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Simple Summary: Pancreatic cancer remains as one of the most life-threatening cancers with a 5-year overall survival rate less than 6%. As a transmembrane protein, capillary formation gene 2 (CMG2) mediates cell–matrix adhesion and migration. Recent studies have revealed emerging roles of CMG2 in various cancers. This study aimed to evaluate expression of CMG2 in pancreatic cancer and its implication in the disease progression and distant metastasis. Interestingly, the significant upregulation of CMG2 was seen in pancreatic cancer, which was associated with poor survival and distant metastases highlighting the potential of targeting this molecule for the prevention of dissemination of pancreatic cancer cells. Capillary morphogenesis gene 2 (CMG2) mediates cell–matrix interactions to facilitate cell adhesion and migration. CMG2 has been implicated in the disease progression of breast cancer, prostate cancer and gastric cancer. The present study aims to determine the role of CMG2 in the disease progression and peritoneal metastasis of pancreatic cancer. Pancreatic tumour samples were collected from Peking University Cancer Hospital. CMG2 expression was determined using quantitative PCR. After the creation of knockdown and overexpression of CMG2 in pancreatic cancer cells, the effect of CMG2 on several cell functions and adhesion to the peritoneum was examined. Potential pathways regulated by CMG2 were found via proteomics analysis and drug tests. CMG2 was upregulated in pancreatic cancer tissues and associated with a poor prognosis. CMG2 was increased in metastatic lesions and those primary tumours with distant metastases. CMG2 promotes cell–cell, cell–matrix and cell–hyaluronic acid adhesion, which may be mediated by epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK) pathway activation. [ABSTRACT FROM AUTHOR]

Context.--Pleural pathology has been dominated by discussions relating to the diagnosis, prognosis, etiology, and management of malignant mesothelioma. However, there exists a diverse group of other neoplasms that involve the pleura; the most common by far is metastatic carcinoma, usually of pulmonary origin. Other metastatic tumors of varied histogenesis do occur but are less common. Primary pleural neoplasms other than diffuse malignant mesothelioma are either uncommon or rare and have received less attention. Objective.--To provide a review of those diverse tumors that can involve the pleura other than mesothelioma in order to facilitate their accurate diagnosis. Data Sources.--Review of relevant literature published via PubMed and other search engines. Conclusions.--A wide variety of tumors can involve the pleura. In most cases, the approach of considering the morphologic features with appropriate immunohistochemistry, in the correct clinical context, allows for a confident diagnosis. For a number of those soft tissue tumors that are well recognized in the pleura, such as solitary fibrous tumor, desmoid-type fibromatosis, synovial sarcoma, and epithelioid hemangioendothelioma, novel markers now exist based on an understanding of the individual tumors' molecular characteristics. Primary pleural lymphomas are rare with poor prognosis. They represent localized specific diffuse large B-cell lymphomas, with either post-germinal center B-cell or plasma cell lineage, arising in the context of either immunodeficiency or immune sequestration and with viral infection. doi: 10.5858/arpa.2017-0537-RA, The World Health Organization (WHO) classification of tumors of the pleura recognizes, based on morphology codes, 3 broad histogenetic classes of neoplasm, namely mesothelial tumors, mesenchymal tumors, and lymphoproliferative disorders. [...]

Objectives: Recombinant granulocyte colony‐stimulating factor (G‐CSF) is frequently administered to patients with cancer to enhance granulocyte recovery post‐chemotherapy. Clinical trials have also used G‐CSF to modulate myeloid cell function in pregnancy and inflammatory diseases. Although the contribution of G‐CSF to expanding normal granulocytes is well known, the effect of this cytokine on the phenotype and function of immunosuppressive granulocytic cells remains unclear. Here, we investigate the impact of physiological and iatrogenic G‐CSF on an as yet undescribed granulocyte phenotype and ensuing outcome on T cells in the settings of cancer and pregnancy. Methods: Granulocytes from patients treated with recombinant G‐CSF, patients with late‐stage cancer and women enrolled on a trial of recombinant G‐CSF were phenotyped by flow cytometry. The ability and mechanism of polarised granulocytes to suppress T‐cell proliferation were assessed by cell proliferation assays, flow cytometry and ELISA. Results: We observed that G‐CSF leads to a significant upregulation of CD14 expression on CD15+ granulocytes. These CD15+CD14+ cells are identified in the blood of patients with patients undergoing neutrophil mobilisation with recombinant G‐CSF, and physiologically in women early in pregnancy or in those treated as a part of a clinical trial. Immunohistochemistry of tumor tissue or placental tissue identified the expression of G‐CSF. The G‐CSF upregulates the release of reactive oxygen species (ROS) in CD15+CD14+ cells leading to the suppression of T‐cell proliferation. Conclusions: G‐CSF induces a population of ROS+ immunosuppressive CD15+CD14+ granulocytes. Strategies for how recombinant G‐CSF can be scheduled to reduce effects on T‐cell therapies should be developed in future clinical studies. [ABSTRACT FROM AUTHOR]

Background: The etiology of male breast cancer (MBC) is poorly understood. In particular, the extent to which the genetic basis of MBC differs from female breast cancer (FBC) is unknown. A previous genome-wide association study of MBC identified 2 predisposition loci for the disease, both of which were also associated with risk of FBC.Methods: We performed genome-wide single nucleotide polymorphism genotyping of European ancestry MBC case subjects and controls in 3 stages. Associations between directly genotyped and imputed single nucleotide polymorphisms with MBC were assessed using fixed-effects meta-analysis of 1380 cases and 3620 controls. Replication genotyping of 810 cases and 1026 controls was used to validate variants with P values less than 1 × 10-06. Genetic correlation with FBC was evaluated using linkage disequilibrium score regression, by comprehensively examining the associations of published FBC risk loci with risk of MBC and by assessing associations between a FBC polygenic risk score and MBC. All statistical tests were 2-sided.Results: The genome-wide association study identified 3 novel MBC susceptibility loci that attained genome-wide statistical significance (P < 5 × 10-08). Genetic correlation analysis revealed a strong shared genetic basis with estrogen receptor-positive FBC. Men in the top quintile of genetic risk had a fourfold increased risk of breast cancer relative to those in the bottom quintile (odds ratio = 3.86, 95% confidence interval = 3.07 to 4.87, P = 2.08 × 10-30).Conclusions: These findings advance our understanding of the genetic basis of MBC, providing support for an overlapping genetic etiology with FBC and identifying a fourfold high-risk group of susceptible men. [ABSTRACT FROM AUTHOR]

A random beamforming scheme for the Gaussian MIMO broadcast channel with channel quality feedback is investigated and extended. Considering the case where the receivers each have receive antennas, the effects of feeding back various amounts of signal-to-interference-plus-noise ratio (SINR) information are analyzed. Using the results from order statistics of the ratio of a linear combination of exponential random variables, the distribution function of the maximum order statistic of the SINR observed at the receiver is found. The analysis from viewing each antenna as an individual user is extended to allow combining at the receivers, where it is known that the linear MMSE combiner is the optimal linear receiver and the CDF for the SINR after optimal combining is derived. Analytically, using the Delta Method, the asymptotic distribution of the maximum order statistic of the SINR with and without combining is shown to be, in the nomenclature of extreme order statistics, of type 3. The throughput of the feedback schemes are shown to exhibit optimal scaling asymptotically in the number of users. Finally, to further reduce the amount of feedback, a hard threshold is applied to the SINR feedback. The amount of feedback saved by implementing a hard threshold is determined and the effect on the system throughput is analyzed and bounded. [ABSTRACT FROM AUTHOR]

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Background: The etiology of male breast cancer (MBC) is poorly understood. In particular, the extent to which the genetic basis of MBC differs from female breast cancer (FBC) is unknown. A previous genome-wide association study of MBC identified 2 predisposition loci for the disease, both of which were also associated with risk of FBC., Methods: We performed genome-wide single nucleotide polymorphism genotyping of European ancestry MBC case subjects and controls in 3 stages. Associations between directly genotyped and imputed single nucleotide polymorphisms with MBC were assessed using fixed-effects meta-analysis of 1380 cases and 3620 controls. Replication genotyping of 810 cases and 1026 controls was used to validate variants with P values less than 1 × 10-06. Genetic correlation with FBC was evaluated using linkage disequilibrium score regression, by comprehensively examining the associations of published FBC risk loci with risk of MBC and by assessing associations between a FBC polygenic risk score and MBC. All statistical tests were 2-sided., Results: The genome-wide association study identified 3 novel MBC susceptibility loci that attained genome-wide statistical significance (P < 5 × 10-08). Genetic correlation analysis revealed a strong shared genetic basis with estrogen receptor-positive FBC. Men in the top quintile of genetic risk had a fourfold increased risk of breast cancer relative to those in the bottom quintile (odds ratio = 3.86, 95% confidence interval = 3.07 to 4.87, P = 2.08 × 10-30)., Conclusions: These findings advance our understanding of the genetic basis of MBC, providing support for an overlapping genetic etiology with FBC and identifying a fourfold high-risk group of susceptible men., (© The Author(s) 2020. Published by Oxford University Press.)