Histology and histopathology Vol.25, nº8 (2010)
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- PublicationOpen AccessSudan Black B treatment reduces autofluorescence and improves resolution of in situ hybridization specific fluorescent signals of brain sections(Murcia: F. Hernández, 2010) Oliveira, V.C.; Carrara, R.C.V.; Simoes, D.L.C.; Saggioro, F.P.; Carlotti, C.G.; Covas, D.T., Jr.; Neder, L.Interference by autofluorescence is one of the major concerns of immunofluorescence analysis of in situ hybridization-based diagnostic assays. We present a useful technique that reduces autofluorescent background without affecting the tissue integrity or direct immunofluorescence signals in brain sections. Using six different protocols, such as ammonia/ethanol, Sudan Black B (SBB) in 70% ethanol, photobleaching with UV light and different combinations of them in both formalin-fixed paraffin-embedded and frozen human brain tissue sections, we have found that tissue treatment of SBB in a concentration of 0.1% in 70% ethanol is the best approach to reduce/eliminate tissue autofluorescence and background, while preserving the specific fluorescence hybridization signals. This strategy is a feasible, non-time consuming method that provides a reasonable compromise between total reduction of the tissue autofluorescence and maintenance of specific fluorescent labels.
- PublicationOpen AccessNew advances on critical implications of tumorand metastasis-initiating cells in cancer progression, treatment resistance and disease recurrence(Murcia: F. Hernández, 2010) Mimeault, M.; Batra, Surinder K.Accumulating lines of experimental evidence have revealed that the malignant transformation of multipotent tissue-resident adult stem/progenitor cells into cancer stem/progenitor cells endowed with a high self-renewal capacity and aberrant multilineage differentiation potential may be at origin of the most types of human aggressive and recurrent cancers. Based on new cancer stem/progenitor cell concepts of carcinogenesis, it is suggested that a small subpopulation of highly tumorigenic and migrating cancer stem/progenitor cells, also designated as cancer- and metastasis-initiating cells, can provide critical roles for primary tumor growth, metastases at distant tissues and organs, treatment resistance and disease relapse. Particularly, cancer initiation and progression to locally invasive and metastatic stages is often associated with a persistent activation of distinct developmental signaling pathways in these immature cells during epithelialmesenchymal transition program. The signaling cascades that are often deregulated in cancer stem/progenitor cells include hedgehog, epidermal growth factor receptor (EGFR), Wnt/ß-catenin, NOTCH, polycomb gene product BMI-1 and/or stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4). Importantly, the results from recent investigations have also indicated that different cancer subtypes may harbor distinct subsets and/or number of cancer-initiating cells during cancer progression as well as before or after therapy initiation and disease recurrence. Therefore, the identification of the molecular transforming events that frequently occur in cancer- and metastasis-initiating cells versus their differentiated progenies is of immense interest to develop new targeting approach for improving current therapies against aggressive, metastatic, recurrent and lethal cancers.
- PublicationOpen AccessThe kinetics and distribution of different macrophage populations in the developing rat skin(Murcia : F. Hernández, 2010) Juniantito, Vetnizah; Izawa, Takeshi; Yamamoto Emi; Kuwamura, Mitsuru; Yamate, JyojiMacrophages play important roles in host defense and homeostasis. In contrast to adulthood, far less is known about macrophage populations in fetuses and neonates. Macrophages were evaluated in the developing rat skin at different anatomical sites (head, anterior dorsal, posterior dorsal, and abdomen) of F344 rats obtained on gestational days 18 and 20, on neonatal days 1-21, and at adult weeks 5-15. The numbers of macrophages in the epidermis, dermis or perifollicular areas that were positive for ED1 (exudative macrophages with activated phagocytosis), ED2 (resident macrophages), and OX6 (antigen-presenting cells) were evaluated. There were no differences in macrophage numbers among the anatomical sites. In the epidermis, only OX6 cells were seen, with gradually increased numbers in neonates and adults. In the dermis, many ED1 cells were already seen in fetuses, and the number peaked on neonatal day 4, and remained at that level until adulthood. By contrast, ED2 and OX6 cells began to be seen after birth and their numbers continued to increase until adulthood; ED2 cells were distributed diffusely in the dermis, whereas ED1 and OX6 cells were present exclusively in the upper dermis. In perifollicular areas, ED1, ED2 and OX6 cells began to be seen after birth, and their numbers gradually increased until adulthood. Some macrophages in dermal and perifollicular areas gave double-positive reactions to ED1+ED2+, ED1+OX6+ or OX6+ED2+. Increased mRNA levels of colony stimulating factor-1 and monocyte chemoattractant protein-1 appeared to correspond to the emergence of rat macrophages. Skin macrophages were shown to be heterogeneous in distribution and function; the information from this study should be very useful for future investigations of experimentally induced rat skin lesions.
- PublicationOpen AccessLiver fibrosis: a dynamic and potentially reversible process(Murcia : F. Hernández, 2010) Povero, Davide; Busletta, Chiara; Novo, Erica; Valfrè di Bonzo, Lorenzo; Cannito, Stefania; Paternostro, Claudia; Parola, MaurizioIn any chronic liver disease (CLDs), whatever the aetiology, reiteration of liver injury results in persisting inflammation and progressive fibrogenesis, with chronic activation of the wound healing response in CLDs, representing a major driving force for progressive accumulation of ECM components, eventually leading to liver cirrhosis. Cirrhosis is characterized by fibrous septa dividing the hepatic parenchyma into regenerative pseudo-lobules, as well as by extensive changes in vascular architecture, the development of portal hypertension and related complications. Liver fibrogenesis (i.e., the dynamic process leading to increased deposition of ECM and much more) can lead to different patterns of fibrosis and is sustained by myofibroblast-like cells (MFs) of different origin, with activated hepatic stellate cells (HSC/MFs) being the major cell type involved. Major pro-fibrogenic mechanisms also include oxidative stress, as well as derangement of epithelial-mesenchymal interactions and, as recently suggested, the process of epithelial to mesenchymal transition (EMT). Liver fibrosis has been considered traditionally as an irreversible process but experimental and clinical literature data published in the last decade have suggested that both the removal of the aetiological agent or condition, as well as an effective therapy, can result in significant regression of liver fibrosis. This is usually associated, particularly in animal models, with induction of apoptosis in MFs but, unfortunately, human HSC/MFs are much more resistant to apoptosis than murine MFs. However, clinical studies provided no unequivocal evidence for a complete reversal of cirrhosis or a significant reversal of vascular changes in conditions of established cirrhosis.
- PublicationOpen AccessAn update on the pathobiological relevance of nuclear receptors for cancers of the head and neck(Murcia : F. Hernández, 2010) Stauber, Roland H.; Wünsch, Desiree; Knauer, Shirley K.; Fetz, VerenaCancers of the head and neck are among the most common neoplasms worldwide, characterized by local tumor aggressiveness, high rate of early recurrence, development of metastasis and second primary tumors. Although disease management of head and neck cancer has improved significantly, overall survival-rates remained largely unchanged over the last decades. Thus, in addition to modern chemo-radiation treatment strategies combined with sophisticated surgery, there is still a need for molecular markers and key regulatory factors exploitable for chemoprevention and targeted therapies. A critical event in carcinogenesis is the uncontrolled modulation of genetic programs, mediated by deregulated signaling cascades, together with downstream transcriptional modulators. Hence, nuclear receptors, belonging to a superfamily of transcription factors implicated in a broad spectrum of physiological and pathophysiological processes, have also been associated with HNC. Enhanced expression of several nuclear receptors has been shown in head and neck cancer cells, and strategies targeting these molecules have been developed and tested in the clinics. In particular, the effects of retinoids targeting nuclear receptors of the thyroid hormone receptor-like receptor subfamily have been vigorously examined in large clinical chemoprevention trials. This review seeks to provide a general overview of nuclear receptors’ molecular functions and summarizes their prognostic/therapeutic relevance, as well as the (pre)clinical studies targeting nuclear receptors in HNC.
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