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Pancreatic Neoplasms: HELP
Articles by Giovanni Brandi
Based on 6 articles published since 2009
(Why 6 articles?)
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Between 2009 and 2019, Giovanni Brandi wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Metastatic pancreatic cancer: is gemcitabine still the best standard treatment? (Review). 2010

Di Marco, Mariacristina / Di Cicilia, Roberto / Macchini, Marina / Nobili, Elisabetta / Vecchiarelli, Silvia / Brandi, Giovanni / Biasco, Guido. ·L. e A. Seràgnoli Department of Hematology and Oncological Sciences, S. Orsola-Malpighi Hospital, University of Bologna, I-40138 Bologna, Italy. mariacristina.dimarco@unibo.it ·Oncol Rep · Pubmed #20372829.

ABSTRACT: Pancreatic ductal adenocarcinoma is the fourth cause of death in the Western world. Surgery remains the only treatment offering an advantage in terms of overall survival (5-year survival range, 15-25%), but unfortunately only 10-20% of patients present resectable disease at the time of diagnosis. Hence chemotherapy, possibly combined with radiation therapy, remains the only treatment option aimed at palliation of symptoms and ensuring a better quality of life. Notwithstanding the efforts to find more effective therapies for the treatment of pancreatic cancer, significant results have not yet been achieved. Increasing interest has focused on integrated treatments, i.e. chemotherapy combined with targeted therapies, and a better selection of patients. This study examines the principal clinical trials that will help give clinicians an overview of the progress made in the systemic therapy for advanced pancreatic cancer patients in recent years.

2 Clinical Trial Alpha-fetoprotein kinetics in patients with hepatocellular carcinoma receiving ramucirumab or placebo: an analysis of the phase 3 REACH study. 2018

Chau, Ian / Park, Joon Oh / Ryoo, Baek-Yeol / Yen, Chia-Jui / Poon, Ronnie / Pastorelli, Davide / Blanc, Jean-Frédéric / Kudo, Masatoshi / Pfiffer, Tulio / Hatano, Etsuro / Chung, Hyun Cheol / Kopeckova, Katerina / Phelip, Jean-Marc / Brandi, Giovanni / Ohkawa, Shinichi / Li, Chung-Pin / Okusaka, Takuji / Hsu, Yanzhi / Abada, Paolo B / Zhu, Andrew X. ·Department of Medicine, Royal Marsden Hospital, Sutton, Surrey, SM2 5PT, UK. Ian.Chau@rmh.nhs.uk. · Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 135-710, Korea. · Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Korea. · Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. · Departmentof Surgery, The University of Hong Kong, Pokfulam, Hong Kong. · Department of Oncology, Santa Maria del Prato Hospital, Feltre (Belluno), 32032, Italy. · Department of Hepato-Gastroenterology and Medical Oncology, CHU de Bordeaux, Hôpital Haut-Lévêque, 33604, Pessac, France. · Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, Osaka-Sayama, 589-8511, Japan. · Department of Medical Oncology, Instituto do Câncer do Estado de São Paulo, São Paulo, 01246-000, Brazil. · Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan. · Department of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, 03722, Korea. · Department of Oncology, University Hospital Motol, 2nd Faculty of Medicine of Charles University, 150 00, Praha, Czech Republic. · Department of Gastroenterology and Digestive Oncology, University Hospital of St Etienne, 42100, Saint Etienne, France. · Department of Experimental, Diagnostic and Specialty Medicine, University Hospital S. Orsola, 40138, Bologna, Italy. · Division of Hepatobiliary and Pancreatic Oncology, Kanagawa Cancer Center, Yokohama, 241-0815, Japan. · Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, 112, Taiwan. · National Yang-Ming University School of Medicine, Taipei, 112, Taiwan. · Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, Tokyo, 104-0045, Japan. · Eli Lilly and Company, New York, NY, 10016, USA. · Eli Lilly and Company, Indianapolis, IN, 46285, USA. · Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Boston, MA, 02114, USA. ·Br J Cancer · Pubmed #29808014.

ABSTRACT: BACKGROUND: Post-hoc analyses of AFP response and progression and their relationship with objective measures of response and survival were performed in patients from REACH. METHODS: Serum AFP was measured at baseline and every 3 cycles (2 weeks/cycle). Associations between AFP and radiographic progression and efficacy end points were analysed. RESULTS: Median percent AFP increase from baseline was smaller in the ramucirumab than in the placebo arm throughout treatment. Time to AFP progression (HR 0.621; P < 0.0001) and to radiographic progression (HR 0.613; P < 0.0001) favoured ramucirumab. Association between AFP and radiographic progression was shown at 6 (OR 6.44, 95% CI 4.03, 10.29; P < 0.0001) and 12 weeks (OR 2.28, 95% CI 1.47, 3.53; P = 0.0002). AFP response was higher with ramucirumab compared with placebo (P < 0.0001). More patients in the ramucirumab arm experienced tumour shrinkage and AFP response compared with placebo. Survival was longer in patients with AFP response (13.6 months) than in patients without (6.2 months), irrespective of treatment (HR 0.457, P < 0.0001). CONCLUSIONS: Treatment with ramucirumab prolonged time to AFP progression, slowed AFP increase and was more likely to induce AFP response. Similar benefits in radiographic progression and response correlated with AFP changes.

3 Article The Italian Rare Pancreatic Exocrine Cancer Initiative. 2019

Brunetti, Oronzo / Luchini, Claudio / Argentiero, Antonella / Tommasi, Stefania / Mangia, Anita / Aprile, Giuseppe / Marchetti, Paolo / Vasile, Enrico / Casadei Gardini, Andrea / Scartozzi, Mario / Barni, Sandro / Delfanti, Sara / De Vita, Fernando / Di Costanzo, Francesco / Milella, Michele / Cella, Chiara Alessandra / Berardi, Rossana / Cataldo, Ivana / Santini, Daniele / Doglioni, Claudio / Maiello, Evaristo / Lawlor, Rita T / Mazzaferro, Vincenzo / Lonardi, Sara / Giuliante, Felice / Brandi, Giovanni / Scarpa, Aldo / Cascinu, Stefano / Silvestris, Nicola. ·1 Medical Oncology Unit, IRCCS Cancer Institute "Giovanni Paolo II" of Bari, Bari, Italy. · 2 Department of Diagnostics and Public Health, Section of Pathology, University of Verona, Verona, Italy. · 3 Molecular Diagnostics and Pharmacogenetics Unit, IRCCS Istituto Tumori "Giovanni Paolo II", Bari, Italy. · 4 Functional Biomorphology Laboratory, IRCCS-Istituto Tumori, Bari, Italy. · 5 Medical Oncology Unit, Hospital of Vicenza, Vicenza, Italy. · 6 Medical Oncology Unit, Sant'Andrea Hospital, University of Rome La Sapienza, Rome, Italy. · 7 Medical Oncology Unit, University Hospital of Pisa, Pisa, Italy. · 8 Medical Oncology Unit, Scientific Institute of Romagna for the Study and Treatment of Cancer (IRST), Meldola, Italy. · 9 Medical Oncology Unit, University of Cagliari, Cagliari, Italy. · 10 Medical Oncology Unit, ASST Bergamo Ovest, Treviglio, Italy. · 11 Medical Oncology Unit, IRCCS Foundation Polyclinic San Matteo, Pavia, Italy. · 12 Medical Oncology Unit, II University of Naples, Naples, Italy. · 13 Medical Oncology Unit, Careggi University Hospital, Florence, Italy. · 14 Medical Oncology Unit, "Regina Elena" National Cancer Institute, Rome, Italy. · 15 Gastrointestinal Medical Oncology and Neuroendocrine Tumors, European Institute of Oncology (IEO), Milan, Italy. · 16 Medical Oncology Unit, Polytechnic University of the Marche, "Ospedali Riuniti Ancona," Ancona, Italy. · 17 Department of Pathology and Diagnostics, University of Verona Hospital Trust, Policlinico GB Rossi, Verona, Italy. · 18 Medical Oncology Unit, University Campus Biomedico, Rome, Italy. · 19 Department of Medical Oncology, IRCCS San Raffaele Scientific Institute, Milan, Italy. · 20 Medical Oncology Unit, IRCCS "Casa Sollievo della Sofferenza" Foundation, San Giovanni Rotondo, Italy. · 21 Arc-Net Centre for Applied Research on Cancer, University and Hospital Trust of Verona, Verona, Italy. · 22 Hepato-Biliary-Pancreatic Surgery, University of Milan, Istituto Nazionale Tumori, Fondazione IRCCS, Milan, Italy. · 23 Medical Oncology Unit, IRCCS Veneto Institute of Oncology (IOV), Padua, Italy. · 24 Hepatobiliary Surgery Unit, IRCCS A. Gemelli Polyclinic Foundation, Catholic University of the Sacred Heart, Rome, Italy. · 25 Oncology Unit, Department of Experimental, Diagnostic and Specialty Medicine, Sant'Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy. · 26 Medical Oncology Unit, Modena Cancer Center, University Hospital of Modena, Modena, Italy. · 27 Scientific Direction, IRCCS Cancer Institute "Giovanni Paolo II" of Bari, Bari, Italy. ·Tumori · Pubmed #30967031.

ABSTRACT: INTRODUCTION: Exocrine pancreatic cancers include common type pancreatic ductal adenocarcinoma and cystic neoplasms, which account for 85% and 10% of cases, respectively. The remaining 5% are rare histotypes, comprising adenosquamous carcinoma, acinar cell carcinoma, signet ring cell carcinoma, medullary carcinoma, pancreatoblastoma, hepatoid carcinoma, undifferentiated carcinoma and its variant with osteoclast-like giant cells, solid pseudopapillary carcinoma, and carcinosarcoma. Due to their low incidence, little knowledge is available on their clinical and molecular features as well as on treatment choices. The national initiative presented here aims at the molecular characterization of series of rare histotypes for which therapeutic and follow-up data are available. METHODS: A nationwide Italian Rare Pancreatic Cancer (IRaPaCa) task force whose first initiative is a multicentric retrospective study involving 21 Italian cancer centers to retrieve histologic material and clinical and treatment data of at least 100 patients with rare exocrine pancreatic cancers has been created. After histologic revision by a panel of expert pathologists, DNA and RNA from paraffin tissues will be investigated by next-generation sequencing using molecular pathway-oriented and immune-oriented mutational and expression profiling panels constructed availing of the information from the International Cancer Genome Consortium. Bioinformatic analysis of data will drive validation studies by immunohistochemistry and in situ hybridization, as well as nanostring assays. CONCLUSIONS: We expect to gather novel data on rare pancreatic cancer types that will be useful to inform the design of therapeutic choices.

4 Article Good performance of platinum-based chemotherapy for high-grade gastroenteropancreatic and unknown primary neuroendocrine neoplasms. 2018

Brandi, Giovanni / Paragona, Marco / Campana, Davide / Brighi, Nicole / Bondi, Arrigo / Pantaleo, Maria Abbondanza / Corbelli, Jody / Barbera, Maria Aurelia / Biasco, Guido. ·a Department of Experimental, Diagnostic and Speciality Medicine , 'L. & A. Seragnoli' Institute of Hematology and Medical Oncology, Sant'Orsola-Malpighi Hospital , Bologna , Italy. · b Interdepartmental Center for Cancer Research (CIRC) , Sant'Orsola-Malpighi Hospital , Bologna , Italy. · c Internal Medicine Unit, Medical and Surgical Sciences Department , Sant'Orsola-Malpighi Hospital , Bologna , Italy. · d Cytological and Pathological Anatomy Unit , Maggiore Hospital , Bologna , Italy. ·J Chemother · Pubmed #28641483.

ABSTRACT: To evaluate efficacy and safety of platinum and etoposide combination in the treatment of advanced gastroenteropancreatic (GEP) and unknown primary (CUP) neuroendocrine carcinomas (NEC), we analysed the records of 21 consecutive patients treated with this regimen from 1999 to 2012. Objective responses were obtained in 11 patients (52%) and disease stability (DS) in 5 (24%). Median progression-free survival (PFS) was 7 months (95% CI, 5.33-8.66). Median overall survival (OS) was 16 months (95% CI, 14.97-17.03). Patients with limited liver disease had a significantly (p = 0.002) better PFS than patients with extrahepatic disease at diagnosis with 9 months (95% CI, 7.14-10.85) vs. 4 months (95% CI, 1.60-6.40). Two patients experienced durable complete response (30 and 90 months). The most common grade 3-4 toxicities were neutropenia (61%), anaemia (50%), nausea and vomiting (27%) and fatigue (22%). The platinum plus etoposide regimen has an acceptable toxicity profile and is effective in patients with GEP and CUP-NECs.

5 Article Estimation of the Survival Benefit Obtainable From Screening for the Early Detection of Pancreatic Cancer. 2016

Cucchetti, Alessandro / Ercolani, Giorgio / Cescon, Matteo / Brandi, Giovanni / Taffurelli, Giovanni / Maroni, Lorenzo / Ravaioli, Matteo / Pezzilli, Raffaele / Pinna, Antonio Daniele. ·From the Department of Medical and Surgical Sciences, S. Orsola-Malpighi Hospital, Alma Mater Studiorum, University of Bologna, Bologna, Italy. ·Pancreas · Pubmed #26646274.

ABSTRACT: OBJECTIVE: The chance to improve survival from pancreatic adenocarcinoma relies on early diagnosis through screening, but any screening program is subject to lead-time bias and no data are available in this regard. Aim of the present study was to evaluate the benefit obtainable from a screening program for early detection of pancreatic adenocarcinoma, considering screen-related biases. METHODS: Monte Carlo simulation was performed using data from 1000 pancreatic cancer patients admitted in a tertiary referral hospital and from pertinent literature. Lead-time bias was assessed and subtracted from expected survival. RESULTS: Mean expected life expectancy was 13.0 months. Assuming a 20%, 30%, or 50% stage III/IV reduction with screening, pancreatic resections would increase from 217 to 290 in front of a 20% stage III/IV reduction to 324 in front of a 30% reduction and to 385 in front of a 50% reduction. After lead-time adjustment, life expectancies were 14.0, 14.6, and 15.9 months, respectively. The number-needed-to-screen calculation suggests that screening can be harmful in a proportion of patients inversely dependent on the length of follow-up and a significant improvement of survival after diagnosis. CONCLUSIONS: Pancreatic adenocarcinoma screening program would probably be successful in the presence of a considerable improvement of postdiagnostic survival; otherwise, it only increases surgical procedure amount.

6 Article Antiprotease strategy in pancreatic cancer treatment: emergence from a preclinical study. 2014

Brandi, Giovanni / Tavolari, Simona / Guarnieri, Tiziana / Di Marco, Mariacristina / Paterini, Paola / Macchini, Marina / Di Girolamo, Stefania / Papi, Alessio / De Rosa, Francesco / Biasco, Guido. ·From the *Department of Experimental, Diagnostic and Specialty Medicine, †"G. Prodi" Interdepartmental Center for Cancer Research (C.I.R.C.), and ‡Center for Applied Biomedical Research (C.R.B.A.), S. Orsola-Malpighi University Hospital; §Department of Biological, Geological and Environmental Sciences; and ∥Department of Medical and Surgical Sciences, S. Orsola-Malpighi University Hospital, Bologna, Italy. ·Pancreas · Pubmed #24201777.

ABSTRACT: OBJECTIVES: Resistance to gemcitabine is one of the main causes of treatment failure in pancreatic cancer. Compelling evidences have shown the involvement of nuclear factor κB (NF-κB) activation in such phenomenon. The protease inhibitor gabexate mesilate has been shown to inhibit NF-κB. We here investigated if combined treatment with this drug could improve gemcitabine antitumoral efficacy in pancreatic cancer cells. METHODS: The effect of gabexate mesilate and gemcitabine, both used at concentrations achievable in human plasma, was assessed on in vitro pancreatic cancer cell growth, invasion, and tumor angiogenesis. The molecular mechanism at the basis of these effects was also investigated. RESULTS: Gabexate mesilate significantly increased gemcitabine anti-invasive and antiangiogenic efficacy. This effect was related to inhibition of gemcitabine-induced NF-κB activation by gabexate mesilate, which prevented RelA/p65 nuclear translocation and resulted in metalloproteinase 2, metalloproteinase 9, vascular endothelial growth factor, and interleukin 8 down-regulation. Combined treatment with gabexate mesilate also inhibited gemcitabine-induced extracellular-regulated kinase 1/2 and AKT activation by increased expression of Raf kinase inhibitor protein and phosphatase and tensin homolog. CONCLUSIONS: Combined treatment with gabexate mesilate sensitizes pancreatic cancer cells to gemcitabine by inhibition of the NF-κB pathway. The efficacy of this therapeutic strategy in pancreatic cancer patients remains to be established and deserves future clinical investigation.