Truini A.,University of Genoa |
Pereira P.S.,Operative Unit of Pathologic Anatomy Hospital Maggiore della Carita of Novara |
Cavazza A.,Operative Unit of Oncology |
Spagnolo P.,University of Basel |
And 8 more authors.
Expert Review of Respiratory Medicine
The epidemic increase of adenocarcinoma histology accounting for more than 50% of primary lung malignancies and the advent of effective molecular targeted-therapies against specific gene alterations characterizing this tumor type have led to the reconsideration of the pathologic classification of lung cancer. The new 2015 WHO classification provided the basis for a multidisciplinary approach emphasizing the close correlation among clinical, radiologic and molecular characteristics and histopathologic pattern of lung adenocarcinoma. The terms 'bronchioloalveolar carcinoma' and 'mixed adenocarcinoma' have been eliminated, introducing the concepts of 'adenocarcinoma in situ' , 'minimally invasive adenocarcinoma' and the use of descriptive predominant patterns in invasive adenocarcinomas (lepidic, acinar, papillary, solid and micropapillary patterns). Invasive mucinous adenocarcinoma' is the new definition for mucinous bronchioloalveolar carcinoma, and some variants of invasive adenocarcinoma have been included, namely colloid, enteric and fetal-type adenocarcinomas. A concise update of the immunomorphologic, radiological and molecular characteristics of the different histologic patterns of lung adenocarcinoma is reported here. © 2015 Informa UK Ltd. Source
Sinagra E.,Cervello |
Perricone G.,Cervello |
Linea C.,Cervello |
Montalbano L.,Cervello |
And 10 more authors.
Case Reports in Gastroenterology
Zollinger-Ellison syndrome is an often progressive, persistent and frequently life-threatening disease, described for the first time as characterized by ulceration of the upper jejunum, hypersecretion of gastric acid and non-beta islet cell tumors of the pancreas; this syndrome is due to the hypersecretion of gastrin. We report a case of Zollinger-Ellison syndrome presenting as severe esophagitis evolving in stenosis, which demonstrates how a delayed diagnosis may induce risk of disease spreading. In this setting new diagnostic approaches, such as somatostatin receptor scanning and positron emission tomography with 68 Ga-labeled octreotide, could be particularly useful, as well as further new therapeutic options, such as molecular targeted treatments and peptide receptor radionuclide therapy, though surgery is currently the only form of curative treatment, and the role of the therapeutic options mentioned needs to be clarified by forthcoming studies. © 2013 S. Karger AG, Basel. Source
Rossi G.,University Hospital Policlinico of Modena |
Cavazza A.,Operative Unit of Oncology |
Spagnolo P.,University of Basel |
Spagnolo P.,University of Padua |
And 13 more authors.
European Respiratory Journal
The term diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) may be used to describe a clinico-pathological syndrome, as well as an incidental finding on histological examination, although there are obvious differences between these two scenarios. According to the World Health Organization, the definition of DIPNECH is purely histological. However, DIPNECH encompasses symptomatic patients with airway disease, as well as asymptomatic patients with neuroendocrine cell hyperplasia associated with multiple tumourlets/carcinoid tumours. DIPNECH is also considered a pre-neoplastic lesion in the spectrum of pulmonary neuroendocrine tumours, because it is commonly found in patients with peripheral carcinoid tumours. In this review, we summarise clinical, physiological, radiological and histological features of DIPNECH and critically discuss recently proposed diagnostic criteria. In addition, we propose that the term "DIPNECH syndrome" be used to indicate a sufficiently distinct patient subgroup characterised by respiratory symptoms, airflow obstruction, mosaic attenuation with air trapping on chest imaging and constrictive obliterative bronchiolitis, often with nodular proliferation of neuroendocrine cells with/without tumourlets/carcinoid tumours on histology. Surgical lung biopsy is the diagnostic gold standard. However, in the appropriate clinical and radiological setting, transbronchial lung biopsy may also allow a confident diagnosis of DIPNECH syndrome. Copyright © ERS 2016. Source
Pacetti U.,Operative Unit of Oncology |
Veltri E.,Unit of Medical Oncology |
Fattoruso S.I.S.,Operative Unit of Oncology |
Cardillo F.D.,Operative Unit of Oncology |
And 3 more authors.
Aim: To evaluate the efficacy of reduction of dexamethasone with a single-dose of palonosetron in preventing acute and delayed nausea and vomiting in patients receiving highly emetogenic chemotherapy (HEC) for early breast cancer. Patients and methods: Chemotherapy-naive patients with breast cancer were given HEC in an adjuvant or neoadjuvant setting. Palonosetron and dexamethasone 4 mg i.v. were given on day 1 and another two administrations of dexamethasone 4 mg i.m. were given on days 2 and 3. The end-point was complete response (CR) and complete control (CC) during the acute and delayed phases. Results: Twenty-six patients were observed. Complete response was achieved in 19 out of 26 patients (72.4%); the same result was shown in 72.4% out of 76 courses given. Conclusion: This alternative schedule suggests efficacy for the control of acute and delayed emesis in moderately emetogenic chemotherapy. Further investigations are required to confirm these results. Source
Ragazzi M.,Operative Unit of Pathology |
Tamagnini I.,Operative Unit of Pathology |
Bisagni A.,Operative Unit of Pathology |
Cavazza A.,Operative Unit of Pathology |
And 9 more authors.
Journal of Clinical Pathology
Aims Identification of epidermal growth factor receptor (EGFR) mutations in lung adenocarcinomas is the single most important predictor of clinical response and outcome using EGFR tyrosine kinase inhibitors (TKIs). EGFR E746-A750del and L858R mutations are the most common gene alterations, also predicting the best clinical response to TKIs. We evaluated the accuracy of EGFR mutation-specific antibodies in a large cohort of lung adenocarcinomas, with different molecular settings and types of tissue samples. Methods 300 lung adenocarcinomas diagnosed on cytology (48 cell blocks), biopsy (157 cases) and surgical resections (95 cases) were selected. All cases were investigated for EGFR by sequencing and two mutationspecific antibodies (clone 6B6 for E746-A750del; clone 43B2 for L858R) were tested using an automated immunostainer. Discordant results were investigated by next-generation sequencing (NGS). Results Overall sensitivity and specificity of mutantspecific antibodies were 58.6% and 98.0%, respectively, and they increased up to 84% and 100% if only tumours harbouring E746-A750del were considered. In 13 discordant cases, NGS confirmed immunohistochemistry results in eight samples. Conclusions The EGFR mutation-specific antibodies have a fair/good sensitivity and good/high specificity in identifying classic mutations, but they cannot replace molecular tests. The antibodies work equally well on biopsies and cell blocks, possibly permitting a rapid screening in cases with poor material. Source