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Pancreatic Neoplasms: HELP
Articles by Antonio Russo
Based on 8 articles published since 2010
(Why 8 articles?)
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Between 2010 and 2020, Antonio Russo wrote the following 8 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Moving the Target on the Optimal Adjuvant Strategy for Resected Pancreatic Cancers: A Systematic Review with Meta-Analysis. 2020

Galvano, Antonio / Castiglia, Marta / Rizzo, Sergio / Silvestris, Nicola / Brunetti, Oronzo / Vaccaro, Giovanni / Gristina, Valerio / Barraco, Nadia / Bono, Marco / Guercio, Giovanni / Graceffa, Giuseppa / Fulfaro, Fabio / Gori, Stefania / Bazan, Viviana / Russo, Antonio. ·Medical Oncology Unit, Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Via del Vespro 129, 90127 Palermo, Italy. · Medical Oncology Unit, IRCCS Istituto Tumori "Giovanni Paolo II" of Bari, Viale Orazio Flacco, 65, 70124 Bari, Italy. · Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Palermo, Via del Vespro 129, 90127 Palermo, Italy. · Oncology Department, IRCCS Sacro Cuore Don Calabria Hospital, 37024 Negrar, Verona, Italy. · Department of Experimental Biomedicine and Clinical Neurosciences, School of Medicine, University of Palermo, Via del Vespro 129, 90127 Palermo, Italy. ·Cancers (Basel) · Pubmed #32110977.

ABSTRACT: Combination regimens have shown superiority over single agents in the adjuvant treatment of resected pancreatic cancer (PC), but there are no data supporting definition of the best regimen. This work aimed to compare the efficacy and safety of mFOLFIRINOX, gemcitabine+capecitabine, and gemcitabine+nab/paclitaxel in PC patients. A meta-analysis was performed for direct comparison between trials comparing combination regimens and gemcitabine monotherapy. Subsequently, an indirect comparison was made between trials investigating the efficacy and safety of mFOLFIRINOX, gemcitabine+capecitabine, and gemcitabine+nab/paclitaxel because of the same control arm (gemcitabine). A total of three studies met the selection criteria and were included in our indirect comparison. Indirect comparisons for efficacy outcomes showed a benefit in terms of DFS (disease-free survival)/EFS (event-free survival)/RFS (relapse-free survival) for both mFOLFIRINOX versus gemcitabine+capecitabine (HR 0.69, 95% CI 0.52-0.91) and versus gemcitabine+nab/paclitaxel (HR 0.67, 95% CI 0.50-0.90). No significant advantage was registered for OS (overall survival). Indirect comparisons for safety showed an increase in terms of G3-5 AEs (with the exception of neutropenia) for mFOLFIRINOX versus gemcitabine+capecitabine (RR 1.24, 95% CI 1.03-1.50), while no significant differences were observed versus gemcitabine+nab/paclitaxel. According to our results, mFOLFIRINOX is feasible and manageable and could represent a first option for fit PC resected patients.

2 Review Molecular profiling of pancreatic neuroendocrine tumors (pNETS) and the clinical potential. 2018

Camilli, Massimiliano / Papadimitriou, Konstantinos / Nogueira, Amanda / Incorvaia, Lorena / Galvano, Antonio / D'Antonio, Federica / Ferri, Jose / Santini, Daniele / Silvestris, Nicola / Russo, Antonio / Peeters, Marc / Rolfo, Christian. ·a Department of Oncology , University Campus Biomedico of Rome , Rome , Italy. · b Oncology Department , Antwerp University Hospital , Edegem , Belgium. · c Phase I-Early Clinical Trials Unit, Oncology Department , Antwerp University Hospital & Center for Oncological Research (CORE) , Antwerp , Belgium. · d Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology , University of Palermo , Palermo , Italy. · e Medical Oncology Department , Oncological institute Giovanni Paolo II , Bari , Italy. ·Expert Rev Gastroenterol Hepatol · Pubmed #29629846.

ABSTRACT: INTRODUCTION: Pancreatic neuroendocrine tumors (pNETs) represent a small part of pancreatic neoplasms, and the knowledge about their indolent clinical course remains a subject of investigation. They occur sporadically or as part of familial cancer syndromes and are classified by WHO in 3 categories. There is ongoing research to understand their molecular profiling and leading mutations. Areas covered: The aim of this review is to clarify the overall aspects of tumorigenesis, to expose the latest developments in understanding the course of the disease and the possible therapeutic implications of these. The review also discusses functional and non-functional pNETs and associated inherited syndromes as well as pNET molecular profiling and its possible guidance in the use of targeted therapy. Expert commentary: In the next decade, a more extensive application of new technologies will help improve quality of life and survival, individualizing treatment protocols and identifying which therapeutic strategy is more suitable for each kind of NET.

3 Review MicroRNA in pancreatic adenocarcinoma: predictive/prognostic biomarkers or therapeutic targets? 2015

Brunetti, Oronzo / Russo, Antonio / Scarpa, Aldo / Santini, Daniele / Reni, Michele / Bittoni, Alessandro / Azzariti, Amalia / Aprile, Giuseppe / Delcuratolo, Sabina / Signorile, Michele / Gnoni, Antonio / Palermo, Loredana / Lorusso, Vito / Cascinu, Stefano / Silvestris, Nicola. ·Medical Oncology Unit, National Cancer Research Centre, Istituto Tumori Giovanni Paolo II, Bari, Italy. · Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy. · Department of Pathology and Diagnostics, University of Verona, Verona, Italy. · Department of Medical Oncology, University Campus Bio-Medico, Rome, Italy. · Department of Medical Oncology, San Raffaele Scientific Institute, Milan, Italy. · AOU Ospedali Riuniti, Polytechnic University of the Marche Region, Ancona, Italy. · Clinical and Preclinical Pharmacology Laboratory, National Cancer Research Centre, Istituto Tumori Giovanni Paolo II, Bari, Italy. · Department of Medical Oncology, University Hospital of Udine, Udine, Italy. · Department of Medical Oncology, Hospital of Taranto, Taranto, Italy. ·Oncotarget · Pubmed #26259238.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a tumor with a poor prognosis, short overall survival and few chemotherapeutic choices. MicroRNAs (miRNAs) are non-coding, single-stranded RNAs of around 22 nucleotides involved in the pathogenic mechanisms of carcinogenesis and metastasis. They have been studied in many tumors in order to identify potential diagnostic, prognostic or therapeutic targets. In the current literature, many studies have analyzed the role of miRNAs in PDAC. In fact, the absence of appropriate biomarkers, the difficultly of early detection of this tumor, and the lack of effective chemotherapy in patients with unresectable disease have focused attention on miRNAs as new, interesting advance in this malignancy. In this review we analyzed the role of miRNAs in PDAC in order to understand the mechanisms of action and the difference between the onco-miRNA and the tumor suppressor miRNA. We also reviewed all the data related to the use of these molecules as predictive as well as prognostic biomarkers in the course of the disease. Finally, the possible therapeutic use of miRNAs or anti-miRNAs in PDAC is also discussed. In conclusion, although there is still no clinical application for these molecules in PDAC, it is our opinion that the preclinical evidence of the role of specific miRNAs in carcinogenesis, the possibility of using miRNAs as diagnostic or prognostic biomarkers, and their potential therapeutic role, warrant future studies in PDAC.

4 Article Prognostic significance of circulating PD-1, PD-L1, pan-BTN3As, BTN3A1 and BTLA in patients with pancreatic adenocarcinoma. 2019

Bian, Benjamin / Fanale, Daniele / Dusetti, Nelson / Roque, Julie / Pastor, Sonia / Chretien, Anne-Sophie / Incorvaia, Lorena / Russo, Antonio / Olive, Daniel / Iovanna, Juan. ·Team Pancreatic Cancer, Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Parc Scientifique et Technologique de Luminy, Marseille, France. · Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy. · Team Immunity and Cancer, Centre de Recherche en Cancérologie de Marseille (CRCM), INSERM U1068, CNRS UMR 7258, Aix-Marseille Université and Institut Paoli-Calmettes, Marseille, France. ·Oncoimmunology · Pubmed #30906655.

ABSTRACT: PDAC is one of the most heterogeneous cancers with low chemotherapeutic sensitivity due to a dense stroma, a weak vasculature and significant biological aggressivity. In cancer, suppressive immune checkpoints are often hyper-activated to ensure an effective evasion of tumor cells from immune surveillance. These immune checkpoints include in part, the B7/butyrophilin-like receptors such as butyrophilin sub-family 3A/CD277 receptors (BTN3A), the B and T lymphocyte attenuator (BTLA) belonging to the B7-like receptors and the programmed death protein (PD-1) with its ligand PD-L1. We evaluated the plasma level of these markers in 32 PDAC patients (learning cohort) by

5 Article Phospho-Akt overexpression is prognostic and can be used to tailor the synergistic interaction of Akt inhibitors with gemcitabine in pancreatic cancer. 2017

Massihnia, Daniela / Avan, Amir / Funel, Niccola / Maftouh, Mina / van Krieken, Anne / Granchi, Carlotta / Raktoe, Rajiv / Boggi, Ugo / Aicher, Babette / Minutolo, Filippo / Russo, Antonio / Leon, Leticia G / Peters, Godefridus J / Giovannetti, Elisa. ·Department of Medical Oncology VU University Medical Center, Cancer Center Amsterdam, CCA room 1.52, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. · Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy. · Metabolic syndrome Research center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. · Cancer Pharmacology Lab, AIRC Start Up Unit, University of Pisa, Pisa, Italy. · Department of Pharmacy, University of Pisa, Pisa, Italy. · Department of Surgery, University of Pisa, Pisa, Italy. · Æterna Zentaris GmbH, Frankfurt am Main, Frankfurt, Germany. · Department of Medical Oncology VU University Medical Center, Cancer Center Amsterdam, CCA room 1.52, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. e.giovannetti@vumc.nl. · Cancer Pharmacology Lab, AIRC Start Up Unit, University of Pisa, Pisa, Italy. e.giovannetti@vumc.nl. ·J Hematol Oncol · Pubmed #28061880.

ABSTRACT: BACKGROUND: There is increasing evidence of a constitutive activation of Akt in pancreatic ductal adenocarcinoma (PDAC), associated with poor prognosis and chemoresistance. Therefore, we evaluated the expression of phospho-Akt in PDAC tissues and cells, and investigated molecular mechanisms influencing the therapeutic potential of Akt inhibition in combination with gemcitabine. METHODS: Phospho-Akt expression was evaluated by immunohistochemistry in tissue microarrays (TMAs) with specimens tissue from radically-resected patients (n = 100). Data were analyzed by Fisher and log-rank test. In vitro studies were performed in 14 PDAC cells, including seven primary cultures, characterized for their Akt1 mRNA and phospho-Akt/Akt levels by quantitative-RT-PCR and immunocytochemistry. Growth inhibitory effects of Akt inhibitors and gemcitabine were evaluated by SRB assay, whereas modulation of Akt and phospho-Akt was investigated by Western blotting and ELISA. Cell cycle perturbation, apoptosis-induction, and anti-migratory behaviors were studied by flow cytometry, AnnexinV, membrane potential, and migration assay, while pharmacological interaction with gemcitabine was determined with combination index (CI) method. RESULTS: Immunohistochemistry of TMAs revealed a correlation between phospho-Akt expression and worse outcome, particularly in patients with the highest phospho-Akt levels, who had significantly shorter overall and progression-free-survival. Similar expression levels were detected in LPC028 primary cells, while LPC006 were characterized by low phospho-Akt. Remarkably, Akt inhibitors reduced cancer cell growth in monolayers and spheroids and synergistically enhanced the antiproliferative activity of gemcitabine in LPC028, while this combination was antagonistic in LPC006 cells. The synergistic effect was paralleled by a reduced expression of ribonucleotide reductase, potentially facilitating gemcitabine cytotoxicity. Inhibition of Akt decreased cell migration and invasion, which was additionally reduced by the combination with gemcitabine. This combination significantly increased apoptosis, associated with induction of caspase-3/6/8/9, PARP and BAD, and inhibition of Bcl-2 and NF-kB in LPC028, but not in LPC006 cells. However, targeting the key glucose transporter Glut1 resulted in similar apoptosis induction in LPC006 cells. CONCLUSIONS: These data support the analysis of phospho-Akt expression as both a prognostic and a predictive biomarker, for the rational development of new combination therapies targeting the Akt pathway in PDAC. Finally, inhibition of Glut1 might overcome resistance to these therapies and warrants further studies.

6 Article Neutrophil/lymphocyte ratio helps select metastatic pancreatic cancer patients benefitting from oxaliplatin. 2016

Formica, Vincenzo / Morelli, Cristina / Ferroni, Patrizia / Nardecchia, Antonella / Tesauro, Manfredi / Pellicori, Stefania / Cereda, Vittore / Russo, Antonio / Riondino, Silvia / Guadagni, Fiorella / Roselli, Mario. ·Department of Systems Medicine, Medical Oncology, Tor Vergata Clinical Center, Tor Vergata University of Rome, Rome, Italy. · San Raffaele Roma Open University, Rome, Italy. · Interinstitutional Multidisciplinary Biobank (BioBIM), IRCCS San Raffaele Pisana, Rome, Italy. · Department of Systems Medicine, Internal Medicine, Tor Vergata Clinical Center, Tor Vergata University of Rome, Rome, Italy. · Section of Medical Oncology, Department of Surgical and Oncology Sciences, University of Palermo, Italy. ·Cancer Biomark · Pubmed #27434293.

ABSTRACT: BACKGROUND: High Neutrophil/Lymphocyte ratio (NLR), as a measure of enhanced inflammatory response, has been negatively associated with prognosis in patients with localized pancreatic ductal adenocarcinoma (PDA). OBJECTIVE: In the present study, we aimed at investigating the prognostic value of NLR in two homogeneous groups of chemotherapy-naïve metastatic PDA patients. Patients were treated with either gemcitabine (GEM) or gemcitabine/oxaliplatin (GEMOXA). We also assessed whether NLR could identify patients benefiting from the use of oxaliplatin. METHODS: Consecutive PDA patients treated at the Medical Oncology Unit of Tor Vergata University Hospital of Rome with either GEM or GEMOXA were included (n= 103). NLR was assessed before and during chemotherapy and correlated with outcome together with common clinical and biochemical variables. RESULTS: Among 17 analyzed variables NLR, Karhofsky Perfomance Status (KPS), d-dimer and erythrocyte sedimentation rate were found to be significantly associated with median Overall Survival (mOS) at the univariate analysis. Only NLR and KPS were independent prognosticator at multivariate analysis, with NLR displaying the highest statistical significance. NLR was also predictive of oxaliplatin activity, as only patients with NLR > 2.5 (cutoff determined upon ROC analysis) derived benefit from GEMOXA over GEM. CONCLUSIONS: NLR is both an independent prognostic and predictive factor in metastatic PDA, since only patients with high NLR seem to benefit from the addition of oxaliplatin. NLR may help select patients for whom a particularly poor prognosis might justify more intensive, yet less tolerable, combination regimens.

7 Article Germline copy number variation in the YTHDC2 gene: does it have a role in finding a novel potential molecular target involved in pancreatic adenocarcinoma susceptibility? 2014

Fanale, Daniele / Iovanna, Juan Lucio / Calvo, Ezequiel Luis / Berthezene, Patrice / Belleau, Pascal / Dagorn, Jean Charles / Bronte, Giuseppe / Cicero, Giuseppe / Bazan, Viviana / Rolfo, Christian / Santini, Daniele / Russo, Antonio. ·University of Palermo, Department of Surgical, Oncological and Stomatological Sciences, Section of Medical Oncology , Via del Vespro 129, 90127 Palermo , Italy +39 091 6552500 ; +011 39 091 6554529 ; antonio.russo@usa.net. ·Expert Opin Ther Targets · Pubmed #24834797.

ABSTRACT: OBJECTIVE: The vast majority of pancreatic cancers occurs sporadically. The discovery of frequent variations in germline gene copy number can significantly influence the expression levels of genes that predispose to pancreatic adenocarcinoma. We prospectively investigated whether patients with sporadic pancreatic adenocarcinoma share specific gene copy number variations (CNVs) in their germline DNA. PATIENTS AND METHODS: DNA samples were analyzed from peripheral leukocytes from 72 patients with a diagnosis of sporadic pancreatic adenocarcinoma and from 60 controls using Affymetrix 500K array set. Multiplex ligation-dependent probe amplification (MLPA) assay was performed using a set of self-designed MLPA probes specific for seven target sequences. RESULTS: We identified a CNV-containing DNA region associated with pancreatic cancer risk. This region shows a deletion of 1 allele in 36 of the 72 analyzed patients but in none of the controls. This region is of particular interest since it contains the YTHDC2 gene encoding for a putative DNA/RNA helicase, such protein being frequently involved in cancer susceptibility. Interestingly, 82.6% of Sicilian patients showed germline loss of one allele. CONCLUSIONS: Our results suggest that the YTHDC2 gene could be a potential candidate for pancreatic cancer susceptibility and a useful marker for early detection as well as for the development of possible new therapeutic strategies.

8 Article Analysis of germline gene copy number variants of patients with sporadic pancreatic adenocarcinoma reveals specific variations. 2013

Fanale, Daniele / Iovanna, Juan Lucio / Calvo, Ezequiel Luis / Berthezene, Patrice / Belleau, Pascal / Dagorn, Jean Charles / Ancona, Chiara / Catania, Giovanna / D'Alia, Paolo / Galvano, Antonio / Gulotta, Eliana / Lo Dico, Silvia / Passiglia, Francesco / Bronte, Giuseppe / Midiri, Massimo / Lo Re, Giuseppe / Cicero, Giuseppe / Bazan, Viviana / Russo, Antonio. ·Section of Medical Oncology, Department of Surgical, Oncological and Stomatological Sciences,University of Palermo, Palermo, Italy. ·Oncology · Pubmed #24217364.

ABSTRACT: OBJECTIVES: The rapid fatality of pancreatic cancer is, in large part, the result of diagnosis at an advanced stage in the majority of patients. Identification of individuals at risk of developing pancreatic adenocarcinoma would be useful to improve the prognosis of this disease. There is presently no biological or genetic indicator allowing the detection of patients at risk. Our main goal was to identify copy number variants (CNVs) common to all patients with sporadic pancreatic cancer. METHODS: We analyzed gene CNVs in leukocyte DNA from 31 patients with sporadic pancreatic adenocarcinoma and from 93 matched controls. Genotyping was performed with the use of the GeneChip Human Mapping 500K Array Set (Affymetrix). RESULTS: We identified 431 single nucleotide polymorphism (SNP) probes with abnormal hybridization signal present in the DNA of all 31 patients. Of these SNP probes, 284 corresponded to 3 or more copies and 147 corresponded to 1 or 0 copies. Several cancer-associated genes were amplified in all patients. Conversely, several genes supposed to oppose cancer development were present as single copy. CONCLUSIONS: These data suggest that a set of 431 CNVs could be associated with the disease. This set could be useful for early diagnosis.