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51.
Amalia Conti Virginia Espina Antonella Chiechi Giovanna Magagnoli Chiara Novello Laura Pazzaglia Irene Quattrini Piero Picci Lance A. Liotta Maria Serena Benassi 《Clinical & experimental metastasis》2014,31(1):15-24
We applied reverse phase protein microarrays technology to map signal pathway interactions in a discovery set of 34 soft tissue sarcoma (STS) bone metastases compared to healthy bone. Proteins associated with matrix remodeling (MMP), adhesion (FAK Y576/577, Syndecan-1), and growth/survival (IGF1R Y1135/1136, PI3K, EGFR) were elevated in metastasis compared to normal bone. Linkage between Syndecan-1, FAK Y576/577, Shc Y317, and EGFR, IGF Y1135/1136, PI3K/AKT was a prominent feature of STS bone metastasis. Elevated linkage between RANKL and 4EBP1 T37/46, EGFR, IGF1R Y1135/1136, Src Y41, Shc Y317, PI3Kp110γ was associated with short survival. Finally, we tested the hypothesis that signal pathway proteins augmented in the STS bone metastasis may provide clues to understand the subset of primary STS that metastasize. The most representative molecules identified in the discovery set were validated on an independent series of 82 primary STS by immunohistochemistry applied to a tissue microarray. The goal was to correlate the molecular profile in the primary tumors with a higher likelihood of metastasis. Elevation of activated kinase substrate endpoints IRS1 S612, 4EBP1 T37/46, FAK Y576/577 and loss of Fibronectin, were associated with a higher likelihood of metastases. These data indicate that the linkage between matrix remodeling, adhesion, and growth signaling may drive STS metastasis and can be the basis for prognostic and therapeutic strategies. 相似文献
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Santiago Nava Amalia M. Barbieri Leticia Maya Rodney Colina Atilio J. Mangold Marcelo B. Labruna José M. Venzal 《Acta tropica》2014
The aim of this work was to describe for the first time the presence of Borrelia burgdorferi sensu lato infecting ticks in Argentina. Unfed specimens of Ixodes pararicinus collected from vegetation in Jujuy Province were tested for Borrelia infection by PCR targeting the gene flagellin (fla), the rrfA-rrlB intergenic spacer region (IGS) and the 16S rDNA (rrs) gene. One male and one female of I. pararicinus collected in Jujuy were found to be positive to Borrelia infection with the three molecular markers tested. Phylogenetically, the Borrelia found in I. pararicinus from Jujuy belongs to the B. burgdorferi s.l complex, and it was similar to one of the genospecies detected in I. aragaoi from Uruguay. Also, this genospecies is closely related to two genospecies known from USA, Borrelia americana and the Borrelia sp. genospecies 1. The epidemiological risk that implies the infection with Borrelia in I. paracinus ticks from Argentina appears to be low because the genospecies detected is not suspected of having clinical relevance and there are no records of Ixodes ticks biting humans in the southern cone of South America. Further studies are needed to assess accurately if there is risk of borreliosis transmitted by ticks in South America. 相似文献
54.
Amalia Schiavetti Carlo Dominici Marco Matrunola Paolo Capocaccia Alberto Ceccamea Manuel A. Castello 《Pediatric blood & cancer》1996,26(3):201-207
The cases of two children under three years of age with primary pulmonary rhabdomyosarcoma and no associated lung malformations are reported and a review of the literature is presented. In both, complete surgical removal of the tumor was performed and histologic examination revealed embryonal subtype. Flow cytometric assessment showed a tumor-cell diploid DNA content. Postoperative radio- and chemotherapy were carried out, but in spite of treatment both girls died because of disease progression, fourteen and nine months after diagnosis. The importance of associated cystic lung malformations and DNA content in predicting clinical outcome of primary pulmonary rhabdomyosarcoma is evaluated. © 1996 Wiley-Liss, Inc. 相似文献
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56.
Peter P. Sfikakis Amalia Zografou Vassilis Viglis Aliki Iniotaki-Theodoraki Ifigenia Piskontaki George C. Tsokos Paul Sfikakis Helen Choremi-Papadopoulou 《Arthritis \u0026amp; Rheumatology》1995,38(5):649-654
Objective. In view of the critical importance of the CD28–CD80 (B7/BB1) costimulatory pathway in antigen-specific T cell activation and clonal expansion, we examined CD28 surface molecule expression in vivo, and T cell receptor/CD3-mediated and B7/BB1-costimulated T cell proliferation in vitro, in rheumatoid arthritis (RA). Methods. Two-color immunofluorescence analyses of peripheral blood and synovial fluid–derived T cells, as well as 3H-thymidine incorporation assays, were performed. Results. In the peripheral blood of 31 patients with active, untreated RA, a mean of 91% (range 48–100%) of CD4+ and 46% (range 13–82%) of CD8+ T cell subsets were CD28+, which was not significantly lower than normal. Although an overall decrease in the number of T cells was not observed, the numbers of CD28+CD8+ T cells were significantly lower in RA patients (mean 233/μl, versus 292/μl in controls), and this decrease was more pronounced in patients with severe disease (mean 172/μl). CD28 expression on peripheral CD8+ T cells in RA patients, but not in healthy individuals, correlated inversely with T cell activation as assessed by HLA–DR antigen expression. In contrast to the peripheral blood, RA synovial fluid T cells were almost exclusively CD28+, suggesting that migration of CD28+CD8+ T cells to active sites of inflammation may occur. In vitro proliferative responses of peripheral blood T cells to B7/BB1 costimulation in the presence of mitogenic doses of anti-CD3 monoclonal antibody were identical in patients with RA and healthy individuals. Conclusion. Functionally intact CD28+ T cells may contribute to the abnormal immunoregulation and joint inflammation in RA. 相似文献
57.
S. Ghazaleh Dashti Julie A. Simpson Amalia Karahalios Vivian Viallon Margarita Moreno-Betancur Lyle C. Gurrin Robert J. MacInnis Brigid M. Lynch Laura Baglietto Howard A. Morris Marc J. Gunter Pietro Ferrari Roger L. Milne Graham G. Giles Dallas R. English 《International journal of cancer. Journal international du cancer》2020,146(6):1541-1552
Adiposity increases estrogen receptor (ER)-positive postmenopausal breast cancer risk. While mechanisms underlying this relationship are uncertain, dysregulated sex-steroid hormone production and insulin signaling are likely pathways. Our aim was to quantify mediating effects of fasting insulin and free estradiol in the adiposity and ER-positive postmenopausal breast cancer association. We used data from a case–cohort study of sex hormones and insulin signaling nested within the Melbourne Collaborative Cohort Study. Eligible women, at baseline, were not diagnosed with cancer, were postmenopausal, did not use hormone therapy and had no history of diabetes or diabetes medication use. Women with ER-negative disease or breast cancer diagnosis within the first follow-up year were excluded. We analyzed the study as a cumulative sampling case–control study with 149 cases and 1,029 controls. Missing values for insulin and free estradiol were multiply imputed with chained equations. Interventional direct (IDE) and indirect (IIE) effects were estimated using regression-based multiple-mediator approach. For women with body mass index (BMI) >30 kg/m2 compared to women with BMI 18.5–25 kg/m2, the risk ratio (RR) of breast cancer was 1.75 (95% confidence interval [CI] 1.05–2.91). The estimated IDE (RR) not through the mediators was 1.03 (95% CI 0.43–2.48). Percentage mediated effect through free estradiol was 72% (IIE-RR 1.56; 95% CI 1.11–2.19). There was no evidence for an indirect effect through insulin (IIE-RR 1.12; 95% CI 0.68–1.84; 28% mediated). Our results suggest that circulating free estradiol plays an important mediating role in the adiposity–breast cancer relationship but does not explain all of the association. 相似文献
58.
Renée T. Fortner Anika Hüsing Laure Dossus Anne Tjønneland Kim Overvad Christina C. Dahm Patrick Arveux Agnès Fournier Marina Kvaskoff Matthias B. Schulze Manuela Bergmann Antonia Trichopoulou Anna Karakatsani Carlo La Vecchia Giovanna Masala Valeria Pala Amalia Mattiello Rosario Tumino Fulvio Ricceri Carla H. van Gils Evelyn M. Monninkhof Catalina Bonet José Ramón Quirós Maria-Jose Sanchez Daniel-Ángel Rodríguez-Palacios Aurelio B Gurrea Pilar Amiano Naomi E. Allen Ruth C. Travis Marc J. Gunter Vivian Viallon Elisabete Weiderpass Elio Riboli Rudolf Kaaks 《International journal of cancer. Journal international du cancer》2020,147(5):1325-1333
Endometrial cancer (EC) incidence rates vary ~10-fold worldwide, in part due to variation in EC risk factor profiles. Using an EC risk model previously developed in the European EPIC cohort, we evaluated the prevention potential of modified EC risk factor patterns and whether differences in EC incidence between a European population and low-risk countries can be explained by differences in these patterns. Predicted EC incidence rates were estimated over 10 years of follow-up for the cohort before and after modifying risk factor profiles. Risk factors considered were: body mass index (BMI, kg/m2), use of postmenopausal hormone therapy (HT) and oral contraceptives (OC) (potentially modifiable); and, parity, ages at first birth, menarche and menopause (environmentally conditioned, but not readily modifiable). Modeled alterations in BMI (to all ≤23 kg/m2) and HT use (to all non-HT users) profiles resulted in a 30% reduction in predicted EC incidence rates; individually, longer duration of OC use (to all ≥10 years) resulted in a 42.5% reduction. Modeled changes in not readily modifiable exposures (i.e., those not contributing to prevention potential) resulted in ≤24.6% reduction in predicted EC incidence. Women in the lowest decile of a risk score based on the evaluated exposures had risk similar to a low risk countries; however, this was driven by relatively long use of OCs (median = 23 years). Our findings support avoidance of overweight BMI and of HT use as prevention strategies for EC in a European population; OC use must be considered in the context of benefits and risks. 相似文献
59.
Preferential chemosensitization of PTEN-mutated prostate cells by silencing the Akt kinase 总被引:5,自引:0,他引:5
Priulla M Calastretti A Bruno P Azzariti A Amalia A Paradiso A Canti G Nicolin A 《The Prostate》2007,67(7):782-789
BACKGROUND: In prostate cancer, mutations of the phosphatase PTEN can activate the kinase cascade PI3K/Akt/mTOR which induces drug resistance. METHODS: Chemosensitization by siRNA targeting Akt was studied in HEK293 cells forced to express CA-Akt or kinase-dead DN-Akt. To decrease drug resistance, Akt was silenced with siRNA in human prostate DU-145 cell line expressing the normal PTEN or in LNCaP and PC3 cell lines expressing mutated-PTEN. Taxol was used for the chemosensitization studies. RESULTS: Silencing Akt in the drug-resistant CA-Akt cells efficiently sensitized cells to antitubule agents, whereas silencing drug-responsive DN-Akt cells did not. Only minor effects were obtained in wild-type HEK293 cells. Potentiation by siRNA of taxol cytotoxicity was significantly greater in mutated-PTEN cells than in prostate cells expressing wild-type PTEN. The apoptotic program induced by taxol was preferentially potentiated by Akt siRNA in PTEN-mutated cell lines as regards the DU-145 cell line. CONCLUSIONS: Silencing Akt in PTEN-mutated prostate cancer cells enhances the antitumor effects of taxol. No siRNA chemosensitization was obtained in prostate cells with wild type PTEN. 相似文献
60.
Paola Russo Mariateresa StiglianiLucia Prota Giulia AuriemmaCarlo Crescenzi Amalia PortaRita P. Aquino 《International journal of pharmaceutics》2013
The aim of this study was to evaluate the permeation properties of gentamicin (G) in a novel dry powder form for inhalation through an artificial mucus model. Moreover, since respiratory infections sustained by Pseudomonas are a major cause of sickness and death in CF patients, the susceptibility of P. aeruginosa to engineered G powders was investigated. 相似文献