No abstract

In spite of a hundred year long history of scientific research compulsive buying has been a hardly known phenomenon until today. Ambiguous scientific information makes it impossible to classify compulsive buying as a separate mental disorder. Recently many researchers have noticed phenomenological compatibility of compulsive buying with behavioural addictions. Nowadays, there is reasonable grounds that compulsive buying disorder can be defined as an addiction. There are many similarities occurring between a consumer type behaviours in compulsive buyers and a pathologic consumption of psychoactive substances which included the obsessive need to consumer or a compulsion to consume, personal dependence and loss of control over self-behaviour, as well as tendencies to the consumption increase. Compulsive buying disorder differs in its course from the compulsive behaviours. A strong compulsion to make a given activity, often impossible to restrain is associated with overwhelming but acceptable desire to purchase a specific item. Due to the latest information about the described phenomenon, it has been decided to present current knowledge of adequate classifications, epidemiology and therapy of compulsive buyers. In the article authors' own standpoint as regards pathogenesis and potential risk factors was described.

ADAMs are a family of transmembrane proteins described for the first time in the 1990's. ADAMs is an abbreviation of "A Disintegrin and Metallo-proteinases". Their earliest known role was involvement in gamete fusion, and their adhesion properties in intercellular interactions also suggested involvement in tumor biology. Further research emphasized the importance of ADAM proteins in the regulation of neoplastic processes due to their influence on adhesion, cell migration, proteolysis and cell signaling. Variable ADAM expression in cancer and normal tissue was the basis for considering these proteins as diagnostic markers. Recent numerous studies have been published suggesting the prognostic value of this protein family members. The ADAMs transmembrane proteins regulate processes associated with carcinogenesis and neoplastic progression, including immune response evasion, growth induction and metastasis. Proteolysis and shedding of membrane proteins and binding integrins by ADAMs lead to the activation of numerous growth factors, changes in the extracellular matrix, adhesion proteins and angiogenesis. ADAMs potential as prognostic and diagnostic markers in cancer treatment is a particularly interesting issue and has great practical significance. There are many new studies concerning ADAMs' roles in carcinogenesis, but there are no recent reviews of the latest developments in this field. The aim of this systematic review is to analyze the results of studies published on ADAMs in the last 5 years, to present their roles in neoplasm pathogenesis and their potential utility in clinical oncology.

No abstract

Background Tumor initiation and subsequent progression are usually long-term processes, spread over time and conditioned by diverse aspects. Many cancers develop on the basis of chronic inflammation; however, despite dozens of years of research, little is known about the factors triggering neoplastic transformation under these conditions. Molecular characterization of both pathogenetic states, i.e., similarities and differences between chronic inflammation and cancer, is also poorly defined. The secretory activity of tumor cells may change the immunophenotype of immune cells and modify the extracellular microenvironment, which allows the bypass of host defense mechanisms and seems to have diagnostic and prognostic value. The phenomenon of immunosuppression is also present during chronic inflammation, and the development of cancer, due to its duration, predisposes patients to the promotion of chronic inflammation. The aim of our work was to discuss the above issues based on the latest scientific insights. A theoretical mechanism of cancer immunosuppression is also proposed. Conclusions Development of solid tumors may occur both during acute and chronic phases of inflammation. Differences in the regulation of immune responses between precancerous states and the cancers resulting from them emphasize the importance of immunosuppressive factors in oncogenesis. Cancer cells may, through their secretory activity and extracellular transport mechanisms, enhance deterioration of the immune system which, in turn, may have prognostic implications.

A total of 94 patients with colorectal cancer (CRC) were included in this study. Lymphocytic infiltration of CD45+ cells in the normal colon was more pronounced than that in the paired tumor stroma (p = 0.0008). The mean immunoscore of CD45+TILs was decreased in CRC compared with the controls (p = 0.0010). The percentage of CD3+ cells was higher in stage II than in stage IV (p = 0.0218) and showed a negative correlation with the TNM classification (r = -0.2867, p = 0.0109). The number of stromal CD4+TILs was higher in stage I than in stage III (p = 0.0116) and IV (p = 0.0104), and there was a negative correlation between this number and the stage (r = -0.3708, p = 0.0008). There was a positive correlation between the Ki-67 and CD45+ (r = 0.2468, p = 0.0294), CD3+ (r = 0.3822, p = 0.0006), and CD4+ cells (r = 0.5465, p < 0.0001). The levels of cancer-associated fibroblast (CAF) markers such as α-SMA, thrombin and fibronectin were significantly higher in CRC than in normal colonic mucosa. The immunohistochemical expression of α-SMA was negatively correlated with TILs, while fibronectin showed positive coexpression. A higher number of cells expressing IL-2Rα, PD-L1, CD33 and CD14 were found in colorectal adenocarcinomas than in controls. The number of CD14+ cells was also dependent on the TNM stage (p = 0.0444) and tumor budding (p = 0.0324). These findings suggest a suppressive impact of CRC on the adaptive immune response and emphasize the importance of CAFs in regulating tumor immunity.

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

The impact of the post-mortem interval (PMI) on the optical molecular characteristics of the colonic mucosa and the gut-associated lymphoid tissue (GALT) were examined by multi-parametric measurements techniques. Inflammatory cells were identified by immunohistochemical staining. Molecular parameters were estimated using the Raman spectroscopy (RS) and Fourier Transform Infrared (FTIR) spectroscopic imaging. The 3D refractive index (3D-RI) distributions of samples were determined using the digital holographic tomography. The distribution of immune cells between post-mortem (PM) and normal controls did show significant differences for CD4 (P = 0.0016) or CD8 (P < 0.0001), whose expression level was decreased in PM cases. No association was found between individual PMI values and inflammatory cell distribution. However, there was a tendency for a negative correlation between CD4+ cells and PMI (r = − 0.542, P = 0.032). The alterations ongoing in post-mortem tissue may suggest that PMI has a suppressive effect on the effector properties of the cell-mediated immunity. Moreover, it was confirmed that spectroscopic and digital holotomographic histology are also a useful technique for characterization of the differences in inflammation of varying intensity and in GALT imaging in a solid tissue. Anatomical location of immune cells and methods of tissue fixation determine the molecular and optical parameters of the examined cases.