scholarly journals Morphological Transformation of Myeloma Cells into Multilobated Plasma Cell Nuclei within 7 Days in a Case of Secondary Plasma Cell Leukemia That Finally Transformed as Anaplastic Myeloma

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Akihito Fujimi ◽  
Yasuhiro Nagamachi ◽  
Naofumi Yamauchi ◽  
Yuji Kanisawa

A 48-year-old man was diagnosed with multiple myeloma (IgG-k) and was treated with high-dose dexamethasone as an induction therapy followed by thalidomide-based regimens. Approximately 22 months after the initial diagnosis, the patient developed secondary plasma cell leukemia (PCL) with a white blood cell (WBC) count of 20.2 × 109/L including 79.5% plasma cells. A G-banding chromosomal analysis in the bone marrow showed an t(11;14) abnormality of up to 5%, which was not detected at initial diagnosis. We immediately started bortezomib and dexamethasone therapy, but in just 7 days, the WBC count elevated to 48.5 × 109/L, and approximately 95% of them were medium-sized atypical lymphoid cells with multilobated nuclei. Although we subsequently initiated alternative regimens, the patient’s condition deteriorated, and he died 4 months after developing PCL. Approximately 2 months before his death, the diameter of myeloma cells in the bone marrow enlarged by approximately twofold, and pleomorphic nuclei were present, indicating an anaplastic myeloma transformation. Concurrently, a 100% increase of the t(11;14) clone frequency was observed in the G-banding-analyzed bone marrow cells. Morphological transformation of myeloma cells into multilobated plasma cell nuclei can be considered as the starting point of the sequential process leading to anaplastic myeloma.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5122-5122
Author(s):  
Albert Oriol ◽  
Ignasi Barba ◽  
Angels Barbera ◽  
Carles Arús ◽  
Jose-Luis Garcia-Dorado ◽  
...  

Abstract Advancements in the pathogenetic pathways in multiple myeloma have led to the identification of several primary and secondary genetic lesions and ultimately to a multiple myeloma genetic classification with prognostic implications. Although disregulation of cyclin activity has been recognized as a key event leading to the multiple myeloma phenotype, little is known about the metabolic consequences of this phenomenon. We have studied intact multiple myeloma cells by high resolution magnetic resonance spectroscopy to establish the metabolomic profiles of different native multiple myeloma cells as compared to other lymphoproliferative disorders. Multiple myeloma cells obtained from bone marrow aspirates (n =15), blood (n =3) or other biologic tissues (n =2) from 20 multiple myeloma patients and separated by density gradient centrifugation were evaluated and metabolic profiles were correlated with cytogenetic characteristics of the disease and patients clinical characteristics. Twelve patients were females (60%) with a median age of 65 years (range 50–82). Multiple myeloma monoclonal proteins were IgG (N=9), IgA (N=5) or BJ (N=6). Five of them (25%) had renal insufficiency. Nine patients (45%) had predominantly extramedullar diesase including four cases of plasma cell leukemia. IgH translocations were identified in 5 samples (25%), hyperploidy in 2 (10%), and other or no genetic lesions in 13 (65%), del13 was present in 9 samples (45%) and p53 alterations in 5 (25%). Bone marrow samples from thirteen patients with conventional multiple myeloma presented a relatively constant metabolic pattern with predominantly lipidic signals and a metilen to metil ratio ranging from 1.9 to 4.9 (median 2.9). No differences in this pattern were observed among subgroups of primary translocations or involvement of Rb and p53 genes. Four patients with plasma cell leukemia and three with predominant extranodal disease presented either non detectable lipid signals (N=3) or a higher metilen to metil ratio ranging from 2.8 to 3.9 (median 3.5). In fact, extranodal or leukemic disease was significantly associated to undetectable lipids (P < 0.031) or the composite variable undetectable lipids or metilen to metil ratio > 3 (P < 0.043). Furthermore, after a median follow-up of 18 months, absence of lipids in the metabolic profile was also associated to a shorter survival (median 0.45 years, 95%CI 0–1.03 versus 3 years, 95%CI 0.95–5.06, P < 0.022). These results suggest that metabolic profiles of different multiple myeloma genetic subtypes share common and reletively constant characteristics, while cells obtained from patients with plasma cell leukemia or predominantly extramedullar disease present a clearly distinct profile, probably reflecting the metabolic effect of clonal evolution at a genetic level.


2020 ◽  
Vol 8 (2) ◽  
pp. 23-24
Author(s):  
Akram Deghady ◽  
Nahla Farahat ◽  
Abeer Elhadidy ◽  
Hanaa Donia ◽  
Hadeer Rashid

Oncotarget ◽  
2016 ◽  
Vol 8 (12) ◽  
pp. 19427-19442 ◽  
Author(s):  
Alexey Zatula ◽  
Aida Dikic ◽  
Celine Mulder ◽  
Animesh Sharma ◽  
Cathrine B. Vågbø ◽  
...  

2013 ◽  
Vol 89 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Eirini Katodritou ◽  
Evangelos Terpos ◽  
Charikleia Kelaidi ◽  
Maria Kotsopoulou ◽  
Sossana Delimpasi ◽  
...  

1993 ◽  
Vol 42 (3) ◽  
pp. 299-304 ◽  
Author(s):  
Hiroshi Tsutani ◽  
Taeko Sugiyama ◽  
Shiro Shimizu ◽  
Hiromichi Iwasaki ◽  
Takanori Ueda ◽  
...  

2007 ◽  
Vol 48 (7) ◽  
pp. 1426-1428 ◽  
Author(s):  
Ridvan Ali ◽  
Meral Beksac ◽  
Fahir Ozkalemkas ◽  
Vildan Ozkocaman ◽  
Atilla Ozkan ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3267-3267
Author(s):  
Natalia C. Gonzalez-Paz ◽  
Scott Van Wier ◽  
Rafael Santana-Davila ◽  
Gregory Ahmann ◽  
Tammy Price-Troska ◽  
...  

Abstract Background: Plasma cell leukemia (PCL) is a rare plasma cell (PC) dyscrasia which may be designated as primary (PPCL) or de novo PCL when recognized at the time of diagnosis and secondary (SPCL) when there is leukemic transformation of a previously recognized multiple myeloma (MM). PCL has been reported to exhibit distinct clinical and immunophenotypic features that distinguish it from MM, but little is known about the specific genetics of this disease. To better understand the genetic features of the clonal PC from PPCL and SCPL we assessed in these patients the molecular and cytogenetic abnormalities most commonly found in MM. Patients and Methods: In our study we analyzed 3 groups of patients; 18 with PPCL, 23 with SPCL and a control group of 345 newly diagnosed MM previously published. Diagnostic criteria for PCL followed the presence of >2 x103/L PC in PB (Kyle et al. Arch Intern Med1974; 133–813–8). Cytogenetic abnormalities were assessed by the c-Ig FISH method; mutational analysis was performed using Conformational-sensitive gel electrophoresis (CSGE). Methylation was analyzed by methyl specific PCR (MSP) after bisulfite genomic DNA modification. Results: Translocation of immunoglobulin heavy chain with Cyclin D1 (t (11; 14)) was present in 76.9% (10 of 13) of PPCL, 71% (5 of 7) of SPCL, in contrast to 15.8% (53 of 336) of MM cases. Translocations’ involving the FGFR3-MMSET genes (4p16.3 locus) and c-MAF (16q32) genes were not observed among 10 patients studied with PPCL, but were present in 12.7 % each in SPCL. The t (4;14)(p16;q32) was present in 12.7% cases of MM and the t(14;16)(q32;q23) was present in 4.6 % of MM cases. Deletion of 17p13.1 (p53 locus) was found in 10% (37 of 345) of MM cases, 53.8% (7 of 13) for PPCL and 42.8% (3 of 7) for SPCL. Deletion of 13q was present in 54.2% (176 of 325) of MM, 76.9 % (10 of 13) of PPCL and 57.1% of SPCL. Ras mutations were found in 15% (2/13) of PPCL, located in codon 1 and 2 of the K-ras gene. In addition, 23% for SPCL presented mutations in the N-ras gene. Two mutations were located in codon 2 of N-ras and 1 patients in showed a mutation in codon 1 of K-ras gene. Ras mutations were present in 27% of MM cases. Mutations for p53 gene were present in 30.7% (4/13) of PPCL, 17% (3/17) for SPCL and 5% for MM. Methylation specific PCR for p16 gene was found in 23% (3/13) of PPCL, 29% of SPCL and 33.9% (149/439) of MM. Hypermethylation of p14 was not detected in PPCL but a 23 % was found in SPCL. Conclusions: In this study we demonstrate that PCs from PPCL more frequently carry the t (11; 14). Comparing SPCL and MM, PC’s from de novo PPCL do not show t (4; 14) or (16; 14). Deletion of 13q was more prevalent among patients with PPCL. Ras mutations appear to be as frequent in MM as in PPCL and SPCL. Mutations in p53 appeared to be more prevalent in PPCL than in SPCL and MM. Hypermethylation of p16 does not differ while hypermethylation of p14 is more frequent in SPCL than PPCL. These characteristics may lead to a different onset or disease evolution of PPCL compared to MM and secondary plasma cell leukemia and this may be important for diagnostic and treatment.


2010 ◽  
Vol 34 (4) ◽  
pp. e104-e105 ◽  
Author(s):  
Paolo Bernardeschi ◽  
Maria Teresa Pirrotta ◽  
Iolanda Montenora ◽  
Gloria Giustarini ◽  
Maria Immacolata Ferreri ◽  
...  

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