Radioterapia de alta precisión en el tratamiento del cáncer: Hadronterapia

Excmo. Sr. Presidente, Excmos. e Ilmos. Sres. Académicos, colegas médicos, físicos y demás personas que han tenido a bien asistir a esta sesión científica que versará sobre la hadronterapia del cáncer. El motivo de mi presencia aquí surgió de la última reunión de la Real Academia, convocatoria en la que nuestro Presidente, el Excmo. Sr. D. Vicente Tormo, nos instó a transmitir a la Sociedad Valenciana avances científicos de actualidad. Pensé entonces en la reciente aprobación por parte del Gobierno de la creación de una Gran Instalación de Física Médica en Valencia, en el marco del Mapa de Estructuras Singulares de España. Y una de las actividades principales de la citada Instalación será la hadronterapia en su vertiente protónica, una forma de radioterapia de altísima precisión en el tratamiento del cáncer, que como oncólogo radioterápico y miembro de la comisión del proyecto, que preside el profesor Bernabeu, catedrático de física, y de la que también es miembro destacado el ilustre académico profesor Llombart, tengo a bien exponerles en esta conferencia

Radioteràpia i els seus avenços recents

Radiotherapy and its Recent Progress.Nowadays, radiation therapy is one of the fundamental pillars in cancer treatment within a multidisciplinary context, which includes other therapies such as surgery and chemotherapy. This paper pinpoints the most relevant historical milestones of radiotherapy and its radiobiological basis. Authorsalso discuss the difference between external radiotherapy and brachytherapy, as well as the role they play in multidisciplinary cancer therapy. Indeed, radiotherapy has seen important breakthroughs inrecent decades, above all due to the development of new technologies and imaging techniques

Primitive neuroectodermal kidney tumor

To the Editor: Primitive neuroectodermal tumors (PNET) and Ewing sarcoma (ES) belong to a group of neoplasms de®ned by neuroectodermal differentiation and a characteristic cytogenetic translocation, t(11;22) (q24;q12) or gene rearrangements between chromosomes 21 and 22 [1]. They are generally aggressive tumors that present as metastatic disease in nearly 50% of the cases. ES is frequently a bone disease, whereas PNET can occur in bones, soft tissues, or any other site. Renal PNETs are extremely rare, with only a few cases reported [2]. We here record an adult with renal PNET and bone metastases at diagnosis. Because these tumor can also be found in children [3] our experience may therefore be helpful to pediatric oncologist

Glutathione and Bcl-2 targeting facilitates elimination by chemoradiotherapy of human A375 melanoma xenografts overexpressing bcl-xl, bcl-2, and mcl-1

<p>Abstract</p> <p>Background</p> <p>Bcl-2 is believed to contribute to melanoma chemoresistance. However, expression of Bcl-2 proteins may be different among melanomas. Thus correlations among expression of Bcl-2-related proteins and <it>in vivo </it>melanoma progression, and resistance to combination therapies, was investigated.</p> <p>Methods</p> <p>Human A375 melanoma was injected s.c. into immunodeficient nude mice. Protein expression was studied in tumor samples obtained by laser microdisection. Transfection of siRNA or ectopic overexpression were applied to manipulate proteins which are up- or down-regulated, preferentially, during melanoma progression. Anti-<it>bcl</it>-2 antisense oligonucleotides and chemoradiotherapy (glutathione-depleting agents, paclitaxel protein-binding particles, daunorubicin, X rays) were administered in combination.</p> <p>Results</p> <p><it>In vivo </it>A375 cells down-regulated pro-apoptotic <it>bax </it>expression; and up-regulated anti-apoptotic <it>bcl-2</it>, <it>bcl-xl</it>, and <it>mcl-1</it>, however only Bcl-2 appeared critical for long-term tumor cell survival and progression <it>in vivo</it>. Reduction of Bcl-2, combined with partial therapies, decreased melanoma growth. But only Bcl-2 targeting plus the full combination of chemoradiotherapy eradicated A375 melanoma, and led to long-term survival (> 120 days) without recurrence in 80% of mice. Tumor regression was not due to immune stimulation. Hematology and clinical chemistry data were within accepted clinical toxicities.</p> <p>Conclusion</p> <p>Strategies to target Bcl-2, may increase the effectiveness of antitumor therapies against melanomas overexpressing Bcl-2 and likely other Bcl-2-related antiapoptotic proteins.</p