Institution
University of Turin
Education•Turin, Piemonte, Italy•
About: University of Turin is a education organization based out in Turin, Piemonte, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 29607 authors who have published 77952 publications receiving 2480900 citations. The organization is also known as: Universita degli Studi di Torino & Università degli Studi di Torino.
Papers published on a yearly basis
Papers
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TL;DR: This work investigates the role of scatter factors and semaphorins in neoplastic disease, and their role in the aberrant counterpart of a physiological programme for organ regeneration and maintenance.
Abstract: Malignant disease occurs when neoplastic cells abandon their primary site of accretion, cross tissue boundaries and penetrate the vasculature to colonize distant sites. This process --metastasis--is the aberrant counterpart of a physiological programme for organ regeneration and maintenance. Scatter factors and semaphorins, together with their receptors, help to orchestrate this programme. What are the differences between physiological and pathological activation of these signalling molecules, and can we exploit them therapeutically to prevent metastasis?
746 citations
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TL;DR: The mutational analysis of PIK3CA and KRAS and evaluation of the PTEN protein status in a cohort of 110 patients with mCRC treated with anti-EGFR moAbs indicate that Pik3CA mutations can independently hamper the therapeutic response to panitumumab or cetuximab in mC RC.
Abstract: The monoclonal antibodies (moAb) panitumumab and cetuximab target the epidermal growth factor receptor (EGFR) and have proven valuable for the treatment of metastatic colorectal cancer (mCRC).EGFR-mediated signaling involves two main intracellular cascades: on one side KRAS activates BRAF, which in turn triggers the mitogen-activated protein kinases.On the other, membrane localization of the lipid kinase PIK3CA counteracts PTEN and promotes AKT1 phosphorylation, thereby activating a parallel intracellular axis. Constitutive activation of KRAS bypasses the corresponding signaling cascade and, accordingly, patients with mCRC bearing KRAS mutations are clinically resistant to therapy with panitumumab or cetuximab.We hypothesized that mutations activating PIK3CA could also preclude responsiveness to EGFR-targeted moAbs through a similar mechanism. Here, we present the mutational analysis of PIK3CA and KRAS and evaluation of the PTEN protein status in a cohort of 110 patients with mCRC treated with anti-EGFR moAbs.We observed 15 (13.6%) PIK3CA and 32 (29.0%) KRAS mutations. PIK3CA mutations were significantly associated with clinical resistance to panitumumab or cetuximab; none of the mutated patients achieved objective response (P = 0.038). When only KRAS wild-type tumors were analyzed, the statistical correlation was stronger (P = 0.016). Patients with PIK3CA mutations displayed a worse clinical outcome also in terms of progression-free survival (P = 0.035). Our data indicate that PIK3CA mutations can independently hamper the therapeutic response to panitumumab or cetuximab in mCRC.When the molecular status of the PIK3CA/PTEN and KRAS pathways are concomitantly ascertained, up to 70% of mCRC patients unlikely to respond to EGFR moAbs can be identified. [Cancer Res 2009;69(5):1851–7]
742 citations
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TL;DR: In this paper, the B3LYP method augmented with a damped empirical dispersion term (−f(R)C6/R6) is shown to yield structures and cohesive energies, for a representative set of molecular crystals, in excellent agreement with experimental data.
Abstract: The B3LYP method augmented with a damped empirical dispersion term (−f(R)C6/R6) is shown to yield structures and cohesive energies, for a representative set of molecular crystals, in excellent agreement with experimental data. Vibrational lattice modes of crystalline urea are also reported to be very close to experiment. The role of the damping function in scaling the dispersion contribution has been analyzed as well as the relevance of the BSSE in the prediction of structure and cohesive energy.
739 citations
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TL;DR: Hyperinsulinemia and insulin resistance occur frequently in patients with NASH; these conditions do not stem from a reduced hepatic insulin extraction but from an enhanced pancreatic insulin secretion compensatory to reduced insulin sensitivity.
735 citations
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TL;DR: It is shown that female mice with a cardiomyocyte-specific deletion of stat3 develop PPCM, implying that inhibition of prolactin release may represent a novel therapeutic strategy for P PCM.
730 citations
Authors
Showing all 30045 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Grätzel | 248 | 1423 | 303599 |
Lewis C. Cantley | 196 | 748 | 169037 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Elio Riboli | 158 | 1136 | 110499 |
Giacomo Bruno | 158 | 1687 | 124368 |
Silvia Franceschi | 155 | 1340 | 112504 |
Thomas E. Starzl | 150 | 1625 | 91704 |
Paolo Boffetta | 148 | 1455 | 93876 |
Marco Costa | 146 | 1458 | 105096 |
Pier Paolo Pandolfi | 146 | 529 | 88334 |
Andrew Ivanov | 142 | 1812 | 97390 |
Chiara Mariotti | 141 | 1426 | 98157 |
Tomas Ganz | 141 | 480 | 73316 |
Jean-Pierre Changeux | 138 | 672 | 76462 |
Dong-Chul Son | 138 | 1370 | 98686 |