scholarly journals Acute myeloid leukaemia relapse presenting as cardiac myeloid sarcoma

2018 ◽  
pp. bcr-2018-224419
Author(s):  
Alexander Waselewski ◽  
Michael Joiner ◽  
Steven Raymond Miller

A 50-year-old woman previously diagnosed with acute myeloid leukaemia presented with a 3-month history of shortness of breath and a right-sided facial rash. A chest CT revealed an intracardiac mass in the right atrium extending into her superior and inferior vena cava. Surgery was performed to remove the mass and pathology was consistent with myeloid sarcoma. After surgery, adjuvant radiation therapy was directed to the residual disease. The patient eventually relapsed in other sites not including the right atrium and eventually succumbed to her disease.

Chemotherapy ◽  
2021 ◽  
pp. 1-5
Author(s):  
Salvatore Perrone ◽  
Elettra Ortu La Barbera ◽  
Federica Viola ◽  
Elena Cipollone ◽  
Maria Cristina Scerpa ◽  
...  

A patient with a therapy-related acute myeloid leukaemia (AML), NPM1<sup>mut</sup>, and FLT3-ITD+ was treated with induction and consolidation with CPX-351, obtaining a complete response (CR) but minimal residual disease persisted positive. Later, she complained progressive burning leg pain, weakening of the right hand and leg muscles, associated with absence of osteotendinous leg reflexes. Examination of cerebrospinal fluid (CSF) showed a meningeal relapse of AML. Moreover, a magnetic resonance imaging (MRI) showed 2 right meningeal implants of myeloid sarcoma and bone marrow revealed haematologic relapse of disease. She was treated with medicated lumbar punctures (LPs) followed by an FLA-Ida scheme, and she achieved a 2nd CR. Unfortunately, the patient developed hyperleucocytosis and reappearance of meningeal myeloid sarcoma at MRI. For this reason, a monotherapy with gilteritinib (an FLT3 inhibitor) was started: after 3 months of therapy, central nervous system (CNS)-disease shrunken and then faded, while AML in the bone marrow achieved only a partial response. This is the 1st report of a positive biological effect of gilteritinib on CNS (meningeal) myeloid sarcoma. There are no studies of gilteritinib concentration into CSF and penetration of gilteritinib into the blood-brain barrier should be further studied, given the paucity of drugs active on CNS relapse of AML. In patients receiving CPX-351 only, diagnostic LP should be considered after induction.


Leukemia ◽  
2017 ◽  
Vol 31 (7) ◽  
pp. 1482-1490 ◽  
Author(s):  
C S Hourigan ◽  
R P Gale ◽  
N J Gormley ◽  
G J Ossenkoppele ◽  
R B Walter

2020 ◽  
Vol 190 (2) ◽  
pp. 198-208
Author(s):  
Kristian Løvvik Juul‐Dam ◽  
Hans B. Ommen ◽  
Charlotte G. Nyvold ◽  
Christiane Walter ◽  
Helen Vålerhaugen ◽  
...  

Leukemia ◽  
2019 ◽  
Vol 34 (5) ◽  
pp. 1266-1277 ◽  
Author(s):  
Gauri Deb ◽  
Bettina Wingelhofer ◽  
Fabio M. R. Amaral ◽  
Alba Maiques-Diaz ◽  
John A. Chadwick ◽  
...  

AbstractThe histone demethylase lysine-specific demethylase 1 (LSD1 or KDM1A) has emerged as a candidate therapeutic target in acute myeloid leukaemia (AML); tranylcypromine-derivative inhibitors induce loss of clonogenic activity and promote differentiation, in particular in the MLL-translocated molecular subtype of AML. In AML, the use of drugs in combination often delivers superior clinical activity. To identify genes and cellular pathways that collaborate with LSD1 to maintain the leukaemic phenotype, and which could be targeted by combination therapies, we performed a genome-wide CRISPR-Cas9 dropout screen. We identified multiple components of the amino acid sensing arm of mTORC1 signalling—RRAGA, MLST8, WDR24 and LAMTOR2—as cellular sensitizers to LSD1 inhibition. Knockdown of mTORC1 components, or mTORC1 pharmacologic inhibition, in combination with LSD1 inhibition enhanced differentiation in both cell line and primary cell settings, in vitro and in vivo, and substantially reduced the frequency of clonogenic primary human AML cells in a modelled minimal residual disease setting. Synergistic upregulation of a set of transcription factor genes associated with terminal monocytic lineage differentiation was observed. Thus, dual mTORC1 and LSD1 inhibition represents a candidate combination approach for enhanced differentiation in MLL-translocated AML which could be evaluated in early phase clinical trials.


2013 ◽  
Vol 127 (4) ◽  
pp. 415-418 ◽  
Author(s):  
C-L Kuo ◽  
Y-B Yu ◽  
W-Y Li ◽  
Y-L Lee

AbstractObjective:We report a rare case of concurrent myeloid sarcoma and acute fulminant invasive fungal sinusitis in a patient with relapsed acute myeloid leukaemia.Case report:A 73-year-old man was diagnosed with acute myeloid leukaemia and developed relapse one year later. After two courses of azacytidine, he began suffering from a dull pain in the left temporal and orbital regions. Sinus computed tomography showed a localised lesion in the left ethmoid sinus, which rapidly progressed to an extensive intracranial mass within one month. Surgical debridement was performed, and histopathological analysis revealed the coexistence of myeloid sarcoma and acute fulminant invasive fungal sinusitis. The patient responded well to prompt surgical debridement, antifungal medication and radiotherapy.Conclusion:Coexistence of sinonasal myeloid sarcoma and acute fulminant invasive fungal sinusitis poses an urgent diagnostic and management challenge to clinicians. Timely recognition of this rare comorbid condition is warranted as application of appropriate treatment can save lives.


2019 ◽  
Vol 8 (2) ◽  
pp. 134 ◽  
Author(s):  
Ghazala Khan ◽  
Kim Orchard ◽  
Barbara-ann Guinn

One of the most promising approaches to preventing relapse is the stimulation of the body’s own immune system to kill residual cancer cells after conventional therapy has destroyed the bulk of the tumour. In acute myeloid leukaemia (AML), the high frequency with which patients achieve first remission, and the diffuse nature of the disease throughout the periphery, makes immunotherapy particularly appealing following induction and consolidation therapy, using chemotherapy, and where possible stem cell transplantation. Immunotherapy could be used to remove residual disease, including leukaemic stem cells from the farthest recesses of the body, reducing, if not eliminating, the prospect of relapse. The identification of novel antigens that exist at disease presentation and can act as targets for immunotherapy have also proved useful in helping us to gain a better understand of the biology that belies AML. It appears that there is an additional function of leukaemia associated antigens as biomarkers of disease state and survival. Here, we discuss these findings.


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