Lipoprotein lipase expression in unmutated CLL patients is the consequence of a demethylation process induced by the microenvironment

MORENO PILAR; ABREU CECILIA; BORGE MERCEDES; PALACIOS FLORENCIA; MORANDE PABLO; PEGAZZANO MARIANA; BIANCHI SERGIO; LANDONI A; AGRELO RUBEN; GIORDANO MIRTA; DIGHIERO GUILLERMO; GAMBERALE ROMINA; OPPEZZO PABLO

LEUKEMIA

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2013 vol. 27 p. 721 - 721

0887-6924

Chronic lymphocytic leukaemia (CLL) can be defined as a low-grade B-cell tumor with antigen-experienced monoclonal CD5+ B cells that, having escaped programmed cell death and undergone cell cycle arrest in the G0/G1 phase, relentlessly accumulate in lymphoid organs and circulate into the peripheral blood.1 This leukemic B-cell accumulation results from a complex balance between activation of cell proliferation and inhibition of apoptotic death.2 During the past few years, several new prognostic markers have emerged in CLL. Among them, the mutational status of the immunoglobulin heavy-chain variable (IGHV) genes is considered one of the strongest. Results from gene expression profile in CLL led us to propose that expression of the lipoprotein lipase (LPL) gene could constitute a suitable surrogate marker of the mutational status of IGHV. Despite the usefulness of LPL for CLL prognosis,5, 6, 7, 8 its functional role and the molecular mechanism regulating its expression remain elusive as yet.