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The CIAO Study (“Complicated Intra-Abdominal infection Observational” Study) is a multicenter investigation performed in 68 medical institutions throughout Europe over the course of a 6-month observational period (January-June 2012).Patients with either community-acquired or healthcare-associated complicated intra-abdominal infections (IAIs) were included in the study.2,152 patients with a mean age of 53.8 years (range: 4–98 years) were enrolled in the study. 46.3% of the patients were women and 53.7% were men. Intraperitoneal specimens were collected from 62.2% of the enrolled patients, and from these samples, a variety of microorganisms were collectively identified.The overall mortality rate was 7.5% (163/2.152).According to multivariate analysis of the compiled data, several criteria were found to be independent variables predictive of patient mortality, including patient age, the presence of an intestinal non-appendicular source of infection (colonic non-diverticular perforation, complicated diverticulitis, small bowel perforation), a delayed initial intervention (a delay exceeding 24 hours), sepsis and septic shock in the immediate post-operative period, and ICU admission.Given the sweeping geographical distribution of the participating medical centers, the CIAO Study gives an accurate description of the epidemiological, clinical, microbiological, and treatment profiles of complicated intra-abdominal infections (IAIs) throughout Europe.

IntroductionSome researchers suggest that cancers located in the right vs. the left side of the colon are different and they can be regarded as distinct disease entities. The aim of this study was to analyze differences in clinical, epidemiological and pathological features of patients with right-sided (RCC) and left-sided (LCC) colon cancer.Material and methodsOne thousand two hundred and twenty-four patients were operated on due to colorectal cancer. A group of 477 patients (254 women, mean age 65.5 ±11 for the whole group) with colon cancer was included (212 RCC vs. 265 LCC).ResultsRight colon cancer patients were older (67.8 ±11.3 vs. 63.2 ±11.2; p = 0.0087). Left colon cancer patients underwent surgery for urgent indications more often (17.0% vs. 8.5%; p = 0006). Tumor diameter was greater in the RCC group (55 ±60 mm vs. 38 ±21 mm; p = 0.0003). Total number of removed lymph nodes was higher in the RCC group (11.7 ±6 vs. 8.3 ±5; p = 0.0001). Lymph node ratio was higher in the LCC group (0.45 ±0.28 vs. 0.30 ±0.25; p = 0.0063). We found a strong positive correlation between tumor diameter and the number of removed lymph nodes in the LCC group (r = 0.531).ConclusionsThese differences may result from the fact that RCC patients are diagnosed at an older age. The smaller number of removed lymph nodes in LCC patients may result in incorrect staging. It is still necessary to find other biological dissimilarities of adenocarcinoma located on different sides of the colon.

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Cancer constitutes a grave problem nowadays in view of the fact that it has become one of the main causes of death worldwide. Poor clinical prognosis is presumably due to cancer cells metabolism as tumor microenvironment is affected by oxidative stress. This event triggers adequate cellular response and thereby creates appropriate conditions for further cancer progression. Endoplasmic reticulum (ER) stress occurs when the balance between an ability of the ER to fold and transfer proteins and the degradation of the misfolded ones become distorted. Since ER is an organelle relatively sensitive to oxidative damage, aforementioned conditions swiftly cause the activation of the unfolded protein response (UPR) signaling pathway. The output of the UPR, depending on numerous factors, may vary and switch between the pro-survival and the pro-apoptotic branch, and hence it displays opposing effects in deciding the fate of the cancer cell. The role of UPR-related proteins in tumorigenesis, such as binding the immunoglobulin protein (BiP) and inositol-requiring enzyme-1α (IRE1α), activating transcription factor 6 (ATF6) or the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), has already been specifically described so far. Nevertheless, due to the paradoxical outcomes of the UPR activation as well as gaps in current knowledge, it still needs to be further investigated. Herein we would like to elicit the actual link between neoplastic diseases and the UPR signaling pathway, considering its major branches and discussing its potential use in the development of a novel, anti-cancer, targeted therapy.

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Tumoural angiogenesis is essential for the growth and spread of breast cancer cells. Therefore the aim of this study was to assess the diagnostic performance of angiogenesis markers in tumours and there reflecting levels in serum of breast cancer patients. Angiogenin, Ang2, fibroblast growth factor basic, intercellular adhesion molecule (ICAM)-1, keratinocyte growth factor (KGF), platelet-derived growth factor-BB, and VEGF-A were measured using a FASTQuant angiogenic growth factor multiplex protein assay. We observed that breast cancer tumours exhibited high levels of PDGF-BB, bFGF and VEGF, and extremely high levels of TIMP-1 and Ang-2, whereas in serum we found significantly higher levels of Ang-2, PDGF-BB, bFGF, ICAM-1 and VEGF in patients with breast cancer compared to the benign breast diseases patients. Moreover, some of these angiogenesis markers evaluated in tumour and serum of breast cancer patients exhibited association with standard clinical parameters, ER status as well as MVD of tumours. Angiogenesis markers play important roles in tumour growth, invasion and metastasis. Our results suggest that analysis of angiogenesis markers in tumour and serum of breast cancer patients using multiplex protein assay can improve diagnosis and prognosis in this diseases.

Background: Cancer cell invasion requires integrins for adhesion/de-adhesion and MMPs for focalized proteolysis. Results: MMP-2 is up-regulated in invasive colorectal tumors and degrades ␤1 integrins. Conclusion: Shedding of the I-like domain from ␤1 integrins results in decreased adhesion and enhanced cell motility. Significance: MMP-2 amplifies the motility of cancer cells, not only degrading extracellular matrix but also reducing the ␤1 integrin expression.