"Europa necesita ser competente para impulsar el crecimiento y, a su vez, España también precisa de esa competitividad en el Viejo Continente para hacerse con un lugar destacado que garantice el desarrollo de su economía.
En este sentido, el sector farmacéutico se erige como una de las alternativas en las que España puede demostrar su potencial.
Carlos González Bosch, presidente de la conocida distribuidora Cofares, asegura que el modelo farmacéutico español ocupa actualmente una destacada posición en el mapa europeo, llegando a afirmar que se trata del "mejor" a nivel mundial.
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Aplidin . Los Resultados de este Estudio Muestran la Actividad Antitumoral de Plitidepsina en 23 Tipos de Tumores, lo que Sugiere la Posibilidad de Investigar este Compuesto en otros Tipos de Tumores .
Congreso Anual de la Asociación Americana para la Investigación del Cáncer (AACR) que tendrá lugar en Filadelfia (EE.UU.) del 18 al 22 de abril.
* Estudio llevado a cabo por Cientificos de : Oncotest GmbH, Freiburg, Germany y Pharma Mar S.A., Madrid, Spain .
* Abstract Number: 4472 .
* Presentation Title: Plitidepsin shows antitumor activity in patient-derived tumor xenografts and hematologic malignancies .
* Presentation Time: Tuesday, Apr 21, 2015, 1:00 PM - 5:00 PM .
Author Block: Armin Maier, Gerhard Kelter, Vincent Vuaroquaux, Pablo M. Avilés Marin, Carmen Cuevas, Carlos M. Galmarini, Heinz H. Fiebig. Oncotest GmbH, Freiburg, Germany; Pharma Mar S.A., Madrid, Spain
Abstract Body:
Plitidepsin is a new marine-derived anti-tumor agent, originally isolated from the tunicate Aplidium albicans that is now fully obtained by total chemical synthesis.
The compound is currently being evaluated in a pivotal phase III trial in patients with refractory/relapsed multiple myeloma. Previous in vitro studies in 26 hematological cell lines demonstrated that plitidepsin was more active in multiple myeloma and non-Hodgkin lymphoma compared to CML, AML and ALL derived cell lines as determined in a 4 day proliferation assay in suspension cultures. We have recently shown that plitidepsin interacts selectively with eEF1A2 (eukaryotic translation elongation factor 1 alpha 2) in tumor cells, which results in apoptotic cell death.
To identify target tumor types for future clinical studies, the inhibition of colony formation of plitidepsin was assessed in vitro in 116 established patient derived xenografts tumor models from 23 different tumor types, including solid tumors and hematological malignancies such as myeloma, leukemia and lymphoma.
The anti-tumor activity of plitidepsin varied depending on the concentration used, achieving a mean IC70 (inhibitory concentration of 70%) value of 3 nM (range between 0.03 nM and >1 µM), which can be also achieved in patients treated using the clinical recommended dose or less. 39 out of 116 tumors showed above average sensitivity (IC70 < 1nM) and IC70 values in these tumors were about 9-fold lower than the mean of all tumors as tested. Sensitive tumor types were seen among different tumor types, such as hematological malignancies, pleuramesothelioma, melanoma, small cell and non-small cell lung cancer (both adeno and large cell), as well as renal cancer. In conclusion plitidepsin showed a broad differential antitumor activity in vitro in hematological malignancies and in solid tumors. Bioinformatic analyses are currently underway to identify biomarkers and/or gene signatures that can predict sensitivity or resistance to plitidepsin for selecting patients being responsive to the drug.
* Estudio llevado a cabo por Cientificos de : Oncotest GmbH, Freiburg, Germany y Pharma Mar S.A., Madrid, Spain .
* Abstract Number: 4472 .
* Presentation Title: Plitidepsin shows antitumor activity in patient-derived tumor xenografts and hematologic malignancies .
* Presentation Time: Tuesday, Apr 21, 2015, 1:00 PM - 5:00 PM .
Author Block: Armin Maier, Gerhard Kelter, Vincent Vuaroquaux, Pablo M. Avilés Marin, Carmen Cuevas, Carlos M. Galmarini, Heinz H. Fiebig. Oncotest GmbH, Freiburg, Germany; Pharma Mar S.A., Madrid, Spain
Abstract Body:
Plitidepsin is a new marine-derived anti-tumor agent, originally isolated from the tunicate Aplidium albicans that is now fully obtained by total chemical synthesis.
The compound is currently being evaluated in a pivotal phase III trial in patients with refractory/relapsed multiple myeloma. Previous in vitro studies in 26 hematological cell lines demonstrated that plitidepsin was more active in multiple myeloma and non-Hodgkin lymphoma compared to CML, AML and ALL derived cell lines as determined in a 4 day proliferation assay in suspension cultures. We have recently shown that plitidepsin interacts selectively with eEF1A2 (eukaryotic translation elongation factor 1 alpha 2) in tumor cells, which results in apoptotic cell death.
To identify target tumor types for future clinical studies, the inhibition of colony formation of plitidepsin was assessed in vitro in 116 established patient derived xenografts tumor models from 23 different tumor types, including solid tumors and hematological malignancies such as myeloma, leukemia and lymphoma.
The anti-tumor activity of plitidepsin varied depending on the concentration used, achieving a mean IC70 (inhibitory concentration of 70%) value of 3 nM (range between 0.03 nM and >1 µM), which can be also achieved in patients treated using the clinical recommended dose or less. 39 out of 116 tumors showed above average sensitivity (IC70 < 1nM) and IC70 values in these tumors were about 9-fold lower than the mean of all tumors as tested. Sensitive tumor types were seen among different tumor types, such as hematological malignancies, pleuramesothelioma, melanoma, small cell and non-small cell lung cancer (both adeno and large cell), as well as renal cancer. In conclusion plitidepsin showed a broad differential antitumor activity in vitro in hematological malignancies and in solid tumors. Bioinformatic analyses are currently underway to identify biomarkers and/or gene signatures that can predict sensitivity or resistance to plitidepsin for selecting patients being responsive to the drug.
'Leer' el ADN para vencer al cáncer . ( Post by Celtia ) .
ÁNGELES LÓPEZ Madrid Actualizado: 15/04/2015 .
Uno de los principales retos de la medicina es adaptar el tratamiento al perfil del paciente y su enfermedad, es decir, dar el fármaco adecuado en su dosis justa.
En Oncología, los avances ocurridos en las últimas décadas han permitido desarrollar terapias con menos efectos secundarios y más eficaces. Ahora se persigue seleccionar el medicamento en función de las características de la persona y de su tumor y para ello se están estudiando cientos de mutaciones genéticas que son las que definen el proceso tumoral y su evolución.
Algunas de estas investigaciones, recogidas hoy en la revista Science Translational Medicine, afinan cómo debe ser esa fotografía del genoma para vencer la batalla final contra el cáncer.
...
Uno de los principales retos de la medicina es adaptar el tratamiento al perfil del paciente y su enfermedad, es decir, dar el fármaco adecuado en su dosis justa.
En Oncología, los avances ocurridos en las últimas décadas han permitido desarrollar terapias con menos efectos secundarios y más eficaces. Ahora se persigue seleccionar el medicamento en función de las características de la persona y de su tumor y para ello se están estudiando cientos de mutaciones genéticas que son las que definen el proceso tumoral y su evolución.
Algunas de estas investigaciones, recogidas hoy en la revista Science Translational Medicine, afinan cómo debe ser esa fotografía del genoma para vencer la batalla final contra el cáncer.
...