Institution
University of Naples Federico II
Education•Naples, Campania, Italy•
About: University of Naples Federico II is a education organization based out in Naples, Campania, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 29291 authors who have published 68803 publications receiving 1920149 citations. The organization is also known as: Università degli Studi di Napoli Federico II & Naples University.
Topics: Population, Cancer, Medicine, Context (language use), Computer science
Papers published on a yearly basis
Papers
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TL;DR: Clinical relevant criteria that can help to guide the physician in the management of patients with impaired or poor ovarian response are proposed, including a more specific new definition of ‘‘low prognosis’’ patients.
314 citations
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TL;DR: The assessment of the negative symptom dimension has recently improved, but even current expert consensus‐based instruments diverge on several aspects and the use of objective measures might contribute to overcome uncertainties about the reliability of rating scales, but these measures require further investigation and validation.
314 citations
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TL;DR: In this paper, the authors evaluated the effectiveness of marine protected areas (MPAs) and found that 3 of 15 Italian marine reserves investigated had adequate enforcement, and that patterns of recovery of target fish were related to enforcement.
314 citations
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TL;DR: Evaluation of neoangiogenesis and of certain growth factors, such as AR, can be useful in addition to conventional pathological staging to select high-risk NSCLC patients who may benefit from post-surgical systemic therapies.
Abstract: We have determined the expression of transforming growth factor alpha (TGF alpha), amphiregulin (AR), CRIPTO, the epidermal growth factor receptor (EGFR), erbB-2, erbB-3, and tumor angiogenesis in a series of 195 patients with stage I-IIIA non-small cell lung cancer (NSCLC) treated with radical surgery to define their usefulness as prognostic indicators of survival. A variable degree of specific staining in cancer cells was observed for the three growth factors and for the three growth factor receptors in the majority of NSCLC patients. A statistically significant association between overexpression of TGF alpha, AR, and CRIPTO was observed. Enhanced expression of AR was significantly correlated with enhanced expression of erbB-2 and advanced T-stage. A direct association was also detected for overexpression of TGF alpha and of erbB-2 or erbB-3, respectively. Sex, tumor size, nodal status, stage, microvessel count, as a measure of neovascularization, and AR overexpression significantly correlated with overall survival at univariate analysis. In a Cox multivariate analysis, the only characteristics with an independent prognostic effect on OAS were microvessel count [relative hazard (RH), 6.61; P < 0.00001), nodal status (RH, 1.59; P = 0.0013), and AR overexpression (RH, 1.72; P = 0.02). These results suggest that evaluation of neoangiogenesis and of certain growth factors, such as AR, can be useful in addition to conventional pathological staging to select high-risk NSCLC patients who may benefit from post-surgical systemic therapies.
314 citations
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TL;DR: It is shown that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC.
Abstract: To define novel pathways that regulate susceptibility to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in non-small cell lung cancer (NSCLC), we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant NSCLC cells, levels of different miRs are increased, and in particular, miR-221 and -222. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. Indeed, transfection with anti-miR-221 and -222 rendered CALU-1-resistant cells sensitive to TRAIL. Conversely, H460-sensitive cells treated with -221 and -222 pre-miRs become resistant to TRAIL. miR-221 and -222 target the 3'-UTR of Kit and p27(kip1) mRNAs, but interfere with TRAIL signaling mainly through p27(kip1). In conclusion, we show that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC.
314 citations
Authors
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Name | H-index | Papers | Citations |
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D. M. Strom | 176 | 3167 | 194314 |
Yang Gao | 168 | 2047 | 146301 |
Robert Stone | 160 | 1756 | 167901 |
Elio Riboli | 158 | 1136 | 110499 |
Barry J. Maron | 155 | 792 | 91595 |
H. Eugene Stanley | 154 | 1190 | 122321 |
Paul Elliott | 153 | 773 | 103839 |
Robert O. Bonow | 149 | 808 | 114836 |
Kai Simons | 147 | 426 | 93178 |
Peter Buchholz | 143 | 1181 | 92101 |
Martino Margoni | 141 | 2059 | 107829 |
H. A. Neal | 141 | 1903 | 115480 |
Luca Lista | 140 | 2044 | 110645 |
Pierluigi Paolucci | 138 | 1965 | 105050 |
Ari Helenius | 137 | 298 | 64789 |