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

MERCEDES BORGE; M. VICTORIA DELPINO; ENRIQUE PODAZA; CARMEN STANGANELLI; VIRGINIA PALAU-NAGORE; ALEJANDRO ROISMAN; IRMA SLAVUTSKY; MARIA F. PALACIOS; IGNACIO LEDESMA; ANTONIO ARRA; ALICIA DIAZ; MIRTA GIORDANO; ROMINA GAMBERALE; RAIMUNDO F. BEZARES

LEUKEMIA AND LYMPHOMA

TAYLOR & FRANCIS LTD

Lugar: Londres; Año: 2016

1042-8194

ReceptorActivator for Nuclear Factor j B Ligand (RANKL) is a member of the TNF-asuperfamily normally produced by osteoblasts and stromal cells, which activatesits receptor RANK present on osteoclasts and osteoclast precursors, thusfavoring their differentiation and activity. An aberrant expression of RANKLwas previously reported in a proportion of B cell malignancies such asChronic lymphocytic leukemia (CLL),[1] multiple myeloma (MM)[1] and follicularlymphoma.[2] Signaling via RANKL in CLL and in MM cells induce the release ofcytokines involved in disease pathophysiology, including IL-6, IL8 andTNF-a,[1] whereas release of soluble RANKL (sRANKL) was observed in MM cells andwas not detected in CLL cells.[1] In line with this, bone destruction is aprominent feature of MM but a rare complication in CLL. We here present a caseof CLL with lytic bone lesions displaying an aberrant release of sRANKL by themalignant cells.