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This article presents a descriptive review of the anatomical and imaging studies of the lymphatic system in the normal and post-operative conditions and attempts to answer the questions of why some people develop lymphoedema after cancer and some do not, and what causes the variability in lymphoedema onset timing.Protein folding is a substantively error prone process, especially when it occurs in the endoplasmic reticulum (ER). The highly exquisite machinery in the ER controls secretory protein folding, recognizes aberrant folding states, and retrotranslocates permanently misfolded proteins from the ER back to the cytosol; these misfolded proteins are then degraded by the ubiquitin-proteasome system termed as the ER-associated degradation (ERAD). The 26S proteasome is a multisubunit protease complex that recognizes and degrades ubiquitinated proteins in an ATP-dependent manner. The complex structure of the 26S proteasome requires exquisite regulation at the transcription, translation, and molecular assembly levels. this website Nuclear factor erythroid-derived 2-related factor 1 (Nrf1; NFE2L1), an ER-resident transcription factor, has recently been shown to be responsible for the coordinated expression of all the proteasome subunit genes upon proteasome impairment in mammalian cells. In this review, we summarize the current knowledge regarding the transcriptional regulation of the proteasome, as well as recent findings concerning the regulation of Nrf1 transcription activity in ER homeostasis and metabolic processes.Despite direct or indirect efforts of the proteomic community, the fraction of blind spots on the protein map is still significant. Almost 11% of human genes encode missing proteins; the existence of which proteins is still in doubt. Apparently, proteomics has reached a stage when more attention and curiosity need to be exerted in the identification of every novel protein in order to expand the unusual types of biomaterials and/or conditions. It seems that we have exhausted the current conventional approaches to the discovery of missing proteins and may need to investigate alternatives. Here, we present an approach to deciphering missing proteins based on the use of non-standard methodological solutions and encompassing diverse MS/MS data, obtained for rare types of biological samples by members of the Russian Proteomic community in the last five years. These data were re-analyzed in a uniform manner by three search engines, which are part of the SearchGUI package. The study resulted in the identification of two missing and five uncertain proteins detected with two peptides. Moreover, 149 proteins were detected with a single proteotypic peptide. Finally, we analyzed the gene expression levels to suggest feasible targets for further validation of missing and uncertain protein observations, which will fully meet the requirements of the international consortium. The MS data are available on the ProteomeXchange platform (PXD014300).Low-grade serous ovarian carcinoma (LGSOC) is a distinct pathologic and clinical entity, characterized by less aggressive biological behavior, lower sensitivity to chemotherapy and longer survival compared with high-grade serous ovarian carcinoma. LGSOC often harbors activating mutations of genes involved in mitogen activated protein kinase (MAPK) pathway. Patients with disease confined to the gonad(s) should undergo bilateral salpingo-oophorectomy, total hysterectomy and comprehensive surgical staging, although fertility-sparing surgery can be considered in selected cases. Women with stage IA-IB disease should undergo observation alone after surgery, whereas observation, chemotherapy or endocrine therapy are all possible options for those with stage IC-IIA disease. Patients with advanced disease should undergo primary debulking surgery with the aim of removing all macroscopically detectable disease, whereas neoadjuvant chemotherapy followed by interval debuking surgery. After surgery, the patients can receive either carboplatin plus paclitaxel followed by endocrine therapy or endocrine therapy alone. Molecularly targeted agents, and especially MEK inhibitors and Cyclin-dependent kinase (CDK) inhibitors, are currently under evaluation. Additional research on the genomics of LGSOC and clinical trials on the combination of MEK inhibitors with hormonal agents, other molecularly targeted agents or metformin, are strongly warranted to improve the prognosis of patients with this malignancy.Inflammatory cells are major players in the onset of cancer. The degree of inflammation and type of inflammatory cells in the tumor microenvironment (TME) are responsible for tilting the balance between tumor progression and regression. Cancer-related inflammation has also been shown to influence the efficacy of conventional therapy. Mononuclear phagocytes (MPs) represent a major component of the inflammatory circuit that promotes tumor progression. Despite their potential to activate immunosurveillance and exert anti-tumor responses, MPs are subverted by the tumor to support its growth, immune evasion, and spread. MP responses in the TME are dictated by a network of stimuli integrated through the cross-talk between activatory and inhibitory receptors. Alterations in receptor expression/signaling can create excessive inflammation and, when chronic, promote tumorigenesis. Research advances have led to the development of new therapeutic strategies aimed at receptor targeting to induce a tumor-infiltrating MP switch from a cancer-supportive toward an anti-tumor phenotype, demonstrating efficacy in different human cancers. This review provides an overview of the role of MP receptors in inflammation-mediated carcinogenesis and discusses the most recent updates regarding their targeting for immunotherapeutic purposes. We focus in particular on the TREM-1 receptor, a major amplifier of MP inflammatory responses, highlighting its relevance in the development and progression of several types of inflammation-associated malignancies and the promises of its inhibition for cancer immunotherapy.Background The rising trend in allergic diseases has developed in parallel with the increasing prevalence of obesity, suggesting a possible association. The links between eating habits and allergies have not been sufficiently clarified. Aim To evaluate the nutritional status, eating habits, and risk factors of obesity and pulmonary function in children with allergic rhinitis. Materials and methods We evaluated 106 children with allergic rhinitis (mean age 12.1 ± 3.4 years; M/F 60/46) from the Department of Allergology. Clinical data were collected regarding allergies, physical activity, nutritional status (Bodystat), dietary habits (Food Frequency Questionnaire validated for the Polish population), skin prick test with aeroallergens (Allergopharma), and spirometry (Jaeger). Results All children suffered from allergic rhinitis; among them, 43 (40.6%) presented symptoms of asthma. There were differences between children with only allergic rhinitis (AR group) and children with both rhinitis and asthma (AA group) in pulmonary function (forced expiratory volume in one second (FEV1) 100 ± 11 vs.