P53 deletion may drive the clinical evolution and treatment response in multiple myeloma.
We report a patient with multiple myeloma presenting with a paraspinal plasmacytoma with a marked dissociation between the response obtained in bone marrow (BM) infiltration and that achieved in soft tissue masses. While a complete remission was reached and maintained in BM, extramedullary plasmacytomas were refractory to every line of treatment. Genetic analysis identified the presence of t(4;14) and RB deletion in myeloma cells of both origins. However, a P53 deletion was only detected in plasma cells from extramedullary plasmacytomas. This finding suggests that P53 deletion has a role in the lack of treatment response of extramedullary plasmacytomas.
López-Anglada
Lucía
L
Servicio de Hematología, Hospital Universitario, Centro de Investigación del Cáncer-IBMCC (USAL-CSIC), Salamanca, Spain.
Gutiérrez
Norma C
NC
García
Juan L
JL
Mateos
María V
MV
Flores
Teresa
T
San Miguel
Jesús F
JF
D002883:Chromosomes, Human, Pair 14 / Q000235:genetics; D002894:Chromosomes, Human, Pair 4 / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D006801:Humans; D008875:Middle Aged; D009101:Multiple Myeloma / Q000235:genetics* / Q000628:therapy; D016609:Neoplasms, Second Primary / Q000235:genetics* / Q000628:therapy; D010954:Plasmacytoma / Q000235:genetics* / Q000628:therapy; D016160:Retinoblastoma Protein / Q000235:genetics; D014178:Translocation, Genetic / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D016160:Retinoblastoma Protein; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53