Purpose Mantle cell lymphoma (MCL) is a rare and aggressive subtype of non-Hodgkin lymphoma that is incurable with standard therapies. The use of gene expression analysis has been of interest, recently, to detect biomarkers for cancer. There is a great need for systemic coexpression network analysis of MCL and this study aims to establish a gene coexpression network to forecast key genes related to the pathogenesis and prognosis of MCL. Methods The microarray dataset GSE93291 was downloaded from the Gene Expression Omnibus database. We systematically identified coexpression modules using the weighted gene coexpression network analysis method (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis were performed on the modules deemed important. The protein–protein interaction networks were constructed and visualized using Cytoscape software on the basis of the STRING website; the hub genes in the top weighted network were identified. Survival data were analyzed using the Kaplan–Meier method and were compared using the log-rank test. Results Seven coexpression modules consisting of different genes were applied to 5,000 genes in the 121 human MCL samples using WGCNA software. GO and KEGG enrichment analysis identified the blue module as one of the most important modules; the most critical pathways identified were the ribosome, oxidative phosphorylation and proteasome pathways. The hub genes in the top weighted network were regarded as real hub genes (IL2RB, CD3D, RPL26L1, POLR2K, KIF11, CDC20, CCNB1, CCNA2, PUF60, SNRNP70, AKT1 and PRPF40A). Survival analysis revealed that seven genes (KIF11, CDC20, CCNB1, CCNA2, PRPF40A, CD3D and PUF60) were associated with overall survival time (p < 0.05). Conclusions The blue module may play a vital role in the pathogenesis of MCL. Five real hub genes (KIF11, CDC20, CCNB1, CCNA2 and PUF60) were identified as potential prognostic biomarkers as well as therapeutic targets with clinical utility for MCL.

Abstract:The ZM-1 tissue microarrayer designed by our groups is manufactured in stainless steel and brass and contains many features that make TMA (tissue microarray) paraffin blocks construction faster and more convenient. By means of ZM-1 tissue microarrayer, biopsy needles are used to punch the donor tissue specimens respectively. All the needles with the punched specimen cylinders are arrayed into the array-board, with an array of small holes dug to fit the needles. All the specimen cylinders arraying and the TMA paraffin block shaping are finished in only one step so that the specimen cylinders and the paraffin of the TMA block can very easily be incorporated and the recipient paraffin blocks need not be made in advance, and the paraffin used is the same as that for conventional pathology purpose. ZM-1 tissue microarrayer is easy to be manufactured, does not need any precision location system, and so is much cheaper than the currently used instrument. Our method's relatively cheap and simple ZM-1 tissue microarrayer technique of constructing TMA paraffin block may facilitate popularization of the TMA technology.

To date, five cases of invasive lobular carcinoma with solid and encapsulated papillary carcinoma (SPC and EPC) growth pattern were reported. In this article, we describe such a case that might represent a diagnostic pitfall. A 61-year-old woman had a mass on the left breast that was characterized by multiple expansile nodules with a fibrous capsule. Tumor cells were arranged in a solid pattern with inconspicuous delicate fibrovascular cores, some were irregular glandular tubes and papillary, similar to the growth pattern of SPC and EPC. The appearance of the tumor surrounding tissue suggested a special type of lobular carcinoma. The diagnosis of invasive lobular carcinoma was confirmed by immunohistochemistry, which revealed negative E-cadherin, positive cytoplasmic P120, and deleted myoepithelium. Next-generation sequencing revealed CDH1 mutations that further proved the diagnosis of invasive lobular carcinoma. The main differential diagnoses for this tumor are SPC, EPC, neuroendocrine carcinoma, and secretory carcinoma, for which immunohistochemical analysis is an essential diagnostic tool. The growth pattern of invasive lobular carcinoma with EPC and SPC is a variant of the invasive lobular carcinoma newly discovered. The understanding of this variant expands the morphological spectrum of invasive lobular carcinoma and will help prevent misdiagnosis.

The diagnosis of primary angiosarcoma of ovary is still a challenge as it has no specific clinical symptoms and is easily confused with other malignant neoplasms in morphology. Here, we described a case of primary ovarian angiosarcoma and reviewed the literature. A 47-year-old female showed a left ovary mass. Grossly, the cut surface of the tumor was solid and gray-white with intermediate texture. Some areas were spongy and atropurpureus with a soft texture. Microscopically, the tumor cells were arranged into a variety of different structures with visible hemorrhage. Immunochemically, the tumor cells were positive for CD31, ERG, Fli1, D2–40 and vimentin in a strong and diffused manner. CD34 stain showed focal positivity. Epithelial markers (e.g. CK, CK7, CK8/18 and PAX8) were all negative. Negative immunostaining for SMA, S-100, P53 and calretinin also were detected. The proliferative index (Ki-67) was approximately 40%. After surgery, the patient was treated with radiotherapy, targeted therapy and immunotherapy. In the 9-month follow-up, the patient was survival without evidence of disease. The diagnosis of ovarian angiosarcoma required the careful observation of morphology and the reasonable application of immunohistochemistry. Targeted therapy and immunotherapy are the potential directions for the treatment of angiosarcoma.

Mitogen- and stress-activated protein kinase (MSK) 1 protein was initially identified as a particularly interesting protein of mitogen-activated protein kinase. It was reported to enhance B cell lymphoma 2-associated death protein's phosphorylation to protect cell death, suggesting that MSK1 represents a new type of anti-cell death gene. Moreover, a recent study has shown that MSK1 is involved in negative feedback pathways that are crucial to prevent uncontrolled inflammation. However, its function and expression in the central nervous system lesion are not been understood very well. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of MSK1 expression in the brain cortex. Double immunofluorescence staining revealed that MSK1 was co-expressed with neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP). Besides, co-localization of MSK1/active caspase 3 and MSK1/proliferating cell nuclear antigen (PCNA) was detected in NeuN and GFAP. We also examined the expression profiles of PCNA and active caspase 3 whose changes were correlated with the expression of MSK1. All our findings suggested that MSK1 might be involved in the pathophysiology of brain after TBI.