carcinoma samples, 3 of 39 (7.7%) hyperplasias, and the 6 prostate cancer cell lines. Among 23 paired prostate carcinoma tissues, 16 tumor samples exhibited the hypermethylation of EphA5, and 15 of these 16 specimens (93.8%) shown the downregulation of EphA5 expression than that of their respectively matched noncancerous samples. Immunostaining analysis demonstrated that the EphA5 protein was absent or down-regulated in 10 of 13 (76.9%) available carcinoma samples, and 8 of these 10 samples (80.0%) exhibited hypermethylation. The frequency of EphA5 methylation was higher in cancer patients with an elevated Gleason score or T3-T4 staging. Following the treatment of 6 prostate cancer cell lines with 5-aza-2′-deoxycytidine, the levels of EphA5 mRNA were significantly increased. Prostate cancer cells invasion and migration were significantly suppressed by ectopic expression of EphA5 in vitro.ConclusionOur study provides evidence that EphA5 is a potential target for epigenetic silencing in primary prostate cancer and is a potentially valuable prognosis predictor and thereapeutic marker for prostate cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1025-3) contains supplementary material, which is available to authorized users.

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This effort investigates the dynamic properties of ejecta from explosively shocked, melted Pb targets. The study shows that the ejecta cloud that expands beyond the shocked surface is characterized by a high density and low velocity fragment layer between the free-surface and the high velocity micro-jetting particle cloud. This slow, dense ejecta layer is liquid micro-spall. The properties of micro-spall layer, such as the mass, density and velocity, were diagnosed in a novel application of an Asay window, while micro-jetting particles by lithium niobate piezoelectric pins and high speed photography. The total mass-velocity distribution of ejecta, including micro-spall fragments and micro-jetting particles, is presented. Furthermore, the sensitivity of ejecta production to slight variations in the shockwave drive using the Asay foil is studied.

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full-dose crizotinib and osimertinib targeting MET amplification sequentially emerging after T790M positivity in EGFR-mutant non-small cell lung cancer. J Thorac Oncol. 2017;12:e85-e88. 4. Li YQ, Song SS, Jiang SH, Zhang XY. Combination therapy of erlotinib/crizotinib in a lung adenocarcinoma patient with primary EGFR mutation plus secondary MET amplification and a novel acquired crizotinibresistant mutation MET G1108C. Ann Oncol. 2017;28: 2622-2624. 5. Baldacci S, Mazieres J, Tomasini P, et al. Outcome of EGFR-mutated NSCLC patients with MET-driven resistance to EGFR tyrosine kinase inhibitors. ALK receptor tyrosine kinase (ALK) fusion is found in many cancers; the highest detection has been in NSCLC. ALK is considered a lung cancer-driven gene, but ALK double fusion is rare. 1 ALK inhibitors are widely used in cancer-targeted therapy now. Alectinib as first-line treatment for ALK-positive NSCLC patients brings about progression-free survival of 25.7 months. 2 However, the sensitivity to ALK inhibitors of different ALK fusion forms is different. 3 Therefore, constantly exploring the new form of ALK fusion and studying its relevance to drug sensitivity has great clinical significance. With the development of next-generation sequencing (NGS) technology, ALK detection is becoming more and more precise. Here we report two novel ALK fusions detected simultaneously in a case of lung adenocarcinoma. The tumor size was significantly reduced after treatment with crizotinib.The patient was a 56-year-old male. In August 2007, during a routine physical examination, computed tomography (CT) screen revealed a lower left lung mass Figure 2. Computed tomography scans of patient #2 treated with osimertinib and crizotinib showing response in cervical metastases (A) at baseline and (B) at 1 month of treatment, and in pleural metastases (C) at baseline and (D) at 1 month of treatment.Drs. Lin and Ren contributed equally to this work.

Background: Intracranial angiomatous meningioma (AM) is a rare subtype of meningioma. Here, we investigated the clinical and pathological features of AMs. Materials and Methods: We performed a retrospective study of 23 intracranial AMs verified by postoperative pathology at Huashan Hospital North between 2013 and 2018. Clinical data, radiological and pathological findings, and information on treatment and outcomes were collected and analyzed. Additionally, the literature on intracranial AMs was reviewed. Results: The sample comprised 13 men and 10 women with AMs. The mean age was 54.2 years, and the mean duration of symptoms was 14.9 months. Headache and epilepsy were the most common symptoms. The most common AMs locations were the cerebral convexity and parasagittal/falx region. The rates of vascular signs, homogeneous enhancement, and peritumoral brain edema (PTBE) on magnetic resonance images were high. Histologically, besides typical meningioma cells, AMs had an abundant vascular component and low Ki-67 index. The extent of PTBE was related to microvessel density (MVD) of tumors, but not to the expression of MMP9 or VEGF. Simpson grade I resection was achieved in 15 cases, and grade II resection was achieved in 7 cases. Twenty-one cases were followed up, and they all had favorable outcomes without recurrence. Conclusion: AM is a type of meningioma with a rich blood supply and distinct clinical and pathological features. It showed a slight male predominance and was common at the cerebral convexity or parasagittal/falx region. Histologically, it showed benign biological characteristics despite frequent and severe PTBE, and the extent of PTBE was related to MVD of tumors. Simpson I resection is the best treatment, and the prognosis is usually good after total tumor removal, while gamma knife is recommended for small residual tumor.