Presentaciones del Zepsyre Lung en el Congreso IASCL :
16 Octubre Presentación Oral :
Actualización de los Datos Finales de Eficacia y Seguridad Obtenidos en el Ensayo de Fase I/II que combina PM1183 (Lurbinectedin) con Doxorrubicina en Cáncer de Pulmón Microcítico (CPM) Recidivante .
17 de Octubre Se Presentará :
El Esquema del Ensayo de Fase III en Curso en la Sesión Titulada " Clinical Design, Statistics and Clinical Trials" .
Tambien el uso de la Combinación de Trabectedin + PLD sin Platino Brinda a los Pacientes Tiempo para Recuperarse de las Toxicidades relacionadas con el Platino y puede Restaurar la Sensibilidad del Platino en las Células Tumorales.
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Future Oncol. 2017 Oct 11.
When Nonplatinum is the answer: the role of trabectedin plus pegylated liposomal doxorubicin in recurrent ovarian cancer.
Colombo N.
Abstract :
Trabectedin + pegylated liposomal doxorubicin (PLD) offers a well tolerated and effective nonplatinum, nontaxane alternative for treatment of ovarian cancer patients with a treatment-free interval after platinum beyond 6 months, especially for those relapsing between 6 and 12 months and those who are not candidates to receive platinum-based therapy. Using the nonplatinum trabectedin + PLD combination gives patients time to recover from platinum-related toxicities and may restore platinum sensitivity in tumor cells. The sequence effect, by which intercalation of trabectedin + PLD between platinum regimens may enhance the activity of next platinum and improve survival, is currently under investigation in the Phase III prospective International Ovarian cancer patients Trial with Yondelis.
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Trabectedin mechanism of action and platinum resistance: molecular rationale.
Ray-Coquard I.
Abstract :
Trabectedin presents a complex mode of action affecting key cell biology processes in tumor cells and in the tumor microenvironment. In ovarian cancer patients with a platinum treatment-free interval of 6-12 months treated with trabectedin + pegylated liposomal doxorubicin (PLD) or single-agent PLD, and retreated with platinum after relapse, overall survival was significantly prolonged in the trabectedin + PLD group. Mechanisms by which trabectedin restores tumor sensitivity to platinum include its interaction with components of the nucleotide excision repair machinery in tumor cells and inhibition of inflammatory mediators such as IL-6 in the tumor microenvironment. Additionally, BRCA mutations and associated homologous recombination repair deficiency may contribute to enhanced sensitivity to trabectedin observed in BRCA-mutated patients with ovarian cancer .
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Platinum or Nonplatinum in Recurrent Ovarian Cancer: that is the question.
Poveda A, Marth C.
Abstract :
Although platinum-based chemotherapy continues to be the first-line option for advanced ovarian cancer and for platinum recurrences beyond 6 months, platinum rechallenge is not the best approach for some patients, such as those with residual toxicities, platinum-related hypersensitivity reactions or limited platinum-sensitivity (i.e., a platinum treatment-free interval [TFIp] of 6-12 months). Results of the MITO-8 study called into question the role of single-agent nonplatinum-based regimens in this specific subset of ovarian cancer patients. The current article summarizes the results of the MITO-8 study highlighting key limitations, and discusses the role of the nonplatinum-based combination of trabectedin + pegylated liposomal doxorubicin in the management of ovarian cancer patients who relapse between 6 and 12 months after last platinum.
Trabectedin presents a complex mode of action affecting key cell biology processes in tumor cells and in the tumor microenvironment. In ovarian cancer patients with a platinum treatment-free interval of 6-12 months treated with trabectedin + pegylated liposomal doxorubicin (PLD) or single-agent PLD, and retreated with platinum after relapse, overall survival was significantly prolonged in the trabectedin + PLD group. Mechanisms by which trabectedin restores tumor sensitivity to platinum include its interaction with components of the nucleotide excision repair machinery in tumor cells and inhibition of inflammatory mediators such as IL-6 in the tumor microenvironment. Additionally, BRCA mutations and associated homologous recombination repair deficiency may contribute to enhanced sensitivity to trabectedin observed in BRCA-mutated patients with ovarian cancer .
