A case of chronic myelomonocytic leukemia presenting rapid swelling of a finger due to leukemic cell invasion

Skin Cancer ◽  
2012 ◽  
Vol 27 (2) ◽  
pp. 158-161
Author(s):  
Mariko KAMO ◽  
Yusuke SHIRAKASHI ◽  
Atsushi FUJIMOTO ◽  
Makoto SUGIURA ◽  
Yasuhiro MOCHIZUKI ◽  
...  
Keyword(s):  
Cell Invasion ◽  
Leukemic Cell ◽  
Chronic Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia

scholarly journals Vasculitis associated with myelodysplastic syndrome and chronic myelomonocytic leukemia: French multicenter case-control study

2020 ◽  
Vol 50 (5) ◽  
pp. 879-884
Author(s):  
Anne Laure Roupie ◽  
Alexis Guedon ◽  
Benjamin Terrier ◽  
Constance Lahuna ◽  
Vincent Jachiet ◽  
...  
Keyword(s):  
Myelodysplastic Syndrome ◽  
Case Control Study ◽  
Case Control ◽  
Chronic Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia ◽  
Control Study

Trisomy 19 as the sole chromosomal abnormality in proliferative chronic myelomonocytic leukemia

2006 ◽  
Vol 30 (8) ◽  
pp. 1043-1047 ◽  
Author(s):  
M. Daskalakis ◽  
N. Mauritzson ◽  
B. Johansson ◽  
K. Bouabdallah ◽  
F. Onida ◽  
...  
Keyword(s):  
Chromosomal Abnormality ◽  
Chronic Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia

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.

Sign in / Sign up

Export Citation Format

Share Document