O The question of diagnosis, treatment and prognosis of myelodysplastic  syndrome

Baidurin, S; Buyalskaya, Anastasia; Shalabayeva, Gaukhar

doi:10.54500/2790-1203.111.1.2022.20-28

Cited by 1 publication

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“…The BM-predominant autoimmunity is amplified by an additional antigenic stimulation ( 84 – 87 ). Th1 immune responses suppress the production of erythrocytes, granulocytes, platelets, and B lymphocytes ( 49 , 55 – 57 , 87 ), which results in clinical and laboratory features of AA and hMDS ( 3 , 4 , 9 , 10 ).…”

Section: Immune Dysregulation and An Inflamed Bme In Ahfmentioning

confidence: 99%

“…The dysregulated growth of leukemic cells results in the overgrowth of their normal counterparts and the suppression of normal blood cell production, clonal hematopoiesis, and corresponding hematological presentations (5)(6)(7)(8). The presence of dysplastic features indicates a diagnosis of MNs, and an increased percentage of myeloblasts is the most significant biomarker representing leukemic hematopoiesis and entry into advanced stages (9,10). Immunological, cytogenetic, and biological molecular analyses can provide valuable information for diagnosis, classification, and risk stratification.…”

Section: General Overview Of Aplastic Anemia and Myeloid Neoplasmsmentioning

confidence: 99%

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When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Zhao,

Ju,

Xiu

et al. 2024

Front. Immunol.

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Aplastic anemia (AA) and hypoplastic myelodysplastic syndrome are paradigms of autoimmune hematopoietic failure (AHF). Myelodysplastic syndrome and acute myeloid leukemia are unequivocal myeloid neoplasms (MNs). Currently, AA is also known to be a clonal hematological disease. Genetic aberrations typically observed in MNs are detected in approximately one-third of AA patients. In AA patients harboring MN-related genetic aberrations, a poor response to immunosuppressive therapy (IST) and an increased risk of transformation to MNs occurring either naturally or after IST are predicted. Approximately 10%–15% of patients with severe AA transform the disease phenotype to MNs following IST, and in some patients, leukemic transformation emerges during or shortly after IST. Phenotypic transformations between AHF and MNs can occur reciprocally. A fraction of advanced MN patients experience an aplastic crisis during which leukemic blasts are repressed. The switch that shapes the disease phenotype is a change in the strength of extramedullary inflammation. Both AHF and MNs have an immune-active bone marrow (BM) environment (BME). In AHF patients, an inflamed BME can be evoked by infiltrated immune cells targeting neoplastic molecules, which contributes to the BM-specific autoimmune impairment. Autoimmune responses in AHF may represent an antileukemic mechanism, and inflammatory stressors strengthen antileukemic immunity, at least in a significant proportion of patients who have MN-related genetic aberrations. During active inflammatory episodes, normal and leukemic hematopoieses are suppressed, which leads to the occurrence of aplastic cytopenia and leukemic cell regression. The successful treatment of underlying infections mitigates inflammatory stress-related antileukemic activities and promotes the penetration of leukemic hematopoiesis. The effect of IST is similar to that of treating underlying infections. Investigating inflammatory stress-powered antileukemic immunity is highly important in theoretical studies and clinical practice, especially given the wide application of immune-activating agents and immune checkpoint inhibitors in the treatment of hematological neoplasms.

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Section: Immune Dysregulation and An Inflamed Bme In Ahfmentioning

confidence: 99%

Section: General Overview Of Aplastic Anemia and Myeloid Neoplasmsmentioning

confidence: 99%

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Zhao,

Ju,

Xiu

et al. 2024

Front. Immunol.

View full text Add to dashboard Cite

show abstract

O The question of diagnosis, treatment and prognosis of myelodysplastic syndrome

Cited by 1 publication

References 0 publications

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

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