Myeloproliferative neoplasms (Registro nro. 22856)
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| 000 -Cabecera | |
|---|---|
| Campo de control interno | 02005nam a2200253 4500 |
| 001 - Número de control | |
| control field | ESSALUD |
| 005 - Fecha y hora de la última transacción | |
| Campo de control | 20260821144938.0 |
| 007 - Tipo material - Descripcion fisica - info general | |
| Tipo material - Descripcion fisica - info general | ta |
| 008 - Elementos de Longitud Fija - Información General | |
| Elementos de Longitud Fija - Información | t pe ||||| |||| 00| 0 spa d |
| 040 ## - Origen de la Catalogación | |
| Origen de la Catalogación | BMG |
| 041 ## - Idioma | |
| Idioma | eng |
| 100 ## - Autor | |
| Autor | Plo, Isabelle |
| Rol del Autor | Autor |
| 9 (RLIN) | 54275 |
| 245 ## - Titulo | |
| Titulo | Myeloproliferative neoplasms |
| 300 ## - Páginas | |
| Paginación | páginas: 788-802 |
| 520 ## - Resumen | |
| Resumen | Classic myeloproliferative neoplasms, including essential thrombocythemia, polycythemia vera, and primary myelofibrosis, are chronic, clonal hematopoietic stem-cell disorders. These disorders are driven by gain-of-function mutations in the genes Janus kinase 2 (JAK2), calreticulin (CALR), or the thrombopoietin receptor (MPL) that activate cytokine signaling. These mutations arise decades before clinical disease develops and confer a clonal advantage that is further shaped by comutations in epigenetic, splicing, or signaling genes. Inflammation enhances clonal dominance, favoring the development of myelofibrosis and thrombotic complications. Disease evolution may culminate in secondary acute myeloid leukemia, which has a poor prognosis. Current therapies primarily aim to control symptoms, thrombosis, and splenomegaly, but they have limited disease-modifying effects, except for pegylated interferon alfa and JAK2 inhibitors in some patients. Emerging therapies that selectively target mutant CALR and JAK2 V617F using immunotherapy and selective inhibitors could be a breakthrough in the treatment of persons with myeloproliferative neoplasms, with the expectation of achieving durable disease modification and potentially clonal eradication. |
| 650 ## - Temas - Descriptores | |
| Temas - Descriptores | CÁNCER |
| 9 (RLIN) | 1231 |
| 650 ## - Temas - Descriptores | |
| Temas - Descriptores | TRATAMIENTOS EN ONCOLOGÍA |
| 9 (RLIN) | 53734 |
| 650 ## - Temas - Descriptores | |
| Temas - Descriptores | ENFERMEDAD INFLAMATORIA |
| 9 (RLIN) | 53667 |
| 650 ## - Temas - Descriptores | |
| Temas - Descriptores | LEUCEMIA |
| 9 (RLIN) | 33873 |
| 650 ## - Temas - Descriptores | |
| Temas - Descriptores | LINFOMA |
| 9 (RLIN) | 39360 |
| 700 ## - Autor Personal | |
| Autor Personal | Vainchenker, William |
| 9 (RLIN) | 54276 |
| 773 0# - Revista (Relacion con el numero) | |
| Host Biblionumber | 22717 |
| Host Itemnumber | 22650 |
| Ciudad, Editorial | Massachusetts NEJM Group |
| Codigo barras item/ejemplar | NEJM12 |
| Titulo de la Revista | The New England Journal of Medicine |
| Número de control de registro | ESSALUD |
| ISSN | 0028-4793 |
| 942 ## - Elementos de Koha | |
| Tipo de Documento | Artículos |
| Fecha procesamiento | 2026-08-21 |
| Catalogador | sqb |
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