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Start Over Author "Burgues, O." Topic breast cancer
5 results on '"Burgues, O."'

1. Non-canonical NF-kappa B pathway activation predicts outcome in borderline oestrogen receptor positive breast carcinoma

Author

Rojo, F, Gonzalez-Perez, A, Furriol, J, Nicolau, MJ, Ferrer, J, Burgues, O, Sabbaghi, M, Gonzalez-Navarrete, I, Cristobal, I, Serrano, L, Zazo, S, Madoz, J, Servitja, S, Tusquets, I, Albanell, J, Lluch, A, Rovira, A, and Eroles, P

Subjects
breast cancer, non-canonical, NF-kappa B, ER-positive
Abstract

Background: NF-kappa B signalling appears deregulated in breast tumours. The purpose of this study was to determine whether the non-canonical NF-kappa B pathway, is activated in oestrogen receptor positive (ER+) breast cancer, to identify any correlation between its activity and the clinico-pathological phenotype and to explore whether NF-kappa B2 and RelB subunits and/or any of their target genes might be used as a predictive marker. Methods: Two independent cohorts of ER+ early breast cancer patients treated with adjuvant endocrine therapy were included in the study. Activation of RelB and NF-kappa B2 subunits was determined in a training set of 121 patients by measuring DNA-binding activities in nuclear extracts from fresh frozen specimens by an ELISA-based assay. Samples of 15 ER - breast cancer patients were also included in the study. In a large validation cohort of 207 patients, nuclear immunostaining of RelB and NF-kappa B2 on formalin-fixed paraffin-embedded specimens was performed. Statistical correlation within clinico-pathological factors, disease-free survival (DFS) and overall survival (OS) was evaluated. Publicly available gene expression and survival data have been interrogated aimed to identify target genes. Results: Activation of NF-kappa B2 and RelB was found in 53.7 and 49.2% of the 121 ER+ tumours analysed, with similar levels to ER - breast tumours analysed in parallel for comparisons. In the validation cohort, we obtained a similar proportion of cases with activation of NF-kappa B2 and RelB (59.9 and 32.4%), with a 39.6% of co-activation. Multiplexing immunofluorescence in breast cancer tissue confirmed an inverse spatial distribution of ER with NF-kappa B2 and RelB nuclear expression in tumour cells. Interestingly, NF-kappa B2 and RelB mRNA expression was inversely correlated with ER gene (ESR1) levels (P

Published
2016

2. Prospective transGEICAM study of the impact of the 21-gene Recurrence Score assay and traditional clinicopathological factors on adjuvant clinical decision making in women with estrogen receptor-positive (ER+) node-negative breast cancer.

Author

Albanell, J., González, A., Ruiz-Borrego, M., Alba, E., García-Saenz, J. A., Corominas, J. M., Burgues, O., Furio, V., Rojo, A., Palacios, J., Bermejo, B., Martínez-García, M., Limon, M. L., Muñoz, A. S., Martín, M., Tusquets, I., Rojo, F., Colomer, R., Faull, I., and Lluch, A.

Subjects
*BREAST cancer, *ESTROGEN receptors, *EPIDERMAL growth factor receptors, *CLINICAL pathology, *DECISION making, *HORMONE therapy, *LONGITUDINAL method
Abstract

Background: This study examined the impact of the Recurrence Score (RS) in Spanish breast cancer patients and explored the associations between clinicopathological markers and likelihood of change in treatment recommendations. Patients and methods: Enrollment was offered consecutively to eligible women with estrogen receptor-positive; human epidermal growth factor receptor 2-negative, node-negative breast cancer. Oncologists recorded treatment recommendation and confidence in it before and after knowing the patient’s RS. Results: Treatment recommendation changed in 32% of 107 patients enrolled: in 21% from chemohormonal (CHT) to hormonal therapy (HT) and in 11% from HT to CHT. RS was associated with the likelihood of change from HT to CHT (P < 0.001) and from CHT to HT (P < 0.001). Confidence of oncologists in treatment recommendations increased for 60% of cases. Higher tumor grade (P = 0.007) and a high proliferative index (Ki-67) (P = 0.023) were significantly associated with a greater chance of changing from HT to CHT, while positive progesterone receptor status (P = 0.002) with a greater probability of changing from CHT to HT. Conclusions: Results from the first prospective European study are consistent with published experience and use of the RS as proposed in European clinical practice guidelines and provide evidence on how Oncotype DX and clinicopathological factors are complementary and patient selection may be improved. [ABSTRACT FROM PUBLISHER]

Published
2012
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3. 321P - Clinical application of mutational analysis in breast cancer patients: The relevance of PIK3CA analysis for precision medicine.

Author

Cejalvo, J.M., Moragon, S., Ortega, B., Hernando, C., Martínez, M., Gambardella, V., Tarazona Llavero, N., Roda, D., Burgues, O., Alonso, E., Simón, S., Poveda, J., Rentero, P., Zuñiga, S., Bermejo, B., Lluch, A., and Cervantes, A.

Subjects
*BREAST cancer, *CLINICAL medicine, *INDIVIDUALIZED medicine, *CLINICAL drug trials, *CANCER patients
Abstract

The identification of biomarkers to drive treatment is one of the most important objectives of precision medicine. During last years, the role of PIK3CA mutations have been related to clinical benefit deriving from treatment with PI3K, and mTOR inhibitors. In breast cancer (BC), PIK3CA mutations are widely present and the use, in clinical trials, of selective inhibitors improved clinical outcomes. The aim of this study is to assess the value of a monocentric genomic screening program to select patients for trials with experimental targeted agents. We examined PIK3CA mutation in a cohort of 312 metastatic BC patients diagnosed at Hospital Clínico València-INCLIVA from Jan-13 to Apr-19. The sequencing of hotspot mutations was performed in primary (29.9%) and metastatic tissue (70.1%). We used two different technologies: MassARRAY technology (Sequenom MassARRAY, OncoCarta v1.0) and Iluminia MiSeq System (customised panel, OncoSpot v.1). Hotspots were selected according to databases already published. To be diagnosed as mutated, tumors needed to harbor at least 5% of mutant alleles. 7 clinical trials against PI3K pathway were available. PIK3CA analysis was performed in 312 paraffin embedded tumor samples, in which only 5.8% the analysis was not possible due to low quality of DNA. The distribution of BC subtypes were 77.6% Luminal, 13.9% HER2, and 8.5% triple negative (TN). PIK3CA mutations were detected in 96 patients (32.7%). In Luminal, PIK3CA mutations reached 36.8% while only 19.5% in HER2 and 16.0% in TN, respectively. A wide spectrum of PIK3CA mutations was found: H1047R (38.5%), E545K (30.2%), E542K (19.8%), R88Q (3.1%), M1043I (3.1%), N345K (2.1%), P539R (1.0%), K111E (1.0%), C420R (1.0%). One hundred and ninety (64.6%) patients were included in clinical trials, and 74 (38.9%) were treated with PI3K, AKT and mTOR inhibitors. PIK3CA mutations were widely present among luminal BC, being actually a specific target for new drugs. PIK3CA mutational analysis was easily and successfully performed in our center. The identification of PIK3CA hotspots mutations lead to the access for our patient to novel drugs into clinical trials, achieving relevant clinical benefits in most of the cases. The authors. Has not received any funding. A. Lluch: Advisory / Consultancy: Novartis; Advisory / Consultancy: Pfizer; Advisory / Consultancy: Roche/Genentech; Advisory / Consultancy: Eisai; Advisory / Consultancy: Celgene. A. Cervantes: Advisory / Consultancy: Merk serono; Advisory / Consultancy: Roche; Advisory / Consultancy: Beigine; Advisory / Consultancy: Bayer; Advisory / Consultancy: Servier; Advisory / Consultancy: Lilly; Advisory / Consultancy: Novartis; Advisory / Consultancy: Takeda; Advisory / Consultancy: Astelas; Advisory / Consultancy: Pierre Fabre; Speaker Bureau / Expert testimony: Foundation Medicine. All other authors have declared no conflicts of interest. [ABSTRACT FROM AUTHOR]

Published
2019
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5. Predicting response and survival in chemotherapy-treated triple-negative breast cancer

Author

Lourdes Calvo, Brandy Pitcher, Chun-Yang Fan, Álvaro Rodríguez-Lescure, Lisa A. Carey, Blanca Munárriz, William T. Barry, Eric P. Winer, Eva Carrasco, Marc L. Citron, Aleix Prat, Nuria Ribelles, Maggie C.U. Cheang, Elaine R. Mardis, MC Liu, Manuel Ruiz-Borrego, Jose Ignacio Chacon, A. Arcusa, Rafael Caballero, Joan Albanell, E. Alba, Tammi L. Vickery, Matthew J. Ellis, Joel S. Parker, A. Lluch, Clifford A. Hudis, Yufeng Li, Miguel Angel Seguí-Palmer, Ángel L Guerrero, Barbara Adamo, Arrate Plazaola, Margaret L. Gulley, Miguel Martin, Octavio Burgues, José A. López, Maria Vidal, Zhiyuan Hu, Charles M. Perou, Universitat de Barcelona, [Prat,A, Adamo,B, Vidal,M.J] Translational Genomics Group, Vall D'Hebron Institute of Oncology (VHIO) Barcelona, Spain. [Prat,A] Department of Medicine, Universitat Autònoma de Barcelona, Spain. [Lluch,A, Burgues,O] Department of Medical Oncology, Department of Pathology, Hospital Clínico Universitario de Valencia, Spain. [Albanell,J] Department of Medical Oncology, Hospital Del Mar, IMIM, Barcelona, Spain. [Albanell,J] Department of Medical Oncology, Universitat Pompeu Fabra (UPF), Barcelona, Spain. [Barry,W.T] Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, United States. [Fan,C, Parker,J.S, Cheang,M.C.U, Li,Y, Hu,Z, Gulley,M.L, Carey,L.A, Perou,C.M] Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, United States. [Chacón,J.I] Department of Medical Oncology, Hospital Virgen de la Salud, Toledo, Spain. [Parker,J.S, Perou,C.M] Department of Genetics, University of North Carolina, Chapel Hill, NC, United States. [Calvo,L] Department of Medical Oncology, Complexo Hospitalario Universitario de A Coruña, A Coruña, Spain. [Plazaola,A] Department of Medical Oncology, Onkologikoa, San-Sebastián, Spain. [Arcusa,A] Department of Medical Oncology, Consorci Sanitari de Terrassa, Barcelona, Spain. [Seguí-Palmer,M.A] Department of Medical Oncology, Corporació Sanitària Parc Taulí, Sabadell, Spain. [Ribelles,N, Alba,E] Department of Medical Oncology, Department of Pathology, Hospital Universitario Virgen de la Victoria, Málaga, Spain. [Rodríguez-Lescure,A] Department of Medical Oncology, Hospital General de Elche, Alicante, Spain. [Guerrero,A] Department of Medical Oncology, Instituto Valenciano de Oncología (IVO), Valencia, Spain. [Ruiz-Borrego,M] Department of Medical Oncology, Hospital Universitario Virgen Del Rocío, Sevilla, Spain. [Munarriz,B] Department of Medical Oncology, Hospital Universitario la Fe, Valencia, Spain. [López,J.A] Department of Medical Oncology, Hospital San Camilo, Madrid, Spain.[Pitcher,B.N] Alliance Statistical and Data Center, Duke University, Durham, NC, United States. [Liu,M.C] Department of Oncology, Mayo Clinic, Rochester, MN, United States. [Citron,M.L] ProHEALTH Care Assoc., LLP, Lake Success, NY, United States. [Ellis,M.J, Mardis,E, Vickery,T] Department of Oncology, Washington University St. Louis, MO, United States. [Hudis,C.A] Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States. [Winer,E.P] Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States. [Caballero,R, Carrasco,E, Martín,M] GEICAM (Spanish Breast Cancer Research Group), Madrid, Spain. [Martín,M] Department of Medical Oncology, Instituto de Investigación Sanitaria, Hospital Universitario Gregorio Marañón, Madrid, Spain. [Perou,C.M] Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, United States., and This work was supported by funds from the NCI Breast SPORE program Grant No. P50-CA58223-09A1 (CMP), by RO1-CA138255 (CMP), by the Breast Cancer Research Foundation (CMP and MJE), National Cancer Institute (NCI) Strategic Partnering to Evaluate Cancer Signatures Grant No. U01 CA114722-01 (MJE), by the Sociedad Española de Oncología Médica (AP), by FEDER (RETICC-RD12/0036/0051, RD12/0036/0042, RD12/0036/0076, RD12/0036/0070), by Instituto de Salud Carlos III—PI13/01718 (AP), by Banco Bilbao Vizcaya Argentaria (BBVA) Foundation (AP) and by the Alliance Statistics and Data Center (U10-CA33601).

Subjects
Oncology, Cancer Research, Análisis de supervivencia, Colorectal cancer, Triple Negative Breast Neoplasms, Named Groups::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings], chemotherapy, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings], Cohort Studies, Prostate cancer, 0302 clinical medicine, Clinical trials, Breast cancer, Quimioteràpia, Triple-negative breast cancer, Subtypes, 0303 health sciences, Health Care::Health Care Quality, Access, and Evaluation::Quality of Health Care::Health Care Evaluation Mechanisms::Statistics as Topic::Survival Analysis [Medical Subject Headings], subtypes, Genomics, Middle Aged, 3. Good health, Treatment Outcome, Estudi de casos, 030220 oncology & carcinogenesis, Female, Neoadjuvant, Basal like, intrinsic, medicine.medical_specialty, Antineoplastic Agents, basal like, Càncer de mama, 03 medical and health sciences, breast cancer, Internal medicine, genomics, medicine, Humans, Chemotherapy, Lung cancer, Diseases::Neoplasms::Neoplasms by Site::Breast Neoplasms [Medical Subject Headings], Survival analysis, 030304 developmental biology, Proportional hazards model, business.industry, neoadjuvant, Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings], Neoplasias de la mama triple negativas, Antineoplásicos, medicine.disease, Survival Analysis, Expressió gènica, Intrisic, Check Tags::Female [Medical Subject Headings], Intrinsic, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Cohort Studies [Medical Subject Headings], Clinical Study, Gene expression, Case studies, Resultado del tratamiento, Health Care::Health Services Administration::Quality of Health Care::Outcome and Process Assessment (Health Care)::Outcome Assessment (Health Care)::Treatment Outcome [Medical Subject Headings], Skin cancer, business, Assaigs clínics
Abstract

This work was presented, in part, as an oral communication at the ASCO 2012 annual meeting (Abstract #10500). Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; BACKGROUND In this study, we evaluated the ability of gene expression profiles to predict chemotherapy response and survival in triple-negative breast cancer (TNBC). METHODS Gene expression and clinical-pathological data were evaluated in five independent cohorts, including three randomised clinical trials for a total of 1055 patients with TNBC, basal-like disease (BLBC) or both. Previously defined intrinsic molecular subtype and a proliferation signature were determined and tested. Each signature was tested using multivariable logistic regression models (for pCR (pathological complete response)) and Cox models (for survival). Within TNBC, interactions between each signature and the basal-like subtype (vs other subtypes) for predicting either pCR or survival were investigated. RESULTS Within TNBC, all intrinsic subtypes were identified but BLBC predominated (55-81%). Significant associations between genomic signatures and response and survival after chemotherapy were only identified within BLBC and not within TNBC as a whole. In particular, high expression of a previously identified proliferation signature, or low expression of the luminal A signature, was found independently associated with pCR and improved survival following chemotherapy across different cohorts. Significant interaction tests were only obtained between each signature and the BLBC subtype for prediction of chemotherapy response or survival. CONCLUSIONS The proliferation signature predicts response and improved survival after chemotherapy, but only within BLBC. This highlights the clinical implications of TNBC heterogeneity, and suggests that future clinical trials focused on this phenotypic subtype should consider stratifying patients as having BLBC or not. Yes

Published
2014

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