Institution
Università Campus Bio-Medico
Education•Rome, Italy•
About: Università Campus Bio-Medico is a education organization based out in Rome, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 2829 authors who have published 8519 publications receiving 193689 citations. The organization is also known as: Universita Campus Bio-Medico & Campus Bio-Medico University.
Topics: Population, Cancer, Diabetes mellitus, Breast cancer, Type 1 diabetes
Papers published on a yearly basis
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Daniel J. Klionsky1, Fábio Camargo Abdalla2, Hagai Abeliovich3, Robert T. Abraham4 +1284 more•Institutions (463)
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
4,316 citations
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Katholieke Universiteit Leuven1, Swiss Institute of Bioinformatics2, Aristotle University of Thessaloniki3, Paris Descartes University4, University of Auvergne5, Università Campus Bio-Medico6, University of Turin7, Hebron University8, French Institute of Health and Medical Research9, Seconda Università degli Studi di Napoli10, University of Southern Denmark11, Odense University Hospital12, Cliniques Universitaires Saint-Luc13, University Hospital of Lausanne14
TL;DR: This is the largest cohort to date of patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab plus chemotherapy in the pre-KRAS selection era and confirmed that, if KRAS is not mutated, assessing BRAF, NRAS, and PIK3CA population response rates confirmed that.
Abstract: Background Following the discovery that mutant KRAS is associated with resistance to anti-epidermal growth factor receptor (EGFR) antibodies, the tumours of patients with metastatic colorectal cancer are now profiled for seven KRAS mutations before receiving cetuximab or panitumumab. However, most patients with KRAS wild-type tumours still do not respond. We studied the effect of other downstream mutations on the efficacy of cetuximab in, to our knowledge, the largest cohort to date of patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab plus chemotherapy in the pre-KRAS selection era. Methods 1022 tumour DNA samples (73 from fresh-frozen and 949 from formalin-fixed, paraffin-embedded tissue) from patients treated with cetuximab between 2001 and 2008 were gathered from 11 centres in seven European countries. 773 primary tumour samples had sufficient quality DNA and were included in mutation frequency analyses; mass spectrometry genotyping of tumour samples for KRAS, BRAF, NRAS, and PIK3CA was done centrally. We analysed objective response, progression-free survival (PFS), and overall survival in molecularly defined subgroups of the 649 chemotherapy-refractory patients treated with cetuximab plus chemotherapy. Findings 40.0% (299/747) of the tumours harboured a KRAS mutation, 14.5% (108/743) harboured a PIK3CA mutation (of which 68.5% [74/108] were located in exon 9 and 20.4% [22/108] in exon 20), 4.7% (36/761) harboured a BRAF mutation, and 2.6% (17/644) harboured an NRAS mutation. KRAS mutants did not derive benefit compared with wild types, with a response rate of 6.7% (17/253) versus 35.8% (126/352; odds ratio [OR] 0.13, 95% CI 0.07-0.22; p<0.0001), a median PFS of 12. weeks versus 24 weeks (hazard ratio [HR] 1 98, 1.66-2.36; p<0.0001), and a median overall survival of 32 weeks versus 50 weeks (1.75, 1.47-2.09; p<0.0001). In KRAS wild types, carriers of BRAF and NRAS mutations had a significantly lower response rate than did BRAF and NRAS wild types, with a response rate of 8.3% (2/24) in carriers of BRAF mutations versus 38.0% in BRAF wild types (124/326; OR 0.15, 95% CI 0.02-0.51; p=0.0012); and 7.7% (1/13) in carriers of NRAS mutations versus 38.1% in NRAS wild types (110/289; OR 0.14, 0.007-0.70; p=0.013). PIK3CA exon 9 mutations had no effect, whereas exon 20 mutations were associated with a worse outcome compared with wild types, with a response rate of 0.0% (0/9) versus 36.8% (121/329; OR 0.00,0.00-0.89; p=0.029), a median PFS of 11.5 weeks versus 24 weeks (HR 2.52, 1.33-4.78; p=0.013), and a median overall survival of 34 weeks versus 51 weeks (3.29, 1.60-6.74; p=0.0057). Multivariate analysis and conditional inference trees confirmed that, if KRAS is not mutated, assessing BRAF, NRAS, and PIK3CA exon 20 mutations (in that order) gives additional information about outcome. Objective response rates in our series were 24.4% in the unselected population, 36.3% in the KRAS wild-type selected population, and 41.2% in the KRAS, BRAF, NRAS, and PIK3CA exon 20 wild-type population. Interpretation While confirming the negative effect of KRAS mutations on outcome after cetuximab, we show that BRAF, NRAS, and PIK3CA,exon 20 mutations are significantly associated with a low response rate. Objective response rates could be improved by additional genotyping of BRAF, NRAS, and PIK3CA exon 20 mutations in a KRAS wild-type population.
1,940 citations
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The Catholic University of America1, Royal Prince Alfred Hospital2, University of Toronto3, Centre for Addiction and Mental Health4, Università Campus Bio-Medico5, University of Eastern Finland6, Monash University7, Medical University of South Carolina8, Paris 12 Val de Marne University9, University of Regensburg10, University of Brescia11, University of Göttingen12, Beth Israel Deaconess Medical Center13, University of Siena14, University College London15, Copenhagen University Hospital16, Fukushima Medical University17, University of Tübingen18
TL;DR: These guidelines provide an up-date of previous IFCN report on “Non-invasive electrical and magnetic stimulation of the brain, spinal cord and roots: basic principles and procedures for routine clinical application” and include some recent extensions and developments.
1,850 citations
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Paris 12 Val de Marne University1, French Institute of Health and Medical Research2, University of Göttingen3, Ghent University4, University Hospital of Lausanne5, University of Lisbon6, university of lille7, Università Campus Bio-Medico8, University of Belgrade9, University of Hamburg10, Turku University Hospital11, Aristotle University of Thessaloniki12, University of Regensburg13, University of Bern14, Ludwig Maximilian University of Munich15, University of Siena16, The Catholic University of America17, University College London18, University of Ulm19, Copenhagen University Hospital20, University of Oxford21, University of Barcelona22, University of Tübingen23
TL;DR: There is a sufficient body of evidence to accept with level A (definite efficacy) the analgesic effect of high-frequency rTMS of the primary motor cortex (M1) contralateral to the pain and the antidepressant effect of HF-rT MS of the left dorsolateral prefrontal cortex (DLPFC).
1,554 citations
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TL;DR: The isolation of undifferentiated cells that grow as self-adherent clusters (that are termed “cardiospheres”) from subcultures of postnatal atrial or ventricular human biopsy specimens and from murine hearts are described.
Abstract: Cardiac myocytes have been traditionally regarded as terminally differentiated cells that adapt to increased work and compensate for disease exclusively through hypertrophy. However, in the past few years, compelling evidence has accumulated suggesting that the heart has regenerative potential. Recent studies have even surmised the existence of resident cardiac stem cells, endothelial cells generating cardiomyocytes by cell contact or extracardiac progenitors for cardiomyocytes, but these findings are still controversial. We describe the isolation of undifferentiated cells that grow as self-adherent clusters (that we have termed "cardiospheres") from subcultures of postnatal atrial or ventricular human biopsy specimens and from murine hearts. These cells are clonogenic, express stem and endothelial progenitor cell antigens/markers, and appear to have the properties of adult cardiac stem cells. They are capable of long-term self-renewal and can differentiate in vitro and after ectopic (dorsal subcutaneous connective tissue) or orthotopic (myocardial infarction) transplantation in SCID beige mouse to yield the major specialized cell types of the heart: myocytes (ie, cells demonstrating contractile activity and/or showing cardiomyocyte markers) and vascular cells (ie, cells with endothelial or smooth muscle markers).
1,525 citations
Authors
Showing all 2872 results
Name | H-index | Papers | Citations |
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Robert J. Motzer | 121 | 883 | 80129 |
Nicola Maffulli | 115 | 1570 | 59548 |
Bernard Escudier | 96 | 664 | 53523 |
Paolo Maria Rossini | 94 | 680 | 43935 |
Franco Mandelli | 89 | 720 | 33262 |
Matteo Cesari | 88 | 611 | 35197 |
Ana M. Valdes | 84 | 334 | 26627 |
Mauro Maccarrone | 80 | 533 | 22514 |
Patrizio Pasqualetti | 75 | 321 | 17042 |
Tiziana Bisogno | 75 | 130 | 19445 |
Massimo Inguscio | 74 | 427 | 21507 |
Guido Costamagna | 72 | 656 | 19050 |
Alberto Zangrillo | 70 | 539 | 21474 |
Antonio Abbate | 70 | 507 | 17365 |
Giovanni Landoni | 69 | 611 | 17481 |