scholarly journals Validation of the 2017 revision of the WHO chronic myelomonocytic leukemia categories

2018 ◽  
Vol 2 (15) ◽  
pp. 1807-1816 ◽  
Author(s):  
Sanam Loghavi ◽  
Dawen Sui ◽  
Peng Wei ◽  
Guillermo Garcia-Manero ◽  
Sherry Pierce ◽  
...  

Key Points Validation of the WHO 2017 CMML categories supports distinguishing MP-CMML from MDS–CMML. The prognostic value of the new 3-tiered blast-based CMML stratification scheme is limited.

Blood ◽  
2013 ◽  
Vol 121 (25) ◽  
pp. 5068-5077 ◽  
Author(s):  
Eric Padron ◽  
Jeffrey S. Painter ◽  
Sateesh Kunigal ◽  
Adam W. Mailloux ◽  
Kathy McGraw ◽  
...  

Key Points GM-CSF–dependent STAT5 hypersensitivity is detected in 90% of CMML samples and is enhanced by signaling mutations. Treatment with a GM-CSF–neutralizing antibody and JAK2 inhibitors reveals therapeutic potential.


2017 ◽  
Vol 1 (14) ◽  
pp. 972-979 ◽  
Author(s):  
Yanyan Zhang ◽  
Liang He ◽  
Dorothée Selimoglu-Buet ◽  
Chloe Jego ◽  
Margot Morabito ◽  
...  

Key Points Transgenic mice expressing 3 human cytokines enable expansion of CMML cells with limited stem cell engraftment. The mutational profile of CMML cells that expand in mice mirrors that of patient monocytes.


Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2807-2811 ◽  
Author(s):  
Koichi Takahashi ◽  
Naveen Pemmaraju ◽  
Paolo Strati ◽  
Graciela Nogueras-Gonzalez ◽  
Jing Ning ◽  
...  

Key Points t-CMML is associated with higher-risk cytogenetics and manifests poor prognosis. t-CMML should be recognized as one of the therapy-related myeloid neoplasms.


Blood ◽  
2015 ◽  
Vol 125 (23) ◽  
pp. 3618-3626 ◽  
Author(s):  
Dorothée Selimoglu-Buet ◽  
Orianne Wagner-Ballon ◽  
Véronique Saada ◽  
Valérie Bardet ◽  
Raphaël Itzykson ◽  
...  

Key Points An increase in the classical monocyte subset to >94% of total monocytes discriminates CMML from other monocytoses with high specificity. This characteristic increase in classical monocytes disappears in CMML patients who respond to hypomethylating agents.


Blood ◽  
2017 ◽  
Vol 129 (15) ◽  
pp. 2148-2160 ◽  
Author(s):  
Yuichiro Nakata ◽  
Takeshi Ueda ◽  
Akiko Nagamachi ◽  
Norimasa Yamasaki ◽  
Ken-ichiro Ikeda ◽  
...  

Key Points Acquired expression of CblQ367P induces sustained proliferation of myelomonocytes, multilineage dysplasia, and splenomegaly resembling CMML. Combined inhibition of PI3K and JAK2 efficiently suppressed the growth of CblQ367P-induced CMML cells.


Blood ◽  
2013 ◽  
Vol 121 (15) ◽  
pp. 3005-3015 ◽  
Author(s):  
Esperanza Such ◽  
Ulrich Germing ◽  
Luca Malcovati ◽  
José Cervera ◽  
Andrea Kuendgen ◽  
...  

Key Points CMML is a heterogeneous disorder with a highly variable prognosis that clearly requires a specific and widely accepted prognostic scoring system. CPSS is a powerful prognostic score that defines 4 risk groups for survival and AML evolution, developed and validated in the largest CMML series to date.


2019 ◽  
Vol 3 (7) ◽  
pp. 952-955 ◽  
Author(s):  
Ami B. Patel ◽  
Erin M. Pettijohn ◽  
Sameem M. Abedin ◽  
Evan Raps ◽  
Michael W. Deininger

Key Points CMML patients comprise an elderly and frail patient population with comorbidities that often require surgical intervention. Postsurgical leukemoid reaction, a life-threatening complication in CMML patients, may be driven by molecular mechanisms.


Blood ◽  
2013 ◽  
Vol 121 (12) ◽  
pp. 2186-2198 ◽  
Author(s):  
Raphaël Itzykson ◽  
Olivier Kosmider ◽  
Aline Renneville ◽  
Margot Morabito ◽  
Claude Preudhomme ◽  
...  

Key Points Early clonal dominance may distinguish chronic myelomonocytic leukemia from other chronic myeloid neoplasms with similar gene mutations. Early dominance of TET2-mutated cells in the hematopoietic tissue promotes myeloid differentiation skewing toward the granulomonocytic line.


Blood ◽  
2016 ◽  
Vol 128 (10) ◽  
pp. 1408-1417 ◽  
Author(s):  
Chiara Elena ◽  
Anna Gallì ◽  
Esperanza Such ◽  
Manja Meggendorfer ◽  
Ulrich Germing ◽  
...  

Key Points Risk assessment is crucial in patients with CMML because survival may range from a few months to several years. Integrating clinical features, morphology, and genetic lesions significantly improves risk stratification in CMML.


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