Proteoglycans (PGs), important constituents of the extracellular matrix, have been associated with cancer pathogenesis. Their unique structure consisting of a protein core and glycosaminoglycan chains endowed with fine modifications constitutes these molecules as capable cellular effectors important for homeostasis and contributing to disease progression. Indeed, differential expression of PGs and their interacting proteins has been characterized as specific for disease evolvement in various cancer types. Importantly, PGs to a large extent regulate the bioavailability of hormones, growth factors, and cytokines as well as the activation of their respective receptors which regulate phenotypic diversibility, gene expression and rates of recurrence in specific tumor types. Defining and targeting these effectors on an individual patient basis offers ground for the development of newer therapeutic approaches which may act as either supportive or a substitute treatment to the standard therapy protocols. This review discusses the roles of PGs in cancer progression, developing technologies utilized for the defining of the PG “signature” in disease, and how this may facilitate the generation of tailor-made cancer strategies.

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The epithelial to mesenchymal transition (EMT) program is a crucial component in the processes of morphogenesis and embryonic development. The transition of epithelial to mesenchymal phenotype is associated with numerous structural and functional changes, including loss of cell polarity and tight cell-cell junctions, the acquisition of invasive abilities, and the expression of mesenchymal proteins. The switch between the two phenotypes is involved in human pathology and is crucial for cancer progression. Extracellular matrices (ECMs) are multi-component networks that surround cells in tissues. These networks are obligatory for cell survival, growth, and differentiation as well as tissue organization. Indeed, the ECM suprastructure, in addition to its supportive role, can process and deliver a plethora of signals to cells, which ultimately regulate their behavior. Importantly, the ECM derived signals are critically involved in the process of EMT during tumorigenesis. This review discusses the multilayer interaction between the ECM and the EMT process, focusing on contributions of discrete mediators, a strategy that may identify novel potential target molecules. Developmental Dynamics 247:368-381, 2018. V C 2017 Wiley Periodicals, Inc.

A total of 27 strains of Campylobacter jejuni (24 clinical strains and three laboratory strains) were examined for the presence of point mutations in the quinolone resistance determining region (QRDR) of gyrA gene by nonradioisotopic single‐strand conformation polymorphism (non‐RI SSCP) analysis with silver stain. Direct DNA sequencing of the polymerase chain reaction (PCR)‐amplified DNA fragments confirmed the results obtained by non‐RI SSCP analysis and revealed that in clinical strains high‐level quinolone resistance [minimal inhibitory concentration (MIC) to ciprofloxacin ≥ 16 μg/ml] was closely associated with one type of single‐point mutation at codon 86 (Thr‐lle). Two strains with MICs of 8 and 1 μg/ml showed point mutations at codons 86 and 70, respectively. Furthermore, transitions at codon 119 of the gyrA QRDR were identified in 17 strains. Six types of bands were separated in a single electrophoretic step with silver stain within 2 hours after PCR amplification of the gyrA QRDR as follows: type I associated to mutation at codon 70 (Ala‐Thr), type II to mutation at codon 90 (Asp‐Asn), type III to variant with transition at 119, type IV to wild‐type, type V to mutation at codon 86 (Thr‐lle), and type VI to mutation at codon 86 (Thr‐lle) and transition at codon 119. Using four DNA extracts from Cambylobacter coli organisms as templates for amplification of the gyrA QRDR, no PCR products were obtained. Non‐RI SSCP was proved to be a simple, rapid, and useful screening method for detecting gyrA mutations associated with ciprofloxacin resistance in C. jejuni. © 1996 Wiley‐Liss, Inc.

Three different spotted-fever group rickettsiae-Rickettsia conorii, R. massiliae, and R. rhipicephali-were detected and identified by PCR-restriction fragment length polymorphism analysis in Rhipicephalus ticks collected from domestic animals in the Fokida region of Greece, where a high seroprevalence of antibodies to R. conorii was previously demonstrated. The infection rate of ticks was 1.6%. Moreover, R. conorii was isolated from one Rhipicephalus sanguineus tick.Rickettsia conorii, the causative agent of Mediterranean spotted fever, is an obligate intracellular, gram-negative bacterium that infects humans. It is transmitted by the bite of infected arthropods (1, 9). The presence of the spotted-fever group (SFG) rickettsiae in ticks has been reported in several countries (2, 6-11, 13). Many rickettsiae remain poorly characterized due to the inability to be maintained in mammalian cell culture, embryonated chicken eggs, or small rodents, which have traditionally been the standard maintenance hosts used in rickettsiology. The advents of new culture techniques, such as the shell vial-centrifugation technique, and the detection of rickettsial DNA have increased the number of rickettsial species identified (6).A seroepidemiological survey, using an immunofluorescence assay and a Western blot method, was conducted in three villages (Leukaditi, Vounichora, and Makrini) of the Greek province of Fokida in 1991. This study reported a high seroprevalence of antibodies to R. conorii in humans (46%) (1). In a culture survey of ticks from the same area, strain GS (for "Greek strain") was isolated. This strain is genetically similar to Rickettsia massiliae; moreover, R. conorii was not found (2). As a follow-up to previous studies, we focused our efforts on determining the presence and infection rate of R. conorii in field-collected ticks from the three study villages of the Fokida (Fig. 1).In the summer of 1998 (May to August), a total of 439 ticks collected from goats, sheep, and dogs were examined for the presence of SFG rickettsiae. According to standard taxonomic keys, 207 ticks were identified as Rhipicephalus sanguineus, 94 were identified as Rhipicephalus turanicus, and 138 were identified as Rhipicephalus bursa (8). Each tick was triturated in 500 l of minimum essential medium supplemented with 4% fetal calf serum and 2 mM L-glutamine. Half of the above suspension was used for the detection of rickettsial DNA by PCR, and the rest was used for the isolation of rickettsiae by the shell vial technique (3, 4, 9, 11-13). The DNA extraction from the ticks was performed using the QIAamp tissue kit (Qiagen, Hilden, Germany), according to the instructions of the manufacturer. The primer set Rp.CS.877-Rp.CS.1258n was used to amplify a 381-bp sequence of the citrate synthase gene (9). As a negative control for each tick sample, pure PCR buffer treated in the same way as the tick samples was included. As a positive control, purified DNA from R. conorii (Moroccan strain) was used. The DNA from ticks that were positive for the c...