scholarly journals Sorafenib - induced thyroiditis in patient with a relapse of acute myelomonocytic leukemia with FLT3-ITD mutation

2019 ◽  
Vol 91 (8) ◽  
pp. 93-97 ◽  
Author(s):  
Ya B Balzhanova ◽  
E N Parovichnikova ◽  
A N Sokolov ◽  
V V Ryzhko ◽  
M A Samtsova ◽  
...  
Keyword(s):  
Adverse Event ◽  
Cytotoxic Chemotherapy ◽  
High Incidence ◽  
Myeloid Leukemias ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia ◽  
Treatment Emergent Adverse Event ◽  
Acute Myeloid

Sorafenib has been used in acute myeloid leukemias with FLT3-ITD mutation improving the outcomes. However the high incidence of treatment - emergent adverse event may be associated with treatment using sorafenib with cytotoxic chemotherapy. We have reported a case of severe thyroiditis in patient with a relapse of acute myelomonocytic leukemia.

scholarly journals Post-remission therapy of adult acute myeloid leukemia: High dose cytosine-arabinoside versus other consolidation regimens

2014 ◽  
Vol 67 (3-4) ◽  
pp. 83-90 ◽  
Author(s):  
Vanja Zeremski ◽  
Aleksandar Savic
Keyword(s):  
Acute Myeloid Leukemia ◽  
Cytosine Arabinoside ◽  
Myeloid Leukemia ◽  
Acute Myeloblastic Leukemia ◽  
High Dose ◽  
Study Group ◽  
Consolidation Therapy ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia ◽  
Acute Myeloid

Introduction. Modern therapy makes it possible for 60-80% patients with acute myeloid leukemia to achieve complete remission after induction therapy. However, most of them will relapse within six months to a year without additional cytostatic therapy. The questions regarding post-remission therapy remain unanswered. The objective of this study was to compare the survival and relapse rate among the patients who had received high dose cytosine-arabinoside during consolidation therapy and the patients who had not received high dose cytosine- arabinoside during consolidation therapy. Material and Methods. The study included 59 patients aged 18-60 years with de novo acute myeloid leukemia (except for Acute promyelocytic leukemia, which was excluded according to the French- American-British classification) who achieved complete remission. Thirty-nine patients who received high dose cytosine-arabinoside during consolidation were included in the study group and twenty patients who did not receive high dose cytosinearabinoside during consolidation were in the control group. Results. The results show a statistically significantly longer survival rate (p= 0.003) and a lower relapse rate (p= 0.02) among the study group patients, who received high dose cytosine-arabinoside during consolidation, compared to the controls, who did not receive high dose cytosine-arabinoside. The univariate analysis in the study group suggests that the affiliation to Acute myeloblastic leukemia with maturation and Acute myelomonocytic leukemia subgroups, as well as achieving complete remission after a single induction therapy has the prognostic significance. In the multivariate analysis, only the affiliation to Acute myeloblastic leukemia with maturation and Acute myelomonocytic leukemia subgroups retained the independent prognostic significance. Conclusion. This study has demonstrated that high dose cytosine-arabinoside used for consolidation therapy results in the higher survival rate and lower relapse rate compared to consolidation therapy without high dose cytosine-arabinoside. Only the patients within Acute myeloblastic leukemia with maturation and Acute myelomonocytic leukemia subgroups benefited significantly from high dose cytosine-arabinoside.

scholarly journals Juvenile Myelomonocytic Leukemia (JMML): A Mimicker of KMT2A-Rearranged Acute Myeloid Leukemia (AML)

2020 ◽  
Author(s):  
Ashraf Abdullah Saad
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Hematologic Malignancies ◽  
Driver Mutations ◽  
Juvenile Myelomonocytic Leukemia ◽  
Monosomy 7 ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia ◽  
Acute Myeloid

Juvenile myelomonocytic leukemia (JMML) is the most confusing mimicker of KMT2A-rearranged acute myeloid leukemia (AML). Clinical presentation, age of susceptibility (infancy or early childhood) and abnormal monocytosis are common clinical features. To complicate matters, JMML morphologically resemble acute myelomonocytic leukemia (AML M4) and distinction must be made based on accurate blast and promonocyte counts. As treatment significantly varies, AML/JMML overlap can lead to catastrophic consequences that can be avoided by timely management. Therefore, meticulous knowledge of JMML is essential to treat patients with hematologic malignancies. The pathognomic feature of JMML is increased infiltration of the peripheral blood, bone marrow, and viscera by abnormal myelomonocytic cells. Molecular diagnostics has generated substantial dividends in dissecting the genetic basis of JMML. We can now molecularly confirm the diagnosis of JMML in approximately over 90% of patients who harbor driver mutations in KRAS, NRAS, PTPN11, NF1, or CBL genes. The presence of monosomy 7 is a classic feature of JMML that can support the diagnosis in many cases. On the other hand, cytogenetics and Fluorescence in situ hybridization analysis (FISH) are indispensable to differentiate KMT2A-rearranged AML from JMML. In particular, AML with t(9;11) is associated with monocytic features that can be easily mistaken for JMML.

scholarly journals Asxl1 C-terminal mutation perturbs neutrophil differentiation in zebrafish

Leukemia ◽  
2021 ◽  
Author(s):  
Xiao Fang ◽  
Song’en Xu ◽  
Yiyue Zhang ◽  
Jin Xu ◽  
Zhibin Huang ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Chronic Myelomonocytic Leukemia ◽  
Nonsense Mutations ◽  
Myeloid Malignancies ◽  
A Subunit ◽  
Neutrophil Differentiation ◽  
Polycomb Repressive Complex 1 ◽  
Myelomonocytic Leukemia ◽  
Inhibitor Treatment ◽  
Acute Myeloid

AbstractASXL1 is one of the most frequently mutated genes in malignant myeloid diseases. In patients with myeloid malignancies, ASXL1 mutations are usually heterozygous frameshift or nonsense mutations leading to C-terminal truncation. Current disease models have predominantly total loss of ASXL1 or overexpressed C-terminal truncations. These models cannot fully recapitulate leukemogenesis and disease progression. We generated an endogenous C-terminal-truncated Asxl1 mutant in zebrafish that mimics human myeloid malignancies. At the embryonic stage, neutrophil differentiation was explicitly blocked. At 6 months, mutants initially exhibited a myelodysplastic syndrome-like phenotype with neutrophilic dysplasia. At 1 year, about 13% of mutants further acquired the phenotype of monocytosis, which mimics chronic myelomonocytic leukemia, or increased progenitors, which mimics acute myeloid leukemia. These features are comparable to myeloid malignancy progression in humans. Furthermore, transcriptome analysis, inhibitor treatment, and rescue assays indicated that asxl1-induced neutrophilic dysplasia was associated with reduced expression of bmi1a, a subunit of polycomb repressive complex 1 and a reported myeloid leukemia-associated gene. Our model demonstrated that neutrophilic dysplasia caused by asxl1 mutation is a foundation for the progression of myeloid malignancies, and illustrated a possible effect of the Asxl1-Bmi1a axis on regulating neutrophil development.

Production of granulocyte colony-stimulating factor by acute myelomonocytic leukemia cells

1988 ◽  
Vol 12 (9) ◽  
pp. 745-750 ◽  
Author(s):  
Naoki Shirafuji ◽  
Shigetaka Asano ◽  
Koji Kozai ◽  
Satoshi Takahashi ◽  
Satoru Matsuda ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia ◽  
Stimulating Factor
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