1,721,269 research outputs found
Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies
No full textAbstract: Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults.
Recent advances in understanding its molecular basis have opened the way to new therapeutic
strategies, including targeted therapies. However, despite an improvement in prognosis it has been
documented in recent years (especially in younger patients) that allogenic hematopoietic stem cell
transplantation (allo-HSCT) remains the only curative treatment in AML and the first therapeutic
option for high-risk patients. After allo-HSCT, relapse is still a major complication, and is observed
in about 50% of patients. Current evidence suggests that relapse is not due to clonal evolution,
but instead to the ability of the AML cell population to escape immune control by a variety of
mechanisms including the altered expression of HLA-molecules, production of anti-inflammatory
cytokines, relevant metabolic changes and expression of immune checkpoint (ICP) inhibitors capable
of “switching-o” the immune response against leukemic cells. Here, we review the main mechanisms
of immune escape and identify potential strategies to overcome these mechanism
Cytogenetics and molecular studies for defining the pathogenesis and refining the diagnosis of therapy-related acute myeloid leukemias (T-AML)
No full textLa cellula staminale leucemica ed il suo microambiente” Progetto “Progressi in Biologia e Medicina
No full textIl contributo della citogenetica e della ibridazione in situ nella valutazione della MRD nelle emopatie
No full text
Molecular pathways in myelodysplastic syndromes and acute myeloid leukemia: relationships and distinctions-a review.
No full textThe myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are both hematopoietic stem cell disorders. However, while leukemic stem cells have been revealed by clonal tracking experiments, dysplastic stem cells have never been demonstrated by xeno-transplantation assays because of poor engraftment problems. These engraftment difficulties may be due to the unique nature of MDS genetic lesions that are truly able to recapitulate the disease phenotype. MDS and AML of younger patients harbour clonal yet different chromosomal markers, whereas MDS and AML of the elderly present similar defects. Potential involvement of tumor suppressor genes in MDS has been hypothesized but never confirmed, while cooperation between class I and class II mutations has been identified in AML. The reciprocal interactions between stromal cells and neoplastic clones are disrupted in both MDS and AML. In early MDS, stromal and neoplastic cells produce high levels of inhibitory cytokines, whereas in advanced MDS and AML they produce high levels of anti-apoptotic molecules
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