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8 results on '"Elvira Buxo"'

1. Second-line treatment in advanced gastric cancer: Data from the Spanish AGAMENON registry.

Author

Almudena Cotes Sanchís, Javier Gallego, Raquel Hernandez, Virginia Arrazubi, Ana Custodio, Juana María Cano, Gema Aguado, Ismael Macias, Carlos Lopez, Flora López, Laura Visa, Marcelo Garrido, Nieves Martínez Lago, Ana Fernández Montes, María Luisa Limón, Aitor Azkárate, Paola Pimentel, Pablo Reguera, Avinash Ramchandani, Juan Diego Cacho, Alfonso Martín Carnicero, Mónica Granja, Marta Martín Richard, Carolina Hernández Pérez, Alicia Hurtado, Olbia Serra, Elvira Buxo, Rosario Vidal Tocino, Paula Jimenez-Fonseca, and Alberto Carmona-Bayonas

Subjects
Medicine, Science
Abstract

BackgroundSecond-line treatments boost overall survival in advanced gastric cancer (AGC). However, there is a paucity of information as to patterns of use and the results achieved in actual clinical practice.Materials and methodsThe study population comprised patients with AGC in the AGAMENON registry who had received second-line. The objective was to describe the pattern of second-line therapies administered, progression-free survival following second-line (PFS-2), and post-progression survival since first-line (PPS).Results2311 cases with 2066 progression events since first-line (89.3%) were recorded; 245 (10.6%) patients died during first-line treatment and 1326/2066 (64.1%) received a second-line. Median PFS-2 and PPS were 3.1 (95% CI, 2.9-3.3) and 5.8 months (5.5-6.3), respectively. The most widely used strategies were monoCT (56.9%), polyCT (15.0%), ramucirumab+CT (12.6%), platinum-reintroduction (8.3%), trastuzumab+CT (6.1%), and ramucirumab (1.1%). PFS-2/PPS medians gradually increased in monoCT, 2.6/5.1 months; polyCT 3.4/6.3 months; ramucirumab+CT, 4.1/6.5 months; platinum-reintroduction, 4.2/6.7 months, and for the HER2+ subgroup in particular, trastuzumab+CT, 5.2/11.7 months. Correlation between PFS since first-line and OS was moderate in the series as a whole (Kendall's τ = 0.613), lower in those subjects who received second-line (Kendall's τ = 0.539), especially with ramucirumab+CT (Kendall's τ = 0.413).ConclusionThis analysis reveals the diversity in second-line treatment for AGC, highlighting the effectiveness of paclitaxel-ramucirumab and, for a selected subgroup of patients, platinum reintroduction; both strategies endorsed by recent clinical guidelines.

Published
2020
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5. Data from Identification of Docetaxel Resistance Genes in Castration-Resistant Prostate Cancer

Author

Begoña Mellado, Pedro Gascón, María José Ribal, Elvira Buxo, Raquel Bermudo, Pedro L. Fernández, Susana G. Kalko, Jordi Codony-Servat, and Mercedes Marín-Aguilera

Abstract

Docetaxel-based chemotherapy is the standard first-line therapy in metastatic castration-resistant prostate cancer (CRPC). However, most patients eventually develop resistance to this treatment. In this study, we aimed to identify key molecular genes and networks associated with docetaxel resistance in two models of docetaxel-resistant CRPC cell lines and to test for the most differentially expressed genes in tumor samples from patients with CRPC. DU-145 and PC-3 cells were converted to docetaxel-resistant cells, DU-145R and PC-3R, respectively. Whole-genome arrays were used to compare global gene expression between these four cell lines. Results showed differential expression of 243 genes (P < 0.05, Bonferroni-adjusted P values and log ratio > 1.2) that were common to DU-145R and PC-3R cells. These genes were involved in cell processes like growth, development, death, proliferation, movement, and gene expression. Genes and networks commonly deregulated in both DU-145R and PC-3R cells were studied by Ingenuity Pathways Analysis. Exposing parental cells to TGFB1 increased their survival in the presence of docetaxel, suggesting a role of the TGF-β superfamily in conferring drug resistance. Changes in expression of 18 selected genes were validated by real-time quantitative reverse transcriptase PCR in all four cell lines and tested in a set of 11 FFPE and five optimal cutting temperature tumor samples. Analysis in patients showed a noteworthy downexpression of CDH1 and IFIH1, among others, in docetaxel-resistant tumors. This exploratory analysis provides information about potential gene and network involvement in docetaxel resistance in CRPC. Further clinical validation of these results is needed to develop targeted therapies in patients with CRPC that can circumvent such resistance to treatment. Mol Cancer Ther; 11(2); 329–39. ©2011 AACR.

Published
2023

7. Identification of docetaxel resistance genes in castration-resistant prostate cancer

Author

Elvira Buxo, Jordi Codony-Servat, Raquel Bermudo, Pedro Gascón, Mercedes Marín-Aguilera, Begoña Mellado, Susana G. Kalko, Maria J. Ribal, and Pedro L. Fernández

Subjects
Male, Cancer Research, Cell Survival, medicine.medical_treatment, Antineoplastic Agents, Drug resistance, Docetaxel, Biology, urologic and male genital diseases, Bioinformatics, Transforming Growth Factor beta1, Prostate cancer, Cell Line, Tumor, Gene expression, medicine, Humans, Gene Regulatory Networks, Gene, Oligonucleotide Array Sequence Analysis, Regulation of gene expression, Chemotherapy, Models, Genetic, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Prostatic Neoplasms, medicine.disease, Gene expression profiling, Gene Expression Regulation, Neoplastic, Oncology, Drug Resistance, Neoplasm, Cancer research, Taxoids, Orchiectomy, medicine.drug
Abstract

Docetaxel-based chemotherapy is the standard first-line therapy in metastatic castration-resistant prostate cancer (CRPC). However, most patients eventually develop resistance to this treatment. In this study, we aimed to identify key molecular genes and networks associated with docetaxel resistance in two models of docetaxel-resistant CRPC cell lines and to test for the most differentially expressed genes in tumor samples from patients with CRPC. DU-145 and PC-3 cells were converted to docetaxel-resistant cells, DU-145R and PC-3R, respectively. Whole-genome arrays were used to compare global gene expression between these four cell lines. Results showed differential expression of 243 genes (P < 0.05, Bonferroni-adjusted P values and log ratio > 1.2) that were common to DU-145R and PC-3R cells. These genes were involved in cell processes like growth, development, death, proliferation, movement, and gene expression. Genes and networks commonly deregulated in both DU-145R and PC-3R cells were studied by Ingenuity Pathways Analysis. Exposing parental cells to TGFB1 increased their survival in the presence of docetaxel, suggesting a role of the TGF-β superfamily in conferring drug resistance. Changes in expression of 18 selected genes were validated by real-time quantitative reverse transcriptase PCR in all four cell lines and tested in a set of 11 FFPE and five optimal cutting temperature tumor samples. Analysis in patients showed a noteworthy downexpression of CDH1 and IFIH1, among others, in docetaxel-resistant tumors. This exploratory analysis provides information about potential gene and network involvement in docetaxel resistance in CRPC. Further clinical validation of these results is needed to develop targeted therapies in patients with CRPC that can circumvent such resistance to treatment. Mol Cancer Ther; 11(2); 329–39. ©2011 AACR.

Published
2011

8. Prognostic factors for survival with nab-paclitaxel plus gemcitabine in metastatic pancreatic cancer in real-life practice: the ANICE-PaC study

Author

Ana Fernández, Mercedes Salgado, Adelaida García, Elvira Buxò, Ruth Vera, Jorge Adeva, Paula Jiménez-Fonseca, Guillermo Quintero, Cristina Llorca, Mamen Cañabate, Luis Jesús López, Andrés Muñoz, Patricia Ramírez, Paula González, Carlos López, Margarita Reboredo, Elena Gallardo, Manuel Sanchez-Cánovas, Javier Gallego, Carmen Guillén, Nuria Ruiz-Miravet, Víctor Navarro-Pérez, Juan De la Cámara, Inmaculada Alés-Díaz, Roberto Antonio Pazo-Cid, and Alberto Carmona-Bayonas

Subjects
Metastatic pancreatic adenocarcinoma, Gemcitabine, Nab-paclitaxel, Real-life, First-line chemotherapy, Survival, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Treatment with nab-paclitaxel plus gemcitabine increases survival in patients with metastatic pancreatic cancer. However, the assessment of treatment efficacy and safety in non-selected patients in a real-life setting may provide useful information to support decision-making processes in routine practice. Methods Retrospective, multicenter study including patients with metastatic pancreatic cancer, who started first-line treatment with nab-paclitaxel plus gemcitabine between December 2013 and June 2015 according to routine clinical practice. In addition to describing the treatment pattern, overall survival (OS) and progression-free survival (PFS) were assessed for the total sample and the exploratory subgroups based on the treatment and patients’ clinical characteristics. Results All 210 eligible patients had a median age of 65.0 years (range 37–81). Metastatic pancreatic adenocarcinoma was recurrent in 46 (21.9%) patients and de novo in 164 (78.1%); 38 (18%) patients had a biliary stent. At baseline, 33 (18.1%) patients had an ECOG performance status ≥2. Patients received a median of four cycles of treatment (range 1–21), with a median duration of 3.5 months; 137 (65.2%) patients had a dose reduction of nab-paclitaxel and/or gemcitabine during treatment, and 33 (17.2%) discontinued treatment due to toxicity. Relative dose intensity (RDI) for nab-paclitaxel, gemcitabine, and the combined treatment was 66.7%. Median OS was 7.2 months (95% CI 6.0–8.5), and median PFS was 5.0 months (95% CI 4.3–5.9); 50 patients achieved either a partial or complete response (ORR 24.6%). OS was influenced by baseline ECOG PS, NLR and CA 19.9, but not by age ≥ 70 years and/or the presence of hepatobiliary stent or RDI 3 vs. ≤ 3 (p = 0.043), and baseline CA 19.9 > 37 U/mL vs. ≤37 U/mL (p = 0.004). Conclusions Nab-Paclitaxel plus gemcitabine remain effective in a real-life setting, despite the high burden of dose reductions and poorer performance of these patients. A nomogram to predict survival using baseline ECOG performance status, NLR and CA 19.9 is proposed.

Published
2018
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