000			02005nam a2200253 4500
001			ESSALUD
005			20260821144938.0
007			ta
008			t pe ||||| |||| 00| 0 spa d
040			_aBMG
041			_aeng
100			_aPlo, Isabelle _eAutor _954275
245			_aMyeloproliferative neoplasms
300			_apáginas: 788-802
520			_aClassic 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			_aCÁNCER _91231
650			_aTRATAMIENTOS EN ONCOLOGÍA _953734
650			_aENFERMEDAD INFLAMATORIA _953667
650			_aLEUCEMIA _933873
650			_aLINFOMA _939360
700			_aVainchenker, William _954276
773	0		_022717 _922650 _dMassachusetts NEJM Group _oNEJM12 _tThe New England Journal of Medicine _wESSALUD _x0028-4793
942			_cARTICULOS _e2026-08-21 _zsqb
999			_c22856 _d22856