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Bertani H.,Endoscopia digestiva | Frazzoni M.,Fisiopatologia Digestiva | Dabizzi E.,Endoscopia digestiva | Pigo F.,Endoscopia digestiva | And 5 more authors.
Digestive Diseases and Sciences | Year: 2013

Background: Probe-based confocal laser endomicroscopy (pCLE) is a new technique allowing in vivo detection of neoplastic tissue using a standard endoscope. Aims: Our aim was to compare the incident dysplasia detection rate of biopsies obtained by high-definition white light endoscopy (HD-WLE) or by pCLE in a cohort of patients with Barrett's esophagus (BE) participating in a surveillance program. Methods: Fifty of 100 patients underwent pCLE in addition to HD-WLE. Four-quadrant biopsy specimens according to the Seattle biopsy protocol were obtained in all patients to ensure standard-of-care. Diagnosis of dysplasia/neoplasia was made by a blinded gastrointestinal pathologist. Results: Incident high-grade dysplasia (HGD) and low-grade dysplasia (LGD) were diagnosed in 3/100 and in 16/100 cases. In the HD-WLE group, areas suspicious for neoplasia were not observed and dysplasia was diagnosed in 5/50 (10 %) patients (one with HGD). In the pCLE group, areas suspicious for neoplasia were observed by pCLE in 21/50 (42 %) patients; dysplasia was confirmed in 14 cases (28 %) (two with HGD). The dysplasia detection rate was significantly higher in the pCLE group than in the HD-WLE group (P = 0.04). The sensitivity, specificity, positive and negative predictive values of pCLE for dysplasia were 100, 83, 67, and 100 %, respectively. Conclusions: Incident dysplasia can be more frequently detected by pCLE than by HD-WLE in BE. The higher dysplasia detection rate provided by pCLE could improve the efficacy of BE surveillance programs. © 2012 Springer Science+Business Media, LLC. Source


Bellevicine C.,University of Naples Federico II | Vita G.D.,Anatomia Patologica | Malapelle U.,University of Naples Federico II | Troncone G.,University of Naples Federico II
Seminars in Diagnostic Pathology | Year: 2013

In an increased number of settings, cytology represents the only source of sampling and it often substitutes histology as an independent diagnostic modality. Thus, DNA molecular targets to stratify patients for targeted therapy are often evaluated on cytology. In addition, DNA mutational tests may refine indeterminate thyroid and pancreas cytology. This review discusses the applications and limitations of DNA mutational testing on cytology. With respect to histology, most cytological samples have the advantages of a purer population of tumor cells, with low stromal component, a better preserved DNA, and assessing at the same time of sample collection cellular adequacy for DNA testing. However, since in vitro diagnostic tests are licensed only for paraffin-tissue, all mutational assays on cytology are "home brew," requiring a rigorous validation process. This should take into account not only the performance characteristics of the molecular assay but also features inherent to any given cytological samples, such as its source, preparation type, fixation and staining modalities, and the most effective tumor cell enrichment methods. This calls for a change of cytotechnologists and cytopathologists mentality to collect and process the cytological samples not only for microscopy but also to assess clinically relevant molecular markers. © 2013 Elsevier Inc. Source


Izquierdo M.C.,Autonomous University of Madrid | Sanz A.B.,Servicio de Nefrologia | Mezzano S.,Austral University of Chile | Blanco J.,Anatomia Patologica | And 7 more authors.
Kidney International | Year: 2012

TWEAK (tumor necrosis factor-like weak inducer of apoptosis) is a TNF superfamily cytokine that activates the fibroblast growth factor-inducible 14 (Fn14) receptor. Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRNA for the transmembrane chemokine CXCL16, a T-cell chemoattractant, and Fn14 activation. Exogenous TWEAK increased mouse kidney CXCL16 expression and T-lymphocyte infiltration in vivo, processes inhibited by the NF-B inhibitor parthenolide. Tubular cell CXCL16 was increased in a nephrotoxic tubulointerstitial inflammation model and neutralizing anti-TWEAK antibodies decreased this CXCL16 expression and lymphocyte infiltration. In human kidney biopsies with tubulointerstitial inflammation, tubular cell CXCL16 and Fn14 expressions were associated with inflammatory infiltrates. TWEAK upregulated CXCL16 mRNA expression in cultured renal tubular cells in an NF-B-dependent manner and increased soluble and cellular CXCL16 protein. CXCL16 modestly promoted the expression of cytokines in tubular cells expressing its receptor (CXCR6) and appeared to synergize with TWEAK to promote an inflammatory response; however, it did not modulate tubular cell proliferation or survival. Thus, TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation. © 2012 International Society of Nephrology. Source


Sironi M.,Anatomia Patologica
Updates in Surgery | Year: 2011

Intra-abdominal metastases from breast carcinomas are rarely reported in the literature. Least are those originating from occult breast primary. We report, one case of pancreatic metastasis and one case of metastatic infiltration of the colonic wall, both by occult lobular breast carcinoma. The first patient underwent pancreaticoduodenectomy for obstructive jaundice, with unexpected histological finding of infiltration of distal bile duct, pancreatic gland, portal vein and retroperitoneal soft tissue by lobular carcinoma of the breast. The second patient complained of diffuse abdominal pain associated with constipation and rectal bleeding and underwent endoscopic biopsy of three intestinal strictures, revealing metastatic lobular carcinoma with signet-ring cell morphology. In both cases, a subsequent complete diagnostic work-up demonstrated asymptomatic multiple breast nodules, diagnosed as lobular carcinoma by fine needle aspiration cytology. © 2011 Springer-Verlag. Source


Barbetti V.,University of Florence | Morandi A.,University of Florence | Tusa I.,University of Florence | Digiacomo G.,University of Florence | And 8 more authors.
Oncogene | Year: 2014

The colony-stimulating factor-1 (CSF-1) and its receptor CSF-1R physiologically regulate the monocyte/macrophage system, trophoblast implantation and breast development. An abnormal CSF-1R expression has been documented in several human epithelial tumors, including breast carcinomas. We recently demonstrated that CSF-1/CSF-1R signaling drives proliferation of breast cancer cells via 'classical' receptor tyrosine kinase signaling, including activation of the extracellular signal-regulated kinase 1/2. In this paper, we show that CSF-1R can also localize within the nucleus of breast cancer cells, either cell lines or tissue specimens, irrespectively of their intrinsic molecular subtype. We found that the majority of nuclear CSF-1R is located in the chromatin-bound subcellular compartment. Chromatin immunoprecipitation revealed that CSF-1R, once in the nucleus, binds to the promoters of the proliferation-related genes CCND1, c-JUN and c-MYC. CSF-1R also binds the promoter of its ligand CSF-1 and positively regulates CSF-1 expression. The existence of such a receptor/ligand regulatory loop is a novel aspect of CSF-1R signaling. Moreover, our results provided the first evidence of a novel localization site of CSF-1R in breast cancer cells, suggesting that CSF-1R could act as a transcriptional regulator on proliferation-related genes. © 2014 Macmillan Publishers Limited. Source

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