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| 1 | 肿瘤恶性转化与C/EBPβ和STAT3基因相关(英文)显示文摘The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma,but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPβ and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPβ and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage,whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma,expression of C/EBPβ and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells. | Maria Stella Carro Wei Keat Lim Mariano Javier Alvarez Robert J. Bollo Evan Y. Snyder Erik P. Sulman Sandrine L. Anne Fiona Doetsch Howard Colman Anna Lasorella Ken Aldape Andrea Califano Antonio Iavarone | 2010 | 中华神经外科疾病研究杂志2010，9，1： | 16 |
| 2 | Second line systemic therapies for hepatocellular carcinoma: Reasons for the failure显示文摘Hepatocellular carcinoma(HCC) is the main cause of death in patients with cirrhosis, with an increasing incidence worldwide. Sorafenib is the choice therapy for advanced HCC. Over time several randomized phase Ⅲ trials have been performed testing sunitinib, brivanib, linifanib and other molecules in head-tohead comparison with Sorafenib as first-line treatment for advanced-stage HCC, but none of these has so far been registered in this setting. Moreover, another feared vacuum arises from the absence of molecules registered as second-line therapy for patients who have failed Sorafenib, representing an urgent unmet medical need. To date all molecules tested as second-line therapies for advanced hepatocellular carcinoma, failed to demonstrate an increased survival compared to placebo. What are the possible reasons for the failure? What we should expect in the near future? | Marcello Maida Massimo Iavarone Maurizio Raineri Calogero Cammà Giuseppe Cabibbo | 2015 | World Journal of Hepatology2015，7，17： | 7 |
| 3 | Field‐practice study of sorafenib therapy for hepatocellular carcinoma: A prospective multicenter study in Italy显示文摘 | Massimo Iavarone Giuseppe Cabibbo Fabio Piscaglia Claudio Zavaglia Antonio Grieco Erica Villa Calogero Cammà Massimo Colombo | 2011 | Hepatology2011，，6： | 2 |
| 4 | Sequencing of systemic treatment for hepatocellular carcinoma: Second line competitors显示文摘During the last decades,further knowledge of hepatocellular carcinoma(HCC)molecular mechanisms has led to development of effective systemic treatments including tyrosine kinase inhibitors(TKIs)and immunotherapy.In this review,we describe first and second line systemic treatment options for advanced HCC.Several trials have evaluated new drugs for the treatment of HCC patients:In first line,lenvatinib resulted non-inferior to sorafenib and it can be used as alternative,even in the lack of evidence for sequential treatment options in second line after lenvatinib.Recently,atezolizumab plus bevacizumab have shown superiority over sorafenib in first-line.Sorafenib-regorafenib sequential administration in selected patients has opened a new paradigm of treatment in advanced HCC with a life expectancy exceeding two years.Other TKIs for second line treatment include cabozantinib and ramucirumab(specifically for patients with Alpha-fetoprotein values≥400 ng/mL).The combination of TKIs with immunotherapy may represent a big step forward for these patients in the near future. | Federico Pinero Marcelo Silva Massimo Iavarone | 2020 | World Journal of Gastroenterology2020，26，16： | 2 |
| 5 | PED/PEA-15 gene controls glucose transport and is overexpressed in type2 diabetes mellitus 显示文摘 | Condorelli G Vigliotta G Iavarone C | 1998 | EMB0 J1998，17，： | 1 |
| 6 | Structures elucidation of eu-commioside (2'-O-D-β-D-glucopyranosyl Eucommiol)from Eucom- mia ulmiodes 显示文摘 | Bianco A Bonini C Iavarone C etal | 1956 | Phytochemistry1956，21，1： | 1 |
| 7 | 显示文摘 | Urciuoli P Ghinassi S Iavarone C | 2002 | Chirurgia italiana2002，55，6： | 1 |
| 8 | Systems analysis of plant cell wall degradation by the model filamentous fungus Neurospora crassa显示文摘 | Tian C Beeson W T Iavarone A T | | 0，，： | 1 |
| 9 | PED/PEA-15 gene con- trois glucose transport and is overexpressed in type 2 diabetes mellitus 显示文摘 | Condoreili G Vigliotta C Iavarone C | 1998 | EMBO J1998，17，14： | 1 |
| 10 | Id family of helix-loop-helix proteins in cancer显示文摘 | Perk J Iavarone A Benezra R | 2005 | Nat Rev Cancer2005，5，8： | 1 |
| 11 | Patterns of appearance and risk of misdiagnosis of intrahepatic cholangiocarcinoma in cirrhosis at contrast enhanced ultrasound显示文摘 | Marzia Galassi Massimo Iavarone Sandro Rossi Simona Bota Sara Vavassori Laura Rosa Simona Leoni Laura Venerandi Sara Marinelli Angelo Sangiovanni Letizia Veronese Mirella Fraquelli Alessandro Granito Rita Golfieri Massimo Colombo Luigi Bolondi Fabio Pisca | 2013 | Liver Int2013，，5： | 1 |
| 12 | The protein ENH is a cytoplasmic sequestration factor for Id2 in normal and tumor cells from the nervous system 显示文摘 | Lasorella A Iavarone A | 2006 | Proc Natl Aead Sci USA2006，103，13： | 1 |
| 13 | ID proteins as targets in cancer and tools in neurobiology 显示文摘 | Iavarone I Lasorella A | 2006 | Trends Mol Med2006，12，12： | 1 |
| 14 | Influence of low molecular weight ABS species on properties of PC/ABS system显示文摘 | Geco R Iavarone M | 2000 | Polym Eng Sci2000，40，7： | 1 |
| 15 | Characterisation of hepatitis B virus Xproteln mutants in tumor and non-tumor liver cells using laser capture microdissection显示文摘 | Massimo Iavarone Jean-Baptite Trabut | 2003 | Joural of Hepatology2003，39，： | 1 |
| 16 | Quantitative proteomic approach for cellulose degradation by Neurospora crassa显示文摘 | Phillips C M Iavarone A T Marletta M A | | 0，，09： | 1 |
| 17 | Kip/Cip and Ink4 Cdk inhibitors cooperate to induce cell cycle arrest in response to TGF-beta显示文摘 | Reynisdottir I Polyak K Iavarone A et al | 1995 | Genes Dev1995，9，： | 1 |
| 18 | Id2 specifically alters regulation of the cell cycle by tumor suppressor proteins 显示文摘 | Iavarone A Israel MA | 1996 | Mol Cell Biol1996，16，6： | 1 |
| 19 | ID proteins at the cross-road of development and cancer显示文摘 | Lasorella A Uo T Iavarone A | 2001 | Oncogene2001，20，58： | 1 |
| 20 | The diagnostic and e-conomic impact of contrast imaging techniques in the diagnosis of small hepatocellular carcinoma in cirrhosis 显示文摘 | Sangiovanni A Manini MA Iavarone M | 2010 | Gut2010，59，： | 1 |
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