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| 1 | Molecular mechanism of hepatitis B virus-induced hepatocarcinogenesis显示文摘Hepatitis B virus(HBV) infection is a global public health problem with approximately 2 billion people that have been exposed to the virus. HBV is a member of a family of small, enveloped DNA viruses called hepadnaviruses, and has a preferential tropism for hepatocytes of mammals and birds. Epidemiological studies have proved a strong correlation between chronic hepatitis B virus infection and the development of hepatocellular carcinoma(HCC). HCC is the fifth most common malignancy with about 700000 new cases each year, and more than 50% of them arise in HBV carriers. A large number of studies describe the way in which HBV can contribute to HCC development. Multiple mechanisms have been proposed, including the accumulation of genetic damage due to immune-mediated hepatic inflammation and the induction of oxidative stress. There is evidence of the direct effects of the viral proteins HBx and HBs on the cell biology. Integration of HBV-DNAinto the human genome is considered an early event in the carcinogenic process and can induce, through insertional mutagenesis, the alteration of gene expression and chromosomal instability. HBV has also epigenetic effects through the modification of the genomic methylation status. Furthermore, the virus plays an important role in the regulation of microRNA expression. This review will summarize the many mechanisms involved in HBV-related liver carcinogenesis. | Mirko Tarocchi Simone Polvani Giada Marroncini Andrea Galli | 2014 | World Journal of Gastroenterology2014，20，33： | 35 |
| 2 | Peroxisome proliferator activated receptors at the crossroad of obesity, diabetes, and pancreatic cancer显示文摘Pancreatic ductal adenocarcinoma(PDAC) is the fourth cause of cancer death with an overall survival of 5% at five years. The development of PDAC is characteristically associated to the accumulation of distinctive genetic mutations and is preceded by the exposure to several risk factors. Epidemiology has demonstrated that PDAC risk factors may be non-modifiable risks(sex, age, presence of genetic mutations, ethnicity) and modifiable and co-morbidity factors related to the specific habits and lifestyle. Recently it has become evident that obesity and diabetes are two important modifiable risk factors for PDAC. Obesity and diabetes are complex systemic and intertwined diseases and, over the years, experimental evidence indicate that insulin-resistance, alteration of adipokines, especially leptin and adiponectin, oxidative stress and inflammation may play a role in PDAC. Peroxisome proliferator activated receptor-γ(PPARγ) is a nuclear receptor transcription factor that is implicated in the regulation of metabolism, differentiation and inflammation. PPARγ is a key regulator of adipocytes differentiation, regulates insulin and adipokines production and secretion, may modulate inflammation, and it is implicated in PDAC. PPARγ agonists are used in the treatment of diabetes and oxidative stressassociated diseases and have been evaluated for the treatment of PDAC. PPARγ is at the cross-road of diabetes, obesity, and PDAC and it is an interesting target to pharmacologically prevent PDAC in obese and diabetic patients. | Simone Polvani Mirko Tarocchi Sara Tempesti Lapo Bencini Andrea Galli | 2016 | World Journal of Gastroenterology2016，22，8： | 17 |
| 3 | Antidiabetic thiazolidinediones induce ductal differentiation but not apoptosis in pancreatic cancer cells显示文摘AIM: Thiazolidinediones (TZD) are a new class of oral antidiabetic drugs that have been shown to inhibit growth of same epithelial cancer cells. Although TZD were found to be ligands for peroxisome proliferator-activated receptor γ (PPARγ), the mechanism by which TZD exert their anticancer effect is presently unclear. In this study,we analyzed the mechanism by which TZD inhibit growth of human pancreatic carcinoma cell lines in order to evaluate the potential therapeutic use of these drugs in pancreatic adenocarcinoma.METHODS: The effects of TZD in pancreatic cancer cells were assessed in anchorage-independent growth assay.Expression of PPARγ was measured by reverse-transcription polymerase chain reaction and confirmed by Western blot analysis. PPARγ activity was evaluated by transient reporter gene assay. Flow cytometry and DNA fragmentationassay were used to determine the effect of TZD on cell cycle progression and apoptosis respectively. The effect of TZD on ductal differentiation markers was performed by Western blot.RESULTS: Exposure to TZD inhibited colony formation in a PPARγ-dependent manner. Growth inhibition was linked to G1 phase cell cycle arrest through induction of the ductal differentiation program without any increase of the apoptotic rate.CONCLUSION: TZD treatment in pancreatic cancer cells has potent inhibitory effects on growth by a PPAR-dependent induction of pacreatic ductal differentiation. | Elisabetta Ceni Tommaso Mello Mirko Tarocchi David W Crabb Anna Caldini Pietro Invernizzi Calogero Surrenti Stefano Milani Andrea Galli | 2005 | World Journal of Gastroenterology2005，11，8： | 15 |
| 4 | Nuclear receptors and pathogenesis of pancreatic cancer显示文摘Pancreatic ductal adenocarcinoma(PDAC)is a devastating disease with a median overall survival time of5 mo and the five years survival less than 5%,a rate essentially unchanged over the course of the years.A well defined progression model of accumulation of genetic alterations ranging from single point mutations to gross chromosomal abnormalities has been introduced to describe the origin of this disease.However,due to the its subtle nature and concurring events PDAC cure remains elusive.Nuclear receptors(NR)are members of a large superfamily of evolutionarily conserved ligand-regulated DNA-binding transcription factors functionally involved in important cellular functions ranging from regulation of metabolism,to growth and development.Given the nature of their ligands,NR are very tempting drug targets and their pharmacological modulation has been widely exploited for the treatment of metabolic and inflammatory diseases.There are now clear evidences that both classical ligand-activated and orphan NR are involved in the pathogenesis of PDAC from its very early stages;nonetheless many aspects of their role are not fully understood.The purpose of this review is to highlight the striking connections that link peroxisome proliferator activated receptors,retinoic acid receptors,retinoid X receptor,androgen receptor,estrogen receptors and the orphan NR Nur,chicken ovalbumin upstream promoter transcription factorⅡand the liver receptor homologue-1 receptor to PDAC development,connections that could lead to the identification of novel therapies for this disease. | Simone Polvani Mirko Tarocchi Sara Tempesti Andrea Galli | 2014 | World Journal of Gastroenterology2014，20，34： | 12 |
| 5 | Chemotherapy for hepatocellular carcinoma:The present and the future显示文摘Hepatocellular carcinoma(HCC) is the most common primary tumor of the liver. Its relationship to chronic liver diseases, in particular cirrhosis, develops on a background of viral hepatitis, excessive alcohol intake or metabolic steatohepatitis, leads to a high incidence and prevalence of this neoplasia worldwide. Despite the spread of HCC, its treatment it's still a hard challenge, due to high rate of late diagnosis and to lack of therapeutic options for advanced disease. In fact radical surgery and liver transplantation, the most radical therapeutic approaches, are indicated only in case of early diagnosis. Even local therapies, such as transarterial chemoembolization, find limited indications, leading to an important problem regarding treatment of advanced disease. In this situation, until terminal HCC occurs, systemic therapy is the only possible approach, with sorafenib as the only standard treatment available. Anyway, the efficacy of this drug is limited and many efforts are necessary to understand who could benefit more with this treatment. Therefore, other molecules for a targeted therapy were evaluated, but only regorafenib showed promising results. Beside molecular target therapy, also cytotoxic drugs, in particular oxaliplatinand gemcitabine-based regimens, and immune-checkpoint inhibitors were tested with interesting results. The future of the treatment of this neoplasia is linked to our ability to understand its mechanisms of resistance and to find novel therapeutic targets, with the objective to purpose individualized approaches to patients affected by advanced HCC. | Marco Le Grazie Maria Rosa Biagini Mirko Tarocchi Simone Polvani Andrea Galli | 2017 | World Journal of Hepatology2017，9，21： | 11 |
| 6 | Effect of a counseling-supported treatment with the Mediterranean diet and physical activity on the severity of the non-alcoholic fatty liver disease显示文摘AIM To determine the clinical effectiveness of nutritional counseling on reduction of non-alcoholic fatty liver disease(NAFLD) severity, weight loss, metabolic and anthropometric indexes and liver enzymes.METHODS Forty-six adults with NAFLD received a 6-mo clinical and a dietary intervention(based on Mediterranean diet) carried out respectively by a gastroenterologist and a nutritionist with counseling license. The counseling process consisted of monthly meeting(about 45 min each). The effect of the treatment was evaluated monitoring liver enzymes, metabolic parameters, cardiovascular risk indexes, NAFLD severity [assessed by ultrasound(US)] and related indexes. All parameters were assessed at baseline. Biochemistry was also assessed at mid-and end-interventions and US was repeated at end-intervention.RESULTS The percentage of patients with steatosis grade equal or higher than 2 was reduced from 93% to 48% and steatosis regressed in 9 patients(20%). At the end of the treatment the end-point concerning the weight(i.e., a 7% weight reduction or achievement/maintenance of normal weight) was accomplished by 25 out of 46 patients(i.e., 54.3%). As far as the liver enzymes is concerned, all three liver enzymes significantly decrease during the treatment the normalization was particularly evident for the ALT enzyme(altered values reduced from 67% down to 11%). Several parameters, i.e., BMI, waist circumference, waist-to-hip ratio, AST, ALT, GGT, HDL, serum glucose, Tot-Chol/HDL, LDL/HDL, TG/HDL, AIP, HOMA, FLI, Kotronen index, VAI, NAFLD liver fat score and LAP, showed a significant improvement(P < 0.01) between baseline and end-treatment.CONCLUSION Outcomes of this study further strengthen the hypothesis that Med Diet and more active lifestyle can be considered a safe therapeutic approach for reducing risk and severity of NAFLD and related disease states. The proposed approach may be proposed as a valid and recommended approach for improving the clinical profile of NAFLD patients. | Chiara Gelli Mirko Tarocchi Ludovico Abenavoli Laura Di Renzo Andrea Galli Antonino De Lorenzo | 2017 | World Journal of Gastroenterology2017，23，17： | 8 |
| 7 | Acetaldehyde Inhibits PPARγ via H 2 O 2 -Mediated c-Abl Activation in Human Hepatic Stellate Cells显示文摘 | Elisabetta Ceni David W. Crabb Marco Foschi Tommaso Mello Mirko Tarocchi Valentino Patussi Luca Moraldi Renato Moretti Stefano Milani Calogero Surrenti Andrea Galli | 2006 | Gastroenterology2006，，4： | 2 |
| 8 | Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R显示文摘 | Ferruzzi P Ceni E Tarocchi M Grappone C Milani S Galli A | 2005 | J Clin Endocrinol Metab2005，90，3： | 1 |
| 9 | PPAR γ and Oxidative Stress: Con( β ) Catenating NRF2 and FOXO显示文摘 | Simone Polvani Mirko Tarocchi Andrea Galli Paul Drew | 2012 | PPAR Research2012，，： | 1 |
| 10 | Thiazolidinediones inhibit hepatocarcinogenesis in hepatitis B virus–transgenic mice by peroxisome proliferator‐activated receptor γ–independent regulation of nucleophosmin显示文摘 | Andrea Galli Elisabetta Ceni Tommaso Mello Simone Polvani Mirko Tarocchi Francesca Buccoliero Francesca Lisi Laura Cioni Barbara Ottanelli Valeria Foresta Guido Mastrobuoni Gloriano Moneti Giuseppe Pieraccini Calogero Surrenti Stefano Milani | 2010 | Hepatology2010，，2： | 1 |
| 11 | Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R显示文摘 | Ferruzzi P Ceni E Tarocchi M | 2005 | J Clin Endocrinol Metab2005，90，3： | 1 |
| 12 | PPAR γ and Oxidative Stress: Con( β ) Catenating NRF2 and FOXO显示文摘 | Simone Polvani Mirko Tarocchi Andrea Galli Paul Drew | 2012 | PPAR Research2012，，： | 1 |
| 13 | Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R 显示文摘 | Ferruzzi P Ceni E Tarocchi M | 2005 | J Clin Endocrinol Metab2005，90，3： | 1 |
| 14 | COUP‐TFII in pancreatic adenocarcinoma: Clinical implication for patient survival and tumor progression显示文摘 | Simone Polvani Mirko Tarocchi Sara Tempesti Tommaso Mello Elisabetta Ceni Francesca Buccoliero Massimo D’Amico Vieri Boddi Marco Farsi Silvia Nesi Gabriella Nesi Stefano Milani Andrea Galli | 2014 | Int. J. Cancer2014，，7： | 1 |
| 15 | Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R显示文摘 | Ferruzzi P Ceni E Tarocchi M | 2005 | J Clin Endocrinol Metab2005，90，3： | 1 |
| 16 | Oxidative stress stimulates proliferation and invasiveness of hepatic stellate cells via a MMP2-mediated mechanism显示文摘 | Galli A Svegliati-Baroni G Ceni E Milani S Ridolfi F Salzano R Tarocchi M Grappone C Pellegrini G Benedetti A Surrenti C Casini A | 2005 | Hepatology2005，41，5： | 1 |
| 17 | Thiazolidinediones inhibit growth and invasiveness of the human adrenocortical cancer cell line H295R显示文摘 | Ferruzzi P Ceni E Tarocchi M | 2005 | J Clin Endocrinol Metab2005，90，3： | 1 |
| 18 | Functional linkage of cirrhosis‐predictive single nucleotide polymorphisms of toll‐like receptor 4 to hepatic stellate cell responses显示文摘 | Jinsheng Guo Johnny Loke Feng Zheng Feng Hong Steven Yea Masayuki Fukata Mirko Tarocchi Olivia T. Abar Hongjin Huang John J. Sninsky Scott L. Friedman | 2009 | Hepatology2009，，3： | 1 |
| 19 | PPAR gamma and oxidative stress : Con(beta) eatenating NRF2 and FOXO 显示文摘 | Polvani S Tarocchi M Galli A | 2012 | PPAR Res2012，2012，64： | 1 |
| 20 | COUP‐TFII in pancreatic adenocarcinoma: Clinical implication for patient survival and tumor progression显示文摘 | Simone Polvani Mirko Tarocchi Sara Tempesti Tommaso Mello Elisabetta Ceni Francesca Buccoliero Massimo D’Amico Vieri Boddi Marco Farsi Silvia Nesi Gabriella Nesi Stefano Milani Andrea Galli | 2014 | Int J Cancer2014，，7： | 1 |
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