Acute Myeloid Leukemia (AML) is a life-threatening hematological malignancy where allogeneic stem cell transplantation (SCT) remains the only potentially curative treatment option for these patients. However, relapses occur in 30-40% of patients after SCT and are associated with a poor outcome, with an estimated survival of <6 months. A better understanding of biological mechanisms of leukemia relapse post SCT is essential for optimized treatment outcome and could improve patient monitoring strategies. AML cells often evade immune detection through mechanisms such as genomic loss or downregulation of HLA antigens, immune activating receptors, upregulation of inhibitory receptors, altered metabolic environments, and bone marrow niche remodelling.
An improved understanding of these immune escape mechanisms is necessary to learn about their influences on the composition and function of the cellular and soluble part of the immune system and overall bodily function. By understanding these dynamics, innovative treatment strategies can be developed. Strategies may include targeting suppressive cells or immune evasion mechanisms (e.g using checkpoint marker addressing strategies), or enhancing antileukemic responses using activation strategies (e.g mediated by dendritic cells or employing drugs to increase costimulation).
Moreover, identifying predictive and prognostic markers associated with immune activation or suppression, and evaluating how immune modulatory therapies can change these expressions and environments., remains a priority.
To gather further insight in this complex area we welcome submissions that cover topics in post SCT AML patients suffering from relapses. These include, but are not limited to the following themes:
• Mechanisms of relapse in AML post-transplantation
• Therapeutic strategies for relapse (e.g. chemotherapy, second SCT, cellular and humoral therapies, modulatory/hypomethylating treatments)
• Special treatments addressing immune escape/activation
• The interplay between graft versus host disease (GvHD) and graft versus leukemia (GvL) effects
• Prognostic and predictive markers in the relapse context
Topic Editor Jochen J. Frietsch received financial support from: Stemline, Novartis, Medac, Therakos, abbvie, Jazz, Takeda, Janssen-Cilag. Topic Editor Sala Elisa received financial support from: Medac, Takeda, MSD, Jazz, BMS, Kte/Gilead, Priothera, Avencell, Therakos. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
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