In late 2019 the coronavirus disease‐2019 (COVID‐19) pandemic caused by SARS Coronavirus 2 (SARS‐CoV‐2) started in Wuhan, China. Cancer patients are immunosuppressed from their disease and the therapy they receive.Hematopoietic cell transplant (HCT) recipients are a subgroup of patients that are severely immunocompromised and may be at an even higher risk of a complicated course during this infection.We herein report the outcomes and course of 11 sequential cases of HCT recipients infected by SARS‐CoV‐2 treated in our center.The patients age ranged from 17 to 60 years, the duration from transplant to infection ranged from day +5 to 192 months, 6 patients were post allo-HCT, 4 post auto-HCT and one had both allo and auto-HCT. The presenting symptoms were not different from other viral illnesses. The majority had mild COVID-19 stage, while 3 had moderate stage on presentation. None of the patients required oxygen supplementation nor mechanical ventilation.

MYSM1, located on chromosome 1p32.1, encodes histone H2A deubiquitinase, a transcription regulator involved in DNA damage response. Biallelic MYSM1 variants are linked to rare bone marrow failure syndromes, presenting with cytopenia, B-cell deficiency, hypogammaglobulinemia, and developmental abnormalities. We report four cases of MYSM1 mutations progressing from marrow failure to MDS or AML within 9–10 years. Genetic abnormalities, including TP53 mutation and chromosomal anomalies, suggest clonal evolution. Hematopoietic stem cell transplantation achieved remission in two patients with adverse cytogenetics. Further research is needed to refine management strategies and assess long-term outcomes in MYSM1-associated marrow failure and MDS.

Severe aplastic anemia (SAA) in pregnancy represents a rare but life-threatening clinical challenge. Standard therapies such as hematopoietic stem cell transplantation (HSCT) and immunosuppressive therapy are limited during pregnancy due to safety concerns, leaving supportive care as the mainstay. Thrombopoietin receptor agonists (TPO-RAs) such as eltrombopag have emerged as promising agents in refractory SAA, though evidence of their safety in pregnancy remains scarce. We present the case of a 27-year-old woman with SAA post-allogeneic bone marrow transplant who relapsed during subsequent pregnancies. Her disease course was characterized by recurrent pancytopenia, mixed chimerism, and repeated need for stem cell boosts. During pregnancy in 2023, discontinuation of cyclosporine led to worsening cytopenias, prompting reintroduction of cyclosporine and the continuation of eltrombopag. This combined approach, alongside G-CSF and stem cell boosts, contributed to favorable hematologic stabilization. She successfully delivered a healthy infant and achieved hematologic recovery following a third stem cell boost postpartum. This report highlights the potential utility of TPO-RAs during pregnancy when conventional therapy is limited, while emphasizing the need for vigilant monitoring of maternal–fetal outcomes. A review of the literature suggests that although routine use of eltrombopag in pregnancy is not recommended, it may be considered in refractory SAA cases with careful risk–benefit assessment. The case underscores the role of multidisciplinary care, individualized therapeutic planning, and the need for further studies on TPO-RAs in pregnancy-associated bone marrow failure syndromes.

Inherited bone marrow failure syndromes (IBMFSs) are rare, genetically heterogeneous disorders characterized by BMF with possible increased risk of myeloid malignancies. Recent advances in genomic diagnostic techniques have identified a new IBMFS, including Oncostatin M ( OSM ) deficiency, which is an autosomal recessive condition linked to early-onset BMF with possible predisposition to myelodysplastic syndrome (MDS). OSM is a cytokine in the interleukin-6 family and regulates hematopoiesis through the OSM receptor and leukemia inhibitory factor receptor-mediated signaling, activating pathways essential for hematopoietic stem cell progenitor proliferation and differentiation. The reported cases from consanguineous families presented with early-onset cytopenias of variable severity, and some patients developed MDS. In patients with biallelic variants in OSM , hematologic improvement was observed following eltrombopag in two reported patients, while transfusion dependency and high-risk cytogenetics required hematopoietic stem cell transplantation. OSM deficiency is rare; its mechanistic and clinical parallels with other IBMFS underscore its importance. This review outlines the emerging evidence on OSM’s function in hematopoiesis and its deficiency as a newly recognized IBMFS with a potential predisposition to MDS, highlighting the need for early genetic diagnosis and tailored treatment strategies.