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Background: Breast cancer is a metabolically heterogeneous disease, and although the concept of heterogeneous cancer metabolism is known, its precise role in human breast cancer is yet to be fully elucidated. Methods: We investigated in an explorative approach a cohort of 42 primary mamma carcinoma patients with positron emission tomography/magnetic resonance imaging (PET/MR) prior to surgery, followed by histopathology and molecular diagnosis. From a subset of patients, which showed high metabolic heterogeneity based on tracer uptake and pathology classification, tumour centre and periphery specimen tissue samples were further investigated by a targeted breast cancer gene expression panel and quantitative metabolomics by nuclear magnetic resonance (NMR) spectroscopy. All data were analysed in a combinatory approach. Results: [18F]FDG (2‐deoxy‐2‐[fluorine‐18]fluoro‐d‐glucose) tracer uptake confirmed dominance of glucose metabolism in the breast tumour centre, with lower levels in the periphery. Additionally, we observed differences in lipid and proliferation related genes between luminal A and B subtypes in the centre and periphery. Tumour periphery showed elevated acetate levels and enrichment in lipid metabolic pathways genes especially in luminal B. Furthermore, serine was increased in the periphery and higher expression of thymidylate synthase (TYMS) indicated one‐carbon metabolism increased in tumour periphery. The overall metabolic activity based on [18F]FDG uptake of luminal B subtype was higher than that of luminal A and the difference between the periphery and centre increased with tumour grade. Conclusion: Our analysis indicates variations in metabolism among different breast cancer subtypes and sampling locations which details the heterogeneity of the breast tumours. Correlation analysis of [18F]FDG tracer uptake, transcriptome and tumour metabolites like acetate and serine facilitate the search for new candidates for metabolic tracers and permit distinguishing luminal A and B. This knowledge may help to differentiate subtypes preclinically or to provide patients guide for neoadjuvant therapy and optimised surgical protocols based on individual tumour metabolism. [ABSTRACT FROM AUTHOR]

Reticulocalbin‐1 (RCN1) is expressed aberrantly and at a high level in various tumors, including acute myeloid leukemia (AML), yet its impact on AML remains unclear. In this study, we demonstrate that RCN1 knockdown significantly suppresses the viability of bone marrow mononuclear cells (BMMNCs) from AML patients but does not affect the viability of granulocyte colony‐stimulating factor (G‐CSF)‐mobilized peripheral blood stem cells (PBSCs) from healthy donors in vitro. Downregulation of RCN1 also reduces the viability of AML cell lines. Further studies showed that the RCN1 knockdown upregulates type I interferon (IFN‐1) expression and promotes AML cell pyroptosis through caspase‐1 and gasdermin D (GSDMD) signaling. Deletion of the mouse Rcn1 gene inhibits the viability of mouse AML cell lines but not the hematopoiesis of mouse bone marrow. In addition, RCN1 downregulation in human AML cells significantly inhibited tumor growth in the NSG mouse xenograft model. Taken together, our results suggest that RCN1 may be a potential target for AML therapy. [ABSTRACT FROM AUTHOR]

Cervical squamous cell carcinoma (CSCC) is one of the leading causes of cancer death in women worldwide. Patients with advanced cervical carcinoma always have a poor prognosis once resistant to cisplatin due to the lack of effective treatment. It is urgent to investigate the molecular mechanisms of cisplatin resistance. Circular RNAs (circRNAs) are known to exert their regulatory functions in a series of malignancies. However, their effects on CSCC remain to be elucidated. Here, we found that cytoplasmic circARHGAP5, derived from second and third exons of the ARHGAP5 gene, was downregulated in cisplatin‐resistant tissues compared with normal cervix tissues and untreated cervical cancer tissues. In addition, experiments from overexpression/knockdown cell lines revealed that circARHGAP5 could inhibit cisplatin‐mediated cell apoptosis in CSCC cells both in vitro and in vivo. Mechanistically, circARHGAP5 interacted with AU‐rich element RNA‐binding protein (AUF1) directly. Overexpression of AUF1 could also inhibit cell apoptosis mediated by cisplatin. Furthermore, we detected the potential targets of AUF1 related to the apoptotic pathway and found that bcl‐2‐like protein 11 (BIM) was not only negatively regulated by AUF1 but positively regulated by circARHGAP5, which indicated that BIM mRNA might be degraded by AUF1 and thereby inhibited tumor cell apoptosis. Collectively, our data indicated that circARHGAP5 directly bound to AUF1 and prevented AUF1 from interacting with BIM mRNA, thereby playing a pivotal role in cisplatin resistance in CSCC. Our study provides insights into overcoming cancer resistance to cisplatin treatment. [ABSTRACT FROM AUTHOR]

Lung cancer is a very aggressive cancer characterized with molecular heterogeneities in different subtypes, including lung adenocarcinoma and lung squamous cell carcinoma. However, few related molecular signatures have been established for the treatment of lung cancer subtypes. Polo‐like kinase (PLK) family is a crucial regulator during cell division. Aberrant genetic and epigenetic alteration of PLK members plays a controversial role among different cancers. In this study, we performed an analysis of transcriptional and protein expression to identify overexpressed PLK1/4 and under‐expressed PLK2/3 in lung cancer subtypes. We then analysed biological function of PLKs and related genes. Besides, we estimated a correlation of PLKs with patient's genders and TP53 mutation in lung cancer. Higher PLK1/4 expression was significantly associated with male patient and TP53 mutant status, separately. Moreover, we carried out a methylation profile analysis including methylation level, DNA methyltransferases correlation and survival analysis of global methylation. Global methylation survival analysis showed that prognostic value of PLK1/2/4 methylation remained the same significant trend between two lung cancer subtypes, whereas prognostic value of PLK3 methylation lacked consistency. Taken together, these results provided instructive insights into a comprehensive evaluation for advanced therapeutic strategy based on epigenetic evidences. [ABSTRACT FROM AUTHOR]

Polypyrrole (PPy)/montmorillonite (MMT) nanocompounds were prepared by in situ chemical oxidative polymerization of pyrrole in the presence of MMT. The results indicate PPy is intercalated into MMT interlayers and the morphology of obtained PPy in nanocompounds is changed to flake-like rather than granular particles as pristine PPy. The resultant PPy/MMT nanocompounds and pristine PPy were used as microwave absorbing filler separately to prepare microwave absorbing PPy/MMT and PPy epoxy composites. The results indicate PPy/MMT epoxy composites exhibit much better microwave absorbing properties than those filled by pristine PPy. The maximum reflection loss of 20 wt% PPy/MMT filled composite is −32.63 dB at 10.55 GHz with a matching thickness of 2.8 mm, and the effective absorption bandwidth with the reflection loss below −10 dB is from 8.6 GHz to 12.4 GHz, which almost covers the whole X-band. We postulated that the morphology change of PPy in PPy/MMT and its better dispersion may be responsible for the enhancement of microwave absorption. POLYM. COMPOS., 37:532-538, 2016. © 2014 Society of Plastics Engineers [ABSTRACT FROM AUTHOR]

Low‐cost, low‐power wireless sensor nodes that operate in Cauchy noise are required for applications that are located near highly trafficked roads, highways, and bridges, where solar or other green power operation is desirable. A novel suboptimal Cauchy detector of notable simplicity, suitable for low‐power sensor nodes, is proposed. The novel suboptimal detector approaches the performance of the optimal detector very closely while surpassing the performance of popular previously published suboptimal Cauchy detectors by 1–4 dB. [ABSTRACT FROM AUTHOR]