Lenalidomide is known to be effective in myelodysplastic syndromes (MDS) with del(5q) in improving anemia and suppressing del(5q) cells. MDS with del(5q) shows increase of nonlobulated megakaryocytes. However, histopathology of MDS with del(5q) treated with lenalidomide has not been fully studied. We investigated the morphologic changes in lenalidomide treated low- or intermediate-1-risk MDS with del(5q). All of evaluable patients showed high proportion of nonlobulated megakaryocytes. The nonlobulated megakaryocytes were markedly decreased in 6 patients during therapy in parallel with suppression of del(5q) cells. Our analysis suggests that single allele deletion of common deleted region inhibits nuclear lobulation of megakaryocytes.
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http://dx.doi.org/10.1016/j.leukres.2011.11.011 | DOI Listing |
Clin Lymphoma Myeloma Leuk
October 2024
MDS Unit, AOU Careggi, MD, PhD, University of Florence, Florence, Italy.
Lancet Haematol
November 2024
Center for Accelerating Leukemia/Lymphoma Research at Comprehensive Cancer Center, IRCCS Humanitas Research Hospital, Milan, Italy; Department of Biomedical Sciences, Humanitas University, Milan, Italy. Electronic address:
Leukemia
October 2024
Fondazione Sindromi Mielodisplastiche FISiM-ETS, Bologna, Italy.
Nat Commun
June 2024
Computational Biology Program CIMA-Universidad de Navarra, Cancer Center Clínica Universidad de Navarra (CCUN), IdISNA, Pamplona, Spain.
While myelodysplastic syndromes with del(5q) (del(5q) MDS) comprises a well-defined hematological subgroup, the molecular basis underlying its origin remains unknown. Using single cell RNA-seq (scRNA-seq) on CD34 progenitors from del(5q) MDS patients, we have identified cells harboring the deletion, characterizing the transcriptional impact of this genetic insult on disease pathogenesis and treatment response. Interestingly, both del(5q) and non-del(5q) cells present similar transcriptional lesions, indicating that all cells, and not only those harboring the deletion, may contribute to aberrant hematopoietic differentiation.
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