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Isochromosome 20q- (i(20q-)), as a rare reproducible chromosomal anomaly formed on the basis of 20q-, has not been commonly reported. Due to the rarity of this karyotypic anomaly, the bone marrow morphological characteristics of the patients with i(20q-) have not been clarified until now. In this study, the bone marrow cell morphology from MDS patients with isolated i(20q-), isolated 20q-, and normal karyotype was retrospectively compared and statistically analyzed. The results indicated that the isolated i(20q-) was mostly detected in MDS-MLD patients. The frequency and proportion dysplasia of cytoplasmic vacuolization in erythoid cells and small or unusually large size in myeloid cells of isolated i(20q-) MDS patients were significantly higher than those of normal karyotype MDS patients respectively (P < 0.05); the frequency and proportion dysplasia of decreased granules/agranularity in myeloid cells of isolated i(20q-) MDS patients were higher than those of isolated 20q- MDS patients (P < 0.05). The incidence of some specific morphological manifestations, such as deeply lobulated and hyperlobulated megakaryocytes and hypogranular and vacuolized eosinophils, may be an important morphological implication for the anomaly of isolated i(20q-). These morphological features of dysplasia may be helpful in distinguishing MDS with isolated i(20q-) from those with isolated 20q- and normal karyotype. [ABSTRACT FROM AUTHOR]

Acute graft-versus-host disease (aGvHD) is considered a result of "cytokine storm." Targeted therapeutic interventions on cytokines via ubiquitination regulatory pathways may provide a potential approach for aGvHD treatment. Ubiquitin-specific peptidase 11 (USP11) has been reported to play key roles in a variety of physiopathological processes by regulating the stability and function of several vital protein molecules. However, its role in aGvHD remains unclear. In this study, we identified USP11 was associated with aGvHD in patients. In the aGvHD mouse model, the colon and liver were more seriously affected in recipient mice who received USP11 wt bone marrow (BM) cells and eased after the donor was treated with a USP11 inhibitor or received USP11 ko BM cells. In mouse models, IL-6 was identified as a major effecter in accelerating aGvHD induced by USP11. In the cell model, IL-6 mRNA transcript was affected by USP11. In addition, USP11 also inhibited IL-6 degradation by affecting IL-6 ubiquitination. Furthermore, the positive correlation between USP11 and IL-6 was confirmed in the GvHD patients' samples. Collectively, all results indicated that USP11 played a critical role in the onset and progression of aGvHD. USP11 might be a potential target for aGvHD treatment. [Display omitted] [ABSTRACT FROM AUTHOR]