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1. ESMO Guidance for Reporting Oncology real-World evidence (GROW)

Author

Castelo-Branco, L., Pellat, A., Martins-Branco, D., Valachis, A., Derksen, J.W.G., Suijkerbuijk, K.P.M., Dafni, U., Dellaporta, T., Vogel, A., Prelaj, A., Groenwold, R.H.H., Martins, H., Stahel, R., Bliss, J., Kather, J., Ribelles, N., Perrone, F., Hall, P.S., Dienstmann, R., Booth, C.M., Pentheroudakis, G., Delaloge, S., and Koopman, M.

Published
2023
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4. ESMO Guidance for Reporting Oncology real-World evidence (GROW)

Author

Castelo-Branco, L., primary, Pellat, A., additional, Martins-Branco, D., additional, Valachis, A., additional, Derksen, J.W.G., additional, Suijkerbuijk, K.P.M., additional, Dafni, U., additional, Dellaporta, T., additional, Vogel, A., additional, Prelaj, A., additional, Groenwold, R.H.H., additional, Martins, H., additional, Stahel, R., additional, Bliss, J., additional, Kather, J., additional, Ribelles, N., additional, Perrone, F., additional, Hall, P.S., additional, Dienstmann, R., additional, Booth, C.M., additional, Pentheroudakis, G., additional, Delaloge, S., additional, and Koopman, M., additional

Published
2023
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5. ESMO Guidance for Reporting Oncology real-World evidence (GROW)

Author

Epi Kanker Team B, Cancer, MS Medische Oncologie, Infection & Immunity, Castelo-Branco, L, Pellat, A, Martins-Branco, D, Valachis, A, Derksen, J W G, Suijkerbuijk, K P M, Dafni, U, Dellaporta, T, Vogel, A, Prelaj, A, Groenwold, R H H, Martins, H, Stahel, R, Bliss, J, Kather, J, Ribelles, N, Perrone, F, Hall, P S, Dienstmann, R, Booth, C M, Pentheroudakis, G, Delaloge, S, Koopman, M, Epi Kanker Team B, Cancer, MS Medische Oncologie, Infection & Immunity, Castelo-Branco, L, Pellat, A, Martins-Branco, D, Valachis, A, Derksen, J W G, Suijkerbuijk, K P M, Dafni, U, Dellaporta, T, Vogel, A, Prelaj, A, Groenwold, R H H, Martins, H, Stahel, R, Bliss, J, Kather, J, Ribelles, N, Perrone, F, Hall, P S, Dienstmann, R, Booth, C M, Pentheroudakis, G, Delaloge, S, and Koopman, M

Published
2023

7. Chemotherapy de-escalation using an F-18-FDG-PET-based pathological response-adapted strategy in patients with HER2-positive early breast cancer (PHERGain): a multicentre, randomised, open-label, non-comparative, phase 2 trial

Author

Perez-Garcia J, Gebhart G, Borrego M, Stradella A, Bermejo B, Schmid P, Marme F, Escriva-de-Romani S, Calvo L, Ribelles N, Martinez N, Albacar C, Prat A, Dalenc F, Kerrou K, Colleoni M, Afonso N, Di Cosimo S, Sampayo-Cordero M, Malfettone A, Cortes J, Llombart-Cussac A, and PHERGain Steering Comm Trial Inve

Abstract

Background Several de-escalation approaches are under investigation in patients with HER2-positive, early-stage breast cancer. We assessed early metabolic responses to neoadjuvant trashizumab and pertuzumab using F-18-fluorodeoxyglucose (F-18-FDG)-PET (F-18-FDG-PET) and the possibility of chemotherapy de-escalation using a pathological response-adapted strategy. Methods We did a multicentre, randomised, open-label, non-comparative, phase 2 trial in 45 hospitals in Spain, France, Belgium, Germany, the UK, Italy, and Portugal. Eligible participants were women aged 18 years or older with centrally confirmed, HER2-positive, stage I-IIIA, invasive, operable breast cancer (1.5 cm tumour size) with at least one breast lesion evaluable by 18 F-FDG-PET, an Eastern Cooperative Oncology Group performance status of 0 or 1, and a baseline left ventricular ejection fraction of at least 55%. We randomly assigned participants (1:4), via an interactive response system using central block randomisation with block sizes of five, stratified by hormone receptor status, to either docetaxel (75 mg/m(2) intravenous), carboplatin (area under the concentration-time curve 6 mg/mL per min intravenous), trastuzumab (subcutaneous 600 mg fixed dose), and pertuzumab (intravenous 840 mg loading dose, 420 mg maintenance doses; group A); or trastuzumab and pertuzumab (group B). Hormone receptor-positive patients allocated to group B were additionally given letrozole if postmenopausal (2.5 mg/day orally) or tamoxifen if premenopausal (20 mg/day orally). Centrally reviewed F-18-FDG-PET scans were done before randomisation and after two treatment cycles. Patients assigned to group A completed six cycles of treatment (every 3 weeks) regardless of F-18-FDG-PET results. All patients assigned to group B initially received two cycles of trastuzumab and pertuzumab. F-18-FDG-PET responders in group B continued this treatment for six further cycles; F-18-FDG-PET non-responders in this group were switched to six cycles of docetaxel, carboplatin, trastuzumab, and pertuzumab. Surgery was done 2-6 weeks after the last dose of study treatment. Adjuvant treatment was selected according to the neoadjuvant treatment administered, pathological response, hormone receptor status, and clinical stage at diagnosis. The coprimary endpoints were the proportion of F-18-FDG-PET responders in group B with a pathological complete response in the breast and axilla (ypT0/is ypN0) as determined by a local pathologist after surgery after eight cycles of treatment, and 3-year invasive disease-free survival of patients in group B, both assessed by intention to treat. The definitive assessment of pathological complete response was done at this primary analysis; follow-up to assess invasive disease-free survival is continuing, hence these data are not included in this Article. Safety was assessed in all participants who received at least one dose of study drug. Health-related quality-of-life was assessed with EORTC QLQ-C30 and QLQ-BR23 questionnaires at baseline, after two cycles of treatment, and before surgery. This trial is registered with EudraCT (2016-002676-27) and ClinicalTrials.gov (NCT03161353), and is ongoing. Findings Between rune 26, 2017, and April 24, 2019, we randomly assigned 71 patients to group A and 285 to group B. Median follow-up was 5.7 months (IQR 5.3-6.0). 227 (80%) of 285 patients in group B were F-18-FDGPET responders, of whom 86 (37.9%, 95% CI 31.6-44-5; p

Published
2021

8. Regulatory CDH4 Genetic Variants Associate With Risk to Develop Capecitabine-Induced Hand-Foot Syndrome.

Author

Ruiz-Pinto, S, Pita, G, Martín, M, Nuñez-Torres, R, Cuadrado, A, Shahbazi, MN, Caronia, D, Kojic, A, Moreno, LT, de la Torre-Montero, JC, Lozano, M, López-Fernández, LA, Ribelles, N, García-Saenz, JA, Alba, E, Milne, RL, Losada, A, Pérez-Moreno, M, Benítez, J, González-Neira, A, Ruiz-Pinto, S, Pita, G, Martín, M, Nuñez-Torres, R, Cuadrado, A, Shahbazi, MN, Caronia, D, Kojic, A, Moreno, LT, de la Torre-Montero, JC, Lozano, M, López-Fernández, LA, Ribelles, N, García-Saenz, JA, Alba, E, Milne, RL, Losada, A, Pérez-Moreno, M, Benítez, J, and González-Neira, A

Abstract

Capecitabine-induced hand-foot syndrome (CiHFS) is a common dermatological adverse reaction affecting around 30% of patients with capecitabine-treated cancer, and the main cause of dose reductions and chemotherapy delays. To identify novel genetic factors associated with CiHFS in patients with cancer, we carried out an extreme-phenotype genomewide association study in 166 patients with breast and colorectal capecitabine-treated cancer with replication in a second cohort of 85 patients. We discovered and replicated a cluster of four highly correlated single-nucleotide polymorphisms associated with susceptibility to CiHFS at 20q13.33 locus (top hit = rs6129058, hazard ratio = 2.40, 95% confidence interval = 1.78-3.20; P = 1.2 × 10-8 ). Using circular chromosome conformation capture sequencing, we identified a chromatin contact between the locus containing the risk alleles and the promoter of CDH4, located 90 kilobases away. The risk haplotype was associated with decreased levels of CDH4 mRNA and the protein it encodes, R-cadherin (RCAD), which mainly localizes in the granular layer of the epidermis. In human keratinocytes, CDH4 downregulation resulted in reduced expression of involucrin, a protein of the cornified envelope, an essential structure for skin barrier function. Immunohistochemical analyses revealed that skin from patients with severe CiHFS exhibited low levels of RCAD and involucrin before capecitabine treatment. Our results uncover a novel mechanism underlying individual genetic susceptibility to CiHFS with implications for clinically relevant risk prediction.

Published
2021

15. Abstract P5-12-03: Genome copy number entropy as predictor of response for neoadjuvant therapy in early breast cancer

Author

Alba, E, primary, Rueda, OM, additional, Lluch, A, additional, Albanell, J, additional, Chin, S-F, additional, Chacón, JI, additional, Calvo, L, additional, De la Haba-Rodriguez, J, additional, Bermejo, B, additional, Ribelles, N, additional, Sánchez-Rovira, P, additional, Plazaola, A, additional, Barnadas, A, additional, Cirauqul, B, additional, Ramos, M, additional, Arcusa, A, additional, Carrasco, E, additional, Herranz, J, additional, Chiesa, M, additional, Caballero, R, additional, Santonja, A, additional, Rojo, F, additional, and Caldas, C, additional

Published
2019
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16. Abstract P2-13-04: Impact of the adjuvant treatment with trastuzumab in HER2 positive breast cancer in the real-world setting. Analysis of two cohorts (1997-2005/2006-2015) in 1970 patients

Author

Rodriguez, CA, primary, Garcia-Gomez, J, additional, Ribelles, N, additional, Gavila, J, additional, Pernas, S, additional, Rodriguez-Lescure, A, additional, Urrutikoetxea, A, additional, Pernaut, C, additional, Lopez, A, additional, and Garcia-Mata, J, additional

Published
2019
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18. Central sensitization in breast cancer survivors

Author

Cuesta-Vargas, Antonio I., Roldán-Jimenez, C., Pajares, B., Alba, Emilio, Trinidad-Fernandez, M., Ribelles, N., Garcia-Almeida, J. M., de lo Rios-López, M. J., Tirado-Reyes, M., Sevilla-Castillo, A., other, and, Cuesta-Vargas, Antonio I., Roldán-Jimenez, C., Pajares, B., Alba, Emilio, Trinidad-Fernandez, M., Ribelles, N., Garcia-Almeida, J. M., de lo Rios-López, M. J., Tirado-Reyes, M., Sevilla-Castillo, A., and other, and

Abstract

The goal of this study was to study central sensitization (CS)-related symptoms in breast cancer (BC) survivors and to find if there are differences in clinical and functional variables. In this cross-sectional study, 25 women aged between 32 and 69 years participated. CS pain was measured with the Central Sensitization Inventory (CSI). Forty points was considered the cutoff value. Cancer-related fatigue (CRF), Quality of life, functional capacity, and handgrip strength (HGS) was assessed. A 60% of BC survivors showed a CSI score from 0 to 40, while the rest 40% of women had a score higher than 40, CSI scores being 38.35 ± 14.54 points in the whole sample. Significant differences were found in functional capacity, CRF and QoL (p <.011). However, there were no differences in HGS (p =.089). This is the first study to report BC survivors CS-related symptoms. The high CS-related symptoms group showed differences in some symptoms and functional capacity in this population. Future research including a wider sample and more variables related to pain should be carried out.

Published
2018

19. A Phase II study of Days 1 and 8 cisplatin and recombinant alpha-2B interferon in advanced non-small cell lung cancer

Author

Rosell, R., Carles, J., Ariza, A., Moreno, I., Ribelles, N., Solano, V., Pellicer, I., Barnadas, A., and Abad, A.

Subjects
Interferon -- Health aspects, Interferon alpha -- Health aspects, Cisplatin -- Health aspects, Lung cancer, Non-small cell, Tumor antigens -- Research, Health
Abstract

Preliminary data have suggested that the addition of alpha interferon to cisplatin might enhance the chemotherapeutic effectiveness of the latter drug in the treatment of advanced non-small cell lung cancer. Researchers, therefore, set out to determine if this theory could be confirmed in a clinical trial. A total of 30 patients were treated with cisplatin and alpha interferon. As a part of the evaluation of response to treatment, the researchers determined the expression of the antigens NSE (neuron-specific enolase) and Leu-7 in the tumor cells. One complete response to chemotherapy was observed, as were three partial responses. This 13 percent response rate is not different from that which would have been achieved with cisplatin alone, and there is therefore no support for the hypothesis that alpha interferon enhances the effectiveness of cisplatin. However, an interesting observation was made concerning the two antigens, NSE and Leu-7. Not all patients were tested for NSE, and just under 75 percent of those tested were positive, while only three patients were identified who were positive for Leu-7. However, all four of the patients who responded to treatment were positive for NSE and two were positive for both NSE and Leu-7. The authors suggest that this observation is worthy of further research. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

20. A randomized study of two vindesine plus cisplatin-containing regimens with the addition of mitomycin C or ifosfamide in patients with advanced non-small cell lung cancer

Author

Rosell, R., Abad-Esteve, A., Moreno, I., Barnadas, A., Carles, J., Fernandez, C., Ribelles, N., and Culubret, M.

Subjects
Cancer, Lung cancer, Non-small cell, Cisplatin -- Health aspects, Vindesine -- Health aspects, Ifosfamide -- Health aspects, Mitomycin -- Health aspects, Chemotherapy, Combination -- Evaluation, Health
Abstract

The effectiveness of combining different chemotherapeutic agents is based, at least in part, on determining which agents can work synergistically. That is, if two agents act upon cancer cells in slightly different ways, combining the agents might kill more cancer cells without increasing the toxic effects of either agent. If one of the chemotherapeutic drugs was administered at a higher dose, the toxic side effects would be increased. Cisplatin (P) has been the mainstay of lung cancer chemotherapy for a decade, and is often used in combination with vindesine (V). However, one report suggested a promising improvement in lung cancer survival when mitomycin C (M) was used in combination with vindesine and cisplatin (MVP). To replicate this observation, and extend it, 110 patients were randomly assigned to receive MVP, or a combination of ifosfamide, vindesine, and cisplatin (IVP). Seven patients could not be evaluated; the data on the remaining 103 patients indicated a response rate of 20 percent in the IVP group, and 26 percent in the MVP group, falling far short of the 60 percent survival rate previously reported for MVP. Survival in the IVP group was a median of 30 weeks; in the MVP group survival was a median of 32 weeks. For those who responded to chemotherapy, the median IVP group survival will be over 96 weeks; it was 45 weeks for the MVP group. The two-year survival rates were 26 percent for the IVP group and 0 percent for MVP; the difference was not statistically significant. These results failed to replicate the reported synergistic advantage of the MVP chemotherapeutic regimen and failed to find any significant difference between ifosfamide and mitomycin C when used in combination with vindesine and cisplatin. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

21. Genetic markers of toxicity from capecitabine and other fluorouracil-based regimens: investigation in the QUASAR2 study, systematic review, and meta-analysis

Author

Rosmarin, D, Palles, C, Church, D, Domingo, E, Jones, A, Johnstone, E, Wang, H, Love, S, Julier, P, Scudder, C, Nicholson, G, Gonzalez-Neira, A, Martin, M, Sargent, D, Green, E, McLeod, H, Zanger, U, Schwab, M, Braun, M, Seymour, M, Thompson, L, Lacas, B, Boige, V, Ribelles, N, and Afzal, S

Abstract

PURPOSE: Fluourouracil (FU) is a mainstay of chemotherapy, although toxicities are common. Genetic biomarkers have been used to predict these adverse events, but their utility is uncertain. PATIENTS AND METHODS: We tested candidate polymorphisms identified from a systematic literature search for associations with capecitabine toxicity in 927 patients with colorectal cancer in the Quick and Simple and Reliable trial (QUASAR2). We then performed meta-analysis of QUASAR2 and 16 published studies (n = 4,855 patients) to examine the polymorphisms in various FU monotherapy and combination therapy regimens. RESULTS: Global capecitabine toxicity (grades 0/1/2 v grades 3/4/5) was associated with the rare, functional DPYD alleles 2846T>A and *2A (combined odds ratio, 5.51; P = .0013) and with the common TYMS polymorphisms 5'VNTR2R/3R and 3'UTR 6bp ins-del (combined odds ratio, 1.31; P = 9.4 × 10(-6)). There was weaker evidence that these polymorphisms predict toxicity from bolus and infusional FU monotherapy. No good evidence of association with toxicity was found for the remaining polymorphisms, including several currently included in predictive kits. No polymorphisms were associated with toxicity in combination regimens. CONCLUSION: A panel of genetic biomarkers for capecitabine monotherapy toxicity would currently comprise only the four DPYD and TYMS variants above. We estimate this test could provide 26% sensitivity, 86% specificity, and 49% positive predictive value-better than most available commercial kits, but suboptimal for clinical use. The test panel might be extended to include additional, rare DPYD variants functionally equivalent to *2A and 2846A, though insufficient evidence supports its use in bolus, infusional, or combination FU. There remains a need to identify further markers of FU toxicity for all regimens.

Published
2016

22. A phase II trial of dasatinib (D) in combination with trastuzumab (T) and paclitaxel (P) in the first line treatment of HER2 positive metastatic breast cancer (MBC) patients (pts): GEICAM/2010-04

Author

Ocana Fernandez, A., primary, Ruiz Borrego, M., additional, Gil Martin, M., additional, Antolin, S., additional, Atienza, M., additional, Montaño, A., additional, Ribelles, N., additional, Guerrero, A., additional, Muñoz, M., additional, Fernández-Pérez, I., additional, Urruticoechea, A., additional, Falcon Gonzalez, A., additional, Pernas Simon, S., additional, Prato Varela, J., additional, Escudero, M.J., additional, Benito, S., additional, Caballero, R., additional, Carrasco, E., additional, Rojo, F., additional, and Pandiella, A., additional

Published
2017
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23. Genetic Markers of Toxicity From Capecitabine and Other Fluorouracil-Based Regimens: Investigation in the QUASAR2 Study, Systematic Review, and Meta-Analysis

Author

Rosmarin, D, Palles, C, Church, D, Domingo, E, Jones, A, Johnstone, E, Wang, H, Love, S, Julier, P, Scudder, C, Nicholson, G, Gonzalez-Neira, A, Martin, M, Sargent, D, Green, E, McLeod, H, Zanger, UM, Schwab, M, Braun, M, Seymour, M, Thompson, L, Lacas, B, Boige, V, Ribelles, N, Afzal, S, Enghusen, H, Jensen, SA, Etienne-Grimaldi, MC, Milano, G, Wadelius, M, Glimelius, B, Garmo, H, Gusella, M, Lecomte, T, Laurent-Puig, P, Martinez-Balibrea, E, Sharma, R, Garcia-Foncillas, J, Kleibl, Z, Morel, A, Pignon, JP, Midgley, R, Kerr, D, Tomlinson, I, University of Oxford [Oxford], Spanish National Cancer Research Center (CNIO), Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Mayo Clinic [Rochester], University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC), Molecular Mechanisms of Origin and Treatment of Breast Cancer, Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, University Hospital Tuebingen, The Christie NHS Foundation Trust [Manchester, Royaume-Uni], St James's University Hospital, Leeds Teaching Hospitals NHS Trust, Medical Research Council Clinical Trials Unit (MRC CTU), University College of London [London] (UCL), Institut Gustave Roussy (IGR), Service de biostatistique et d'épidémiologie (SBE), Direction de la recherche clinique [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Oncologie digestive, Département de médecine oncologique [Gustave Roussy], Hospital Universitario Virgen de la Victoria [Malaga, Espagne], Rigshospitalet [Copenhagen], Copenhagen University Hospital, Herlev and Gentofte Hospital, Centre de Lutte contre le Cancer Antoine Lacassagne [Nice] (UNICANCER/CAL), UNICANCER-Université Côte d'Azur (UCA), Uppsala University, Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Institut Català d'Oncologia, Imperial College Healthcare NHS Trust [Londres, Royaume-Uni], Universidad Pública de Navarra [Espagne] = Public University of Navarra (UPNA), Charles University [Prague] (CU), Cytokines : structure, signalisation et prolifération tumorale, Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Paul Papin, and CRLCC Paul Papin

Subjects
Genetic Markers, Polymorphism, Genetic, Drug-Related Side Effects and Adverse Reactions, [SDV]Life Sciences [q-bio], ORIGINAL REPORTS, Thymidylate Synthase, Deoxycytidine, Predictive Value of Tests, Antineoplastic Combined Chemotherapy Protocols, Humans, Fluorouracil, Colorectal Neoplasms, Capecitabine, Dihydrouracil Dehydrogenase (NADP)
Abstract

International audience; Purpose Fluourouracil (FU) is a mainstay of chemotherapy, although toxicities are common. Genetic biomarkers have been used to predict these adverse events, but their utility is uncertain.Patients and Methods We tested candidate polymorphisms identified from a systematic literature search for associations with capecitabine toxicity in 927 patients with colorectal cancer in the Quick and Simple and Reliable trial (QUASAR2). We then performed meta-analysis of QUASAR2 and 16 published studies (n = 4,855 patients) to examine the polymorphisms in various FU monotherapy and combination therapy regimens. Results Global capecitabine toxicity (grades 0/1/2 v grades 3/4/5) was associated with the rare, functional DPYD alleles 2846T>A and *2A (combined odds ratio, 5.51; P = .0013) and with the common TYMS polymorphisms 5′VNTR2R/3R and 3′UTR 6bp ins-del (combined odds ratio, 1.31; P = 9.4 × 10−6). There was weaker evidence that these polymorphisms predict toxicity from bolus and infusional FU monotherapy. No good evidence of association with toxicity was found for the remaining polymorphisms, including several currently included in predictive kits. No polymorphisms were associated with toxicity in combination regimens. Conclusion A panel of genetic biomarkers for capecitabine monotherapy toxicity would currently comprise only the four DPYD and TYMS variants above. We estimate this test could provide 26% sensitivity, 86% specificity, and 49% positive predictive value—better than most available commercial kits, but suboptimal for clinical use. The test panel might be extended to include additional, rare DPYD variants functionally equivalent to *2A and 2846A, though insufficient evidence supports its use in bolus, infusional, or combination FU. There remains a need to identify further markers of FU toxicity for all regimens.

Published
2014

24. Luminal androgen receptor role and pathological complete response rate to neoadjuvant chemotherapy in triple negative breast cancer

Author

Chica-Parrado, M.R., primary, Santonja, A., additional, Lluch-Hernandez, A., additional, Albanell, J., additional, Sanchez-Muñoz, A., additional, Chacón, I., additional, Calvo, L., additional, Sanchez-Rovira, P., additional, De Haba, J.l.a., additional, Vicioso, L., additional, Martin, M., additional, Plazaola, A., additional, Prat, A., additional, Ribelles, N., additional, Sánchez-Aragó, M., additional, Jerez, J.M., additional, Escudero, M.J., additional, Caballero, R., additional, Carrasco, E., additional, and Conejo, E. Alba, additional

Published
2016
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25. Germline genetic background contribution to metastatic dissemination in breast cancer extreme phenotype patients

Author

Santonja, A., primary, Pajares, B., additional, Jiménez-Rodríguez, B., additional, Sousa, C. Fernández-De, additional, Ribelles, N., additional, Lluch-Hernandez, A., additional, Catoira, I., additional, Perez-Ruiz, E., additional, Martin, M., additional, Del Monte-Millan, M., additional, Gonzalez-Neira, A., additional, Pita, G., additional, Pujana, M.A., additional, Ruiz, M., additional, Bonifaci, N., additional, De la Haba, J., additional, Sanchez-Rovira, P., additional, Alba, E., additional, and Romero, A., additional

Published
2016
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26. Abstract P3-07-14: Prosigna® intrinsic subtyping predicts response to neoadjuvant combination therapy in study that includes herceptin within HER2+ (IHC) patients

Author

Santonja, Á, primary, Ribelles, N, additional, Jiménez-Rodríguez, B, additional, Sánchez Rovira, P, additional, Álvarez, M, additional, Vicioso, L, additional, Isabel Fernandez, A, additional, de Luque, V, additional, Fernández de Sousa, C, additional, Villar, E, additional, Zarcos, I, additional, Ramírez, C, additional, González-Hermoso, C, additional, Jeiranian, A, additional, Dowidar, N, additional, Schaper, C, additional, Buckingham, W, additional, Ferree, S, additional, Jiménez, A, additional, Prat, A, additional, and Alba, E, additional

Published
2016
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27. Abstract P3-07-15: Prosigna® subtype correlation is a strong predictor of response to neoadjuvant chemotherapy (NAC) in early breast cancer (EBC) study

Author

Chica Parrado, R, primary, Jiménez-Rodríguez, B, additional, Sánchez Rovira, P, additional, Álvarez, M, additional, Vicioso, L, additional, Fernandez, AI, additional, de Luque, V, additional, José Lozano, M, additional, Villar, E, additional, Zarcos, I, additional, Ramírez, C, additional, González-Hermoso, C, additional, Jeiranian, A, additional, Dowidar, N, additional, Schaper, C, additional, Buckingham, W, additional, Ferree, S, additional, Ribelles, N, additional, Rodrigo, I, additional, Prat, AP, additional, and Alba, E, additional

Published
2016
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29. Genetic markers of toxicity from capecitabine and other fluorouracil-based regimens: Investigation in the QUASAR2 study, systematic review, and meta-analysis

Author

Rosmarin, D., Palles, C., Church, D., Domingo, E., Jones, A., Johnstone, E., Wang, H., Love, S., Julier, P., Scudder, C., Nicholson, G., Gonzalez-Neira, A., Martin, M., Sargent, D., Green, E., McLeod, H., Zanger, U.M., Schwab, M., Braun, M., Seymour, M., Thompson, L., Lacas, B., Boige, V., Ribelles, N., Afzal, S., Enghusen, H., Jensen, S.A., Etienne-Grimaldi, M.-C., Milano, G., Wadelius, M., Glimelius, B., Garmo, H., Gusella, M., Lecomte, T., Laurent-Puig, P., Martinez-Balibrea, E., Sharma, R., Garcia-Foncillas, J., Kleibl, Z., Morel, A., Pignon, J.-P., Midgley, R., Kerr, D., Tomlinson, I., Rosmarin, D., Palles, C., Church, D., Domingo, E., Jones, A., Johnstone, E., Wang, H., Love, S., Julier, P., Scudder, C., Nicholson, G., Gonzalez-Neira, A., Martin, M., Sargent, D., Green, E., McLeod, H., Zanger, U.M., Schwab, M., Braun, M., Seymour, M., Thompson, L., Lacas, B., Boige, V., Ribelles, N., Afzal, S., Enghusen, H., Jensen, S.A., Etienne-Grimaldi, M.-C., Milano, G., Wadelius, M., Glimelius, B., Garmo, H., Gusella, M., Lecomte, T., Laurent-Puig, P., Martinez-Balibrea, E., Sharma, R., Garcia-Foncillas, J., Kleibl, Z., Morel, A., Pignon, J.-P., Midgley, R., Kerr, D., and Tomlinson, I.

Published
2014

30. 239PD - A phase II trial of dasatinib (D) in combination with trastuzumab (T) and paclitaxel (P) in the first line treatment of HER2 positive metastatic breast cancer (MBC) patients (pts): GEICAM/2010-04

Author

Ocana Fernandez, A., Ruiz Borrego, M., Gil Martin, M., Antolin, S., Atienza, M., Montaño, A., Ribelles, N., Guerrero, A., Muñoz, M., Fernández-Pérez, I., Urruticoechea, A., Falcon Gonzalez, A., Pernas Simon, S., Prato Varela, J., Escudero, M.J., Benito, S., Caballero, R., Carrasco, E., Rojo, F., and Pandiella, A.

Published
2017
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32. A Phase I Study of Lde225 in Combination with Docetaxel in Patients with Triple Negative (Tn) Advanced Breast Cancer (Abc): Geicam/2012-12

Author

Martin, M., primary, Ruiz-Borrego, M., additional, Trigo, J.M., additional, Antolin, S., additional, Saenz, J.A. Garcia, additional, Hernando, A., additional, Ocana, A., additional, Rojo, F., additional, López-Tarruella, S., additional, Paz-Ares, L., additional, Ribelles, N., additional, Calvo, L., additional, Moreno, F., additional, Caballero, R., additional, and Carrasco, E., additional

Published
2014
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33. Predicting response and survival in chemotherapy-treated triple-negative breast cancer

Author

Prat, A, primary, Lluch, A, additional, Albanell, J, additional, Barry, W T, additional, Fan, C, additional, Chacón, J I, additional, Parker, J S, additional, Calvo, L, additional, Plazaola, A, additional, Arcusa, A, additional, Seguí-Palmer, M A, additional, Burgues, O, additional, Ribelles, N, additional, Rodriguez-Lescure, A, additional, Guerrero, A, additional, Ruiz-Borrego, M, additional, Munarriz, B, additional, López, J A, additional, Adamo, B, additional, Cheang, M C U, additional, Li, Y, additional, Hu, Z, additional, Gulley, M L, additional, Vidal, M J, additional, Pitcher, B N, additional, Liu, M C, additional, Citron, M L, additional, Ellis, M J, additional, Mardis, E, additional, Vickery, T, additional, Hudis, C A, additional, Winer, E P, additional, Carey, L A, additional, Caballero, R, additional, Carrasco, E, additional, Martín, M, additional, Perou, C M, additional, and Alba, E, additional

Published
2014
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35. Safety of surgery in patients (pts) with locally recurrent (LR) or metastatic breast cancer (mBC) treated with docetaxel (D) plus bevacizurnab (BV) or placebo (PL) in the AVADO phase III study in CANCER RESEARCH, vol 69, issue 2, pp 115S-115S

Author

Cortes, J., Pivot, X., Schneeweiss, A., Wilcken, N., Ellis, P., Linderholm, B K, Ribelles, N., Clemens, M., Haslbauer, F., W. Miles, D., Cortes, J., Pivot, X., Schneeweiss, A., Wilcken, N., Ellis, P., Linderholm, B K, Ribelles, N., Clemens, M., Haslbauer, F., and W. Miles, D.

Abstract

n/a

Published
2009

37. P3-05-04: Changes in Recurrence Risk of Breast Cancer Intrisic Subtypes over Time.

Author

Ribelles, N, primary, Perez-Villa, L, additional, Pajares, B, additional, Jerez, JM, additional, Vicioso, L, additional, Jimenez, B, additional, de, Luque V, additional, Franco, L, additional, Alvarez, M, additional, Perez-Rivas, LG, additional, Sanchez-Muñoz, A, additional, Gallego, E, additional, Marquez, A, additional, Hierro, I, additional, and Alba, E, additional

Published
2011
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38. Recurrence risk of breast cancer intrinsic subtypes over time.

Author

Ribelles, N., primary, Perez-Villa, L., additional, Pajares, B., additional, Jerez, J. M., additional, Vicioso, L., additional, Jimenez, B., additional, de Luque, V., additional, Franco, L., additional, Alvarez, M., additional, Perez-Rivas, L. G., additional, Sanchez-Muñoz, A., additional, Gallego, E., additional, Marquez, A., additional, Hierro, I., additional, and Alba, E., additional

Published
2011
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39. Is it Possible to Increase pCR in the Neoadjuvant Treatment With a Dose-Dense/Sequential Combination?

Author

Sánchez-Muñoz, Alfonso, primary, Dueñas-García, R., additional, Jaén-Morago, A., additional, Carrasco, E., additional, Chacón, I., additional, García-Tapiador, A. M., additional, Ortega-Granados, A. L., additional, Martínez-Ortega, E., additional, Ribelles, N., additional, Fernández-Navarro, M., additional, de la Torre-Cabrera, C., additional, Dueñas, B., additional, Rueda, A. I., additional, Martínez, J., additional, Tortosa, C. Ramírez, additional, Martín-Salvago, M. D., additional, and Sánchez-Rovira, P., additional

Published
2010
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40. 0145 First safety data from a randomised phase III trial comparing adjuvant epirubicin–cyclophosphamide → docetaxel (EC → T) vs ET → capecitabine (X) in N+ operable breast cancer (BC)

Author

Martín, M., primary, Lluch, A., additional, Ruiz-Simón, A., additional, Ribelles, N., additional, Ruiz-Borrego, M., additional, Rodríguez-Lescure, A., additional, Muñoz, M., additional, Ramos, M., additional, González, S., additional, and Margelí, M., additional

Published
2009
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46. Neoadjuvant chemotherapy with a dose-dense sequential combination of epirubicin and cyclophosphamide followed by paclitaxel and gemcitabine ± trastuzumab in stage II and III breast cancer. Correlation between pathologic complete response (pCR) and biologic markers

Author

Sanchez, A., primary, Dueñas-García, R., additional, Jaén-Morago, A., additional, Chacón, I., additional, García-Tapiador, A., additional, Martínez-Ortega, E., additional, de la Torre-Cabrera, C., additional, Dueñas, B., additional, Ribelles, N., additional, and Sánchez-Rovira, P., additional

Published
2007
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