Soluble RANKL production by leukemic cells in a case of chronic lymphocytic leukemia with bone destruction

DELPINO M.V; PALAU-NAGORE V; PALACIOS M.F; DIAZ A; BEZARES FR; BORGE M; STANGANELLI C; SLAVUTSKY I; ARRA A; GAMBERALE R; PODAZA E.A; ROISMAN A; LEDESMA I; GIORDANO M

LEUKEMIA AND LYMPHOMA

TAYLOR & FRANCIS LTD

Lugar: Londres; Año: 2016 vol. 25 p. 1 - 4

1042-8194

Receptor Activator for Nuclear Factor j B Ligand(RANKL) is a member of the TNF-a superfamily normallyproduced by osteoblasts and stromal cells, whichactivates its receptor RANK present on osteoclasts andosteoclast precursors, thus favoring their differentiationand activity. An aberrant expression of RANKL was previouslyreported in a proportion of B cell malignanciessuch as Chronic lymphocytic leukemia (CLL),[1] multiplemyeloma (MM)[1] and follicular lymphoma.[2]Signaling via RANKL in CLL and in MM cells induce therelease of cytokines involved in disease pathophysiology,including IL-6, IL8 and TNF-a,[1] whereas releaseof soluble RANKL (sRANKL) was observed in MM cellsand was not detected in CLL cells.[1] In line with this,bone destruction is a prominent feature of MM but arare complication in CLL. We here present a case ofCLL with lytic bone lesions displaying an aberrantrelease of sRANKL by the malignant cells.