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Your search keyword '"Severi, P."' showing total 10 results
Start Over Author "Severi, P." Journal british journal of cancer
10 results on '"Severi, P."'

1. Prognostic role of pre-diagnostic circulating inflammatory biomarkers in breast cancer survival: evidence from the EPIC cohort study

Author

Castro-Espin, Carlota, Cairat, Manon, Navionis, Anne-Sophie, Dahm, Christina C., Antoniussen, Christian S., Tjønneland, Anne, Mellemkjær, Lene, Mancini, Francesca Romana, Hajji-Louati, Mariem, Severi, Gianluca, Le Cornet, Charlotte, Kaaks, Rudolf, Schulze, Matthias B., Masala, Giovanna, Agnoli, Claudia, Sacerdote, Carlotta, Crous-Bou, Marta, Sánchez, Maria-Jose, Amiano, Pilar, Chirlaque, María-Dolores, Guevara, Marcela, Smith-Byrne, Karl, Heath, Alicia K., Christakoudi, Sofia, Gunter, Marc J., Rinaldi, Sabina, Agudo, Antonio, and Dossus, Laure

Published
2024
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2. Dietary intake of total, heme and non-heme iron and the risk of colorectal cancer in a European prospective cohort study

Author

Aglago, Elom K., Cross, Amanda J., Riboli, Elio, Fedirko, Veronika, Hughes, David J., Fournier, Agnes, Jakszyn, Paula, Freisling, Heinz, Gunter, Marc J., Dahm, Christina C., Overvad, Kim, Tjønneland, Anne, Kyrø, Cecilie, Boutron-Ruault, Marie-Christine, Rothwell, Joseph A., Severi, Gianluca, Katzke, Verena, Srour, Bernard, Schulze, Matthias B., Wittenbecher, Clemens, Palli, Domenico, Sieri, Sabina, Pasanisi, Fabrizio, Tumino, Rosario, Ricceri, Fulvio, Bueno-de-Mesquita, Bas, Derksen, Jeroen W. G., Skeie, Guri, Jensen, Torill Enget, Lukic, Marko, Sánchez, Maria-Jose, Amiano, Pilar, Colorado-Yohar, Sandra, Barricarte, Aurelio, Ericson, Ulrika, van Guelpen, Bethany, Papier, Keren, Knuppel, Anika, Casagrande, Corinne, Huybrechts, Inge, Heath, Alicia K., Tsilidis, Konstantinos K., and Jenab, Mazda

Published
2023
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3. Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort: the ELAPSE project

Author

Chen, Jie, Rodopoulou, Sophia, Strak, Maciej, de Hoogh, Kees, Taj, Tahir, Poulsen, Aslak Harbo, Andersen, Zorana J., Bellander, Tom, Brandt, Jørgen, Zitt, Emanuel, Fecht, Daniela, Forastiere, Francesco, Gulliver, John, Hertel, Ole, Hoffmann, Barbara, Hvidtfeldt, Ulla Arthur, Verschuren, W. M. Monique, Jørgensen, Jeanette T., Katsouyanni, Klea, Ketzel, Matthias, Lager, Anton, Leander, Karin, Liu, Shuo, Ljungman, Petter, Severi, Gianluca, Boutron-Ruault, Marie-Christine, Magnusson, Patrik K. E., Nagel, Gabriele, Pershagen, Göran, Peters, Annette, Rizzuto, Debora, van der Schouw, Yvonne T., Samoli, Evangelia, Sørensen, Mette, Stafoggia, Massimo, Tjønneland, Anne, Weinmayr, Gudrun, Wolf, Kathrin, Brunekreef, Bert, Raaschou-Nielsen, Ole, and Hoek, Gerard

Published
2022
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4. The combined activation of KCa3.1 and inhibition of Kv11.1/hERG1 currents contribute to overcome Cisplatin resistance in colorectal cancer cells

Author

Pillozzi, Serena, D'Amico, Massimo, Bartoli, Gianluca, Gasparoli, Luca, Petroni, Giulia, Crociani, Olivia, Marzo, Tiziano, Guerriero, Angela, Messori, Luigi, Severi, Mirko, Udisti, Roberto, Wulff, Heike, Chandy, K George, Becchetti, Andrea, and Arcangeli, Annarosa

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Colo-Rectal Cancer, Digestive Diseases, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Apoptosis, Benzothiazoles, Cell Cycle, Cell Line, Tumor, Cell Survival, Cisplatin, Colorectal Neoplasms, Drug Resistance, Neoplasm, Drug Synergism, ERG1 Potassium Channel, HCT116 Cells, HT29 Cells, Humans, Inhibitory Concentration 50, Intermediate-Conductance Calcium-Activated Potassium Channels, Mice, Potassium Channel Blockers, Pyrazoles, Riluzole, SKA-31, E4031, Cisplatin uptake, preclinical mouse models, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BACKGROUND:Platinum-based drugs such as Cisplatin are commonly employed for cancer treatment. Despite an initial therapeutic response, Cisplatin treatment often results in the development of chemoresistance. To identify novel approaches to overcome Cisplatin resistance, we tested Cisplatin in combination with K+ channel modulators on colorectal cancer (CRC) cells. METHODS:The functional expression of Ca2+-activated (KCa3.1, also known as KCNN4) and voltage-dependent (Kv11.1, also known as KCNH2 or hERG1) K+ channels was determined in two CRC cell lines (HCT-116 and HCT-8) by molecular and electrophysiological techniques. Cisplatin and several K+ channel modulators were tested in vitro for their action on K+ currents, cell vitality, apoptosis, cell cycle, proliferation, intracellular signalling and Platinum uptake. These effects were also analysed in a mouse model mimicking Cisplatin resistance. RESULTS:Cisplatin-resistant CRC cells expressed higher levels of KCa3.1 and Kv11.1 channels, compared with Cisplatin-sensitive CRC cells. In resistant cells, KCa3.1 activators (SKA-31) and Kv11.1 inhibitors (E4031) had a synergistic action with Cisplatin in triggering apoptosis and inhibiting proliferation. The effect was maximal when KCa3.1 activation and Kv11.1 inhibition were combined. In fact, similar results were produced by Riluzole, which is able to both activate KCa3.1 and inhibit Kv11.1. Cisplatin uptake into resistant cells depended on KCa3.1 channel activity, as it was potentiated by KCa3.1 activators. Kv11.1 blockade led to increased KCa3.1 expression and thereby stimulated Cisplatin uptake. Finally, the combined administration of a KCa3.1 activator and a Kv11.1 inhibitor also overcame Cisplatin resistance in vivo. CONCLUSIONS:As Riluzole, an activator of KCa3.1 and inhibitor of Kv11.1 channels, is in clinical use, our results suggest that this compound may be useful in the clinic to improve Cisplatin efficacy and overcome Cisplatin resistance in CRC.

Published
2018

5. Circulating androgen receptor gene amplification and resistance to 177Lu-PSMA-617 in metastatic castration-resistant prostate cancer: results of a Phase 2 trial

Author

De Giorgi, Ugo, Sansovini, Maddalena, Severi, Stefano, Nicolini, Silvia, Monti, Manuela, Gurioli, Giorgia, Foca, Flavia, Casadei, Chiara, Conteduca, Vincenza, Celli, Monica, Di Iorio, Valentina, Calistri, Daniele, Matteucci, Federica, von Eyben, Finn Edler, Attard, Gerhardt, and Paganelli, Giovanni

Published
2021
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7. PREDICT Plus: development and validation of a prognostic model for early breast cancer that includes HER2

Author

Wishart, GC, Bajdik, CD, Dicks, E, Provenzano, E, Schmidt, MK, Sherman, M, Greenberg, DC, Green, AR, Gelmon, KA, Kosma, V-M, Olson, JE, Beckmann, MW, Winqvist, R, Cross, SS, Severi, G, Huntsman, D, Pylkäs, K, Ellis, I, Nielsen, TO, Giles, G, Blomqvist, C, Fasching, PA, Couch, FJ, Rakha, E, Foulkes, WD, Blows, FM, Bégin, LR, van't Veer, LJ, Southey, M, Nevanlinna, H, Mannermaa, A, Cox, A, Cheang, M, Baglietto, L, Caldas, C, Garcia-Closas, M, and Pharoah, PDP

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Clinical Research, Cancer, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Adult, Aged, Breast Neoplasms, Cohort Studies, Female, Humans, Middle Aged, Models, Statistical, Prognosis, Proportional Hazards Models, Receptor, ErbB-2, Reproducibility of Results, Young Adult, breast cancer, HER2, prognostic model, Receptor, erbB-2, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Predict (www.predict.nhs.uk) is an online, breast cancer prognostication and treatment benefit tool. The aim of this study was to incorporate the prognostic effect of HER2 status in a new version (Predict+), and to compare its performance with the original Predict and Adjuvant!. The prognostic effect of HER2 status was based on an analysis of data from 10 179 breast cancer patients from 14 studies in the Breast Cancer Association Consortium. The hazard ratio estimates were incorporated into Predict. The validation study was based on 1653 patients with early-stage invasive breast cancer identified from the British Columbia Breast Cancer Outcomes Unit. Predicted overall survival (OS) and breast cancer-specific survival (BCSS) for Predict+, Predict and Adjuvant! were compared with observed outcomes. All three models performed well for both OS and BCSS. Both Predict models provided better BCSS estimates than Adjuvant!. In the subset of patients with HER2-positive tumours, Predict+ performed substantially better than the other two models for both OS and BCSS. Predict+ is the first clinical breast cancer prognostication tool that includes tumour HER2 status. Use of the model might lead to more accurate absolute treatment benefit predictions for individual patients.

Published
2012

8. Evaluation of variation in the phosphoinositide-3-kinase catalytic subunit alpha oncogene and breast cancer risk

Author

Stevens, KN, Garcia-Closas, M, Fredericksen, Z, Kosel, M, Pankratz, VS, Hopper, JL, Dite, GS, Apicella, C, Southey, MC, Schmidt, MK, Broeks, A, Van ‘t Veer, LJ, Tollenaar, RAEM, Fasching, PA, Beckmann, MW, Hein, A, Ekici, AB, Johnson, N, Peto, J, dos Santos Silva, I, Gibson, L, Sawyer, E, Tomlinson, I, Kerin, MJ, Chanock, S, Lissowska, J, Hunter, DJ, Hoover, RN, Thomas, GD, Milne, RL, Pérez, JI Arias, González-Neira, A, Benítez, J, Burwinkel, B, Meindl, A, Schmutzler, RK, Bartrar, CR, Hamann, U, Ko, YD, Brüning, T, Chang-Claude, J, Hein, R, Wang-Gohrke, S, Dörk, T, Schürmann, P, Bremer, M, Hillemanns, P, Bogdanova, N, Zalutsky, JV, Rogov, YI, Antonenkova, N, Lindblom, A, Margolin, S, Mannermaa, A, Kataja, V, Kosma, V-M, Hartikainen, J, Chenevix-Trench, G, Chen, X, Peterlongo, P, Bonanni, B, Bernard, L, Manoukian, S, Wang, X, Cerhan, J, Vachon, CM, Olson, J, Giles, GG, Baglietto, L, McLean, CA, Severi, G, John, EM, Miron, A, Winqvist, R, Pylkäs, K, Jukkola-Vuorinen, A, Grip, M, Andrulis, I, Knight, JA, Glendon, G, Mulligan, AM, Cox, A, Brock, IW, Elliott, G, Cross, SS, Pharoah, PP, Dunning, AM, Pooley, KA, Humphreys, MK, Wang, J, Kang, D, Yoo, K-Y, Noh, D-Y, Sangrajrang, S, Gabrieau, V, Brennan, P, McKay, J, Anton-Culver, H, Ziogas, A, and Couch, FJ

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Genetics, Cancer, Breast Cancer, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Breast Neoplasms, Case-Control Studies, Class I Phosphatidylinositol 3-Kinases, Female, Genetic Predisposition to Disease, Genetic Variation, Humans, Phosphatidylinositol 3-Kinases, genetic susceptibility, neoplasms, association study, GENICA Network, kConFab Investigators, Australian Ovarian Cancer Study Group, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundSomatic mutations in phosphoinositide-3-kinase catalytic subunit alpha (PIK3CA) are frequent in breast tumours and have been associated with oestrogen receptor (ER) expression, human epidermal growth factor receptor-2 overexpression, lymph node metastasis and poor survival. The goal of this study was to evaluate the association between inherited variation in this oncogene and risk of breast cancer.MethodsA single-nucleotide polymorphism from the PIK3CA locus that was associated with breast cancer in a study of Caucasian breast cancer cases and controls from the Mayo Clinic (MCBCS) was genotyped in 5436 cases and 5280 controls from the Cancer Genetic Markers of Susceptibility (CGEMS) study and in 30 949 cases and 29 788 controls from the Breast Cancer Association Consortium (BCAC).ResultsRs1607237 was significantly associated with a decreased risk of breast cancer in MCBCS, CGEMS and all studies of white Europeans combined (odds ratio (OR)=0.97, 95% confidence interval (CI) 0.95-0.99, P=4.6 × 10(-3)), but did not reach significance in the BCAC replication study alone (OR=0.98, 95% CI 0.96-1.01, P=0.139).ConclusionCommon germline variation in PIK3CA does not have a strong influence on the risk of breast cancer.

Published
2011

9. Effect of tamoxifen and transdermal hormone replacement therapy on cardiovascular risk factors in a prevention trial

Author

Decensi, A, Robertson, C, Rotmensz, N, Severi, G, Maisonneuve, P, Sacchini, V, Boyle, P, Costa, A, and Veronesi, U

Abstract

The combination of tamoxifen and transdermal hormone replacement therapy (HRT) may potentially reduce risks and side-effects of either agent, but an adverse interaction could attenuate their beneficial effects. We assessed the effects of their combination on cardiovascular risk factors within a prevention trial of tamoxifen. Baseline and 12-month measurements of total, low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, platelets and white blood cells were obtained in the following four groups: tamoxifen (n = 1117), placebo (n = 1112), tamoxifen and HRT (n = 68), placebo and HRT (n = 87). The analysis was further extended to women who were on HRT at randomization but discontinued it during the 12-month intervention period (n = 33 on tamoxifen and n = 35 on placebo) and to women who were not on HRT but started it during intervention (n = 36 in both arms of the study). Compared with small changes in the placebo group, tamoxifen was associated with changes in total, LDL- and HDL-cholesterol of approximately -9%, -19% and +0.2% in continuous HRT users compared with -9%, -14% and -0.8% in never HRT users. Similarly, there was no interaction on platelet count. In contrast, the decrease in total and LDL-cholesterol levels induced by tamoxifen was blunted by two-thirds in women who started HRT while on tamoxifen (P = 0.051 for the interaction term). We conclude that the beneficial effects of tamoxifen on cardiovascular risk factors are unchanged in current HRT users, whereas they may be attenuated in women who start transdermal HRT while on tamoxifen. Whereas a trial of tamoxifen in women already on transdermal HRT is warranted, prescription of HRT during tamoxifen may attenuate its activity.

Published
1998
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