36 research outputs found

    Local reactions to tick bites

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    A retrospective histological and immunohistochemical study has been carried out in 25 cases of tick bites recorded in our Departments. The samples that included an attached tick showed a cement cone anchoring the mouthparts to the skin and a blood-soaked, spongiform appearance of the superficial dermis, with a mild neutrophilic and eosinophilic infiltration. The vessels displayed a loose multilayered endothelial proliferation, with plump endothelia, permeated with erythrocytes. A few of them were severed, allowing copious blood extravasation. The established lesions included the following: erythema chronicum migrans-like cases, foreign body granulomas-sometimes containing remnants of the mouthparts-cutaneous lymphoid hyperplasia, either of the T-cell or the B-cell type, and tick-bite alopecia. In both the T-cell and B-cell pseudolymphomas, several vessels showed concentric endothelial and perithelial proliferation similar to that seen in the acute lesions. In the tick-bite alopecia, a lymphocytic infiltrate attacked the permanent portion of the hair follicles, whose reaction was a noticeable hyperplasia of the fibrous sheaths, although only a minority of the hairs was destroyed. The observed alterations are specific in the acute lesions and in the alopecia, where they directly arise as a result of the interactions between the host's tissues and the antihemostatic, anti-inflammatory, and immunomodulatory chemicals contained in the tick saliva. In the other lesions, the changes seem less characteristic, although the fragments of mouthparts and the special vascular changes provide a clue to their etiolog

    Reelin expression in human prostate cancer: a marker of tumor aggressiveness based on correlation with grade.

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    Reelin is a glycoprotein that plays a critical role in the regulation of neuronal migration during brain development and, since reelin has a role in the control of cell migration, it might represents an important factor in cancer pathology. In this study, 66 surgical specimens of prostate cancer were analyzed for reelin expression by immunohistochemical method. The reelin expression was correlated with Gleason score and individual Gleason patterns. Reelin expression was found in 39% prostate cancers. Stromal tissues, normal epithelial cells and prostate intraepithelial neoplasia (PIN) of any grade around and distant from cancer were always negative for reelin. Reelin was found in malignant prostatic epithelial glands of 50% cases Gleason score 10, 52% Gleason score 9, 56% Gleason score 8, 18% Gleason score 7, while no sample of prostate cancers with Gleason score 6 showed reelin expression (P=0,005). As reelin staining is frequently found in high Gleason score prostate cancers, we explored whether reelin expression is influenced by single Gleason patterns

    Havep53 gene mutations and protein expression a different biological significance in colorectal cancer?

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    p53 alterations are considered the most common genetic events in many types of neoplasms, including colorectal carcinoma (CRC). These alterations include mutations of the gene and/or overexpression of the protein. The aim of our study was to assess whether in 160 patients undergoing resective surgery for primary operable CRC there was an association between p53 mutations and protein over-expression and between these and other biological variables, such as cell DNA content (DNA-ploidy) and S-phase fraction (SPF), and the traditional clinicopathological variables. p53 mutations, identified by PCR-SSCP-sequencing analysis, were found in 68/160 patients (43%) and positive staining for p53 protein, detected with the monoclonal antibody DO-7, was present in 48% (77/160) of the cases, with agreement of 57% (91/160). In particular, a significant association was found between increased p53 expression and genetic alterations localized in the conserved regions of the gene or in the L3 DNA-binding domain and the specific type of mutation. Furthermore, both overexpression of p53 and mutations in the conserved areas of the gene were found more frequently in distal than in proximal CRCs, suggesting that they might be "biologically different diseases." Although p53 mutations in conserved areas were associated with flow cytometric variables, overexpression of p53 and mutations in its L3 domain were only related respectively to DNA-aneuploidy and high SPF. These data may reflect the complex involvement of p53 in the different pathways regulating cell-cycle progression. In conclusion, the combination of the mutational status and immunohistochemistry of p53, and flow cytometric data may provide an important insight into the biological features of CRCs

    TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

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    The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutations in K-Ras. p16INK4A promoter hypermethylation was found in 14% (4/28) of PAs and 100% (5/5) carcinomas. All genetic and epigenetic alterations were detected exclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggests that TP53 mutations and p16INK4A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in the malignant progression of PA into carcinoma. J. Cell. Physiol. 207: 654–659, 2006. 2006 Wiley-Liss, Inc

    Detection and quantification of mammaglobin in the blood of breast cancer patients: can it be useful as a potential clinical marker? Preliminary results of a GOIM (Gruppo Oncologico dell'Italia Meridionale) prospective study.

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    BACKGROUND: Mammaglobin is expressed mainly in mammary tissue, overexpressed in breast cancer (BC) and rarely in other tissue. The aim of this study was to assess the sensitivity and specificity of transcript MGB1 detection and to evaluate the role of MGB1 as potential clinical marker for the detection of disseminated cancer cells in the blood of BC patients. PATIENTS AND METHODS: A consecutive series of 23 BC tissues, 36 peripheral blood BC samples and 35 healthy peripheral blood samples was prospectively recruited to investigate MGB1 expression by means of a quantitative Real Time RT-PCR assay. RESULTS: MGB1 overexpression in tissue samples of BC patients is significantly associated only with high level of Ki67 (P <0.05). None of the samples from peripheral blood of 35 healthy female individuals were positive for MGB1 transcript. In contrast MGB1 mRNA expression was detected in three of 36 (8%) peripheral blood of BC patients. CONCLUSIONS: Our preliminary results demonstrate that the detection of MGB1 transcript in peripheral blood of BC patients was specific but with low sensitivity. MGB1 overexpression by itself or in combination with Ki67 might be considered an index of BC progression

    TP53 mutations and S-Phase fraction are independent prognostic indicators in locally advanced laryngeal squamous cell carcinoma

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    Larynx tumor is a rare neoplasia that represent only the 2% of all human tumor. In particular, the 90% of tumor that occur in this organ correspond to the laryngeal squamous cell carcinoma (LSCC). From the biomolecular point of view, it was shown that the TP53 gene mutations are the most common events observed in the early phases of LSCC carcinogenesis. However, them prognostic significance remains controversial. Besides, the prognostic significance of DNA ploidy has been well established for other solid tumors, but its role in LSCC is still controversial. The aim of this study was, therefore, to prospectively evaluate the prognostic significance of TP53 mutations, DNA-ploidy and S-phase fraction (SPF) in LSCC patients. Prospective analysis of 81 patients who underwent resective surgery for primary operable locally advanced LSCC patients (stages III and IV) was performed. Tumor DNA was screened for TP53 mutations by PCR/SSCP and sequencing; DNA flow cytometry was performed on mechanically disaggregated sample of frozen tumor tissue. The median follow-up time in our study group was 71 months (range 11-137 months). Fourthy-four percent of patients (36/81) have, at least, a mutation in the TP53 gene. Of them, 22% (8/36) have double mutations and 6% (2/36) have triple mutations. In total, 47 TP53 mutations were observed. The majority (42%) of these occur in exon 5 (20/47), while the mutations in exons 6, 7 and 8 are represented in 14, 7 and 6 patients respectively (30%, 15% and 13%). The flow cytometry analysis showed that sixty-three percent of the cases (51/81) were DNA aneuploidy and 14% of these (7/51) were multiclonal. LSCC patients were divided into two groups using median SPF level as cut-off point: low SPF 15.1 % and high SPF >15.1 %, Even though it seems that TP53 mutations promotes the LSCC carcinogenesis in young people (p< 0.05), there was not any association between this variable and the clinicopathological or the other biomolecular variables. At univariate analysis, the Kaplan and Meier text show that DNA aneuploidy, high SPF, any TP53 mutations and, in particular, the mutations that occur in exons 5 and 8 proved to be significantly related to quicker disease relapse and short OS. At multivariate analysis, the Cox proportional hazards model show that the major significant predictors for both disease relapse and death were high SPF and any TP53 mutations. In conclusion, any TP53 mutations, more than specific mutations in exon 5 and 8, are important biological indicators to predict the outcome of patients indicating these mutations have biological relevance in terms of LSCC disease course. Our study has also identify high SPF as independent prognostic factors in locally advanced LSCC patients

    Perineural pattern of aggregation of cellular blue nevus: probable histoarchitectural reminiscence of histogenesis

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    A striking feature of cellular blue nevus consists in the presence, in its histologic picture, of numerous hypertrophic nerves and nerve-like figures, positive for histochemical and immunohistochemical methods for nerve fibers and myelin sheaths. These findings, first described in Masson's original article and repeatedly highlighted in the past for their possible histogenetic significance, are currently considered as merely coincidental. However, the thin conventional histologic sections, catching only short tracts of the nerves, preclude a correct observation of their route and do not allow us to verify if there is an architectural relationship between them and the nevus as a whole. With this aim, we observed a few specimens of cellular blue nevus on digitally overlapped images of contiguous 25-[mu]m-thick sections, processed with Winkelmann's technique of silver impregnation for nerve fibers, which supplied an overall, 3-dimensional view of the lesions and the nerves running through them. In these images, the lobular form of the nevus could be seen gathering around a branching hypertrophic nerve, whose stem stretched vertically from the depth to the most superficial tract of the lesion. The nevus cell aggregates invested the stem and the limbs individually, and these followed the curvilinear contour of the nevus lobules. Our images represent evidence of a preferential perineural aggregation of cellular blue nevus, at least in its lobular form. This indicates that the numerous nerves and the neuroid figures, observed in detail-but within a limited perspective- in the conventional sections, are not merely coincidental and they could indeed be a sign of neural differentiation and/or a clue to the possible neural origin of the nevu
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