Acute promyelocytic leukaemia complicating multiple myeloma: evidence of different cell lineages.
The association of leukemia and multiple myeloma is well described usually as a complication of chemotherapy but also in the absence of chemotherapy or at diagnosis. Such leukemias are typically acute myeloid leukemia (AML), particularly myelomonocytic subtype, and cases of acute promyelocytic leuke (APL) are rarely reported. Controversy exists as to whether myeloma and AML originate from a single haematopoietic progenitor or arise from different cell lineages. We report a case of a 58 year old female who developed APL 10 months following diagnosis of nonsecretory light chain (kappa) myeloma which had been treated with local spinal irradiation and low dose oral melphalan and prednisone. Clonality had originally been demonstrated by light chain restriction (kappa) of her bone marrow plasma cells whilst immunoglobulin heavy chain and T cell receptor genes were germ line. At development of APL cytogenetics revealed t(15;17) and PML-RAR fusion gene was detected by RT-PCR. The patient was treated with all-trans retinoic acid (ATRA) and received 2 cycles of consolidation chemotherapy with Idarubicin. Following this therapy the t(15;17) and PML-RAR were both undetectable whilst the clonal population of kappa staining plasma cells persisted. This particular patient represents a rare case of APL complicating multiple myeloma with persistence of the myeloma clone but disappearance of PML-RAR alpha RNA following therapy. This case study appears to support the argument that the APL and myeloma originated from distinct cell lineages.
Dunkley
S
S
Institute of Haematology, Royal Prince Alfred Hospital, Camperdown, NSW, Australia.
Gibson
J
J
Iland
H
H
Li
C
C
Joshua
D
D
D000903:Antibiotics, Antineoplastic / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D014408:Biomarkers, Tumor / Q000032:analysis / Q000235:genetics; D019070:Cell Lineage; D002884:Chromosomes, Human, Pair 15 / Q000235:genetics / Q000648:ultrastructure; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics / Q000648:ultrastructure; D002999:Clone Cells / Q000473:pathology; D003131:Combined Modality Therapy; D004164:Diphosphonates / Q000627:therapeutic use; D054278:Embryonal Carcinoma Stem Cells; D005260:Female; D015328:Gene Rearrangement, B-Lymphocyte, Light Chain; D006801:Humans; D015255:Idarubicin / Q000627:therapeutic use; D007145:Immunoglobulin kappa-Chains / Q000235:genetics; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy / Q000235:genetics / Q000473:pathology*; D008558:Melphalan / Q000008:administration & dosage; D008875:Middle Aged; D009101:Multiple Myeloma / Q000188:drug therapy / Q000473:pathology* / Q000532:radiotherapy; D009194:Myeloma Proteins / Q000235:genetics; D009363:Neoplasm Proteins / Q000032:analysis / Q000235:genetics; D009378:Neoplasms, Multiple Primary / Q000473:pathology*; D014411:Neoplastic Stem Cells / Q000473:pathology*; D015514:Oncogene Proteins, Fusion / Q000032:analysis / Q000235:genetics; D010014:Osteolysis / Q000188:drug therapy / Q000209:etiology; D000077268:Pamidronate; D011241:Prednisone / Q000008:administration & dosage; D012074:Remission Induction; D014178:Translocation, Genetic; D014212:Tretinoin / Q000627:therapeutic use
D000903:Antibiotics, Antineoplastic; D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D004164:Diphosphonates; D007145:Immunoglobulin kappa-Chains; D009194:Myeloma Proteins; D009363:Neoplasm Proteins; D015514:Oncogene Proteins, Fusion; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; D014212:Tretinoin; D000077268:Pamidronate; D008558:Melphalan; D011241:Prednisone; D015255:Idarubicin