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The progression of myelodysplastic syndromes (MDS) to secondary acute myeloid leukemia (sAML), classified under AML with myelodysplasia-related changes (AML-MRC), is a multi-step process driven by the dynamic interplay between cell-intrinsic genetic events and extrinsic microenvironmental remodeling. In this review, we discuss how these changes foster clonal selection and leukemic transformation. Emerging insights from single-cell technologies are highlighted, revealing the dynamic heterogeneity of MDS stem cells and their niche. Finally, we discussed the clinical implications of these mechanisms, including their impact on risk stratification, therapy failure (particularly after hypomethylating agents), and the development of novel treatment strategies aimed at intercepting progression. Integrating molecular findings with clinical translation is essential for improving outcomes in this high-risk disease continuum.

The most prevalent kind of acute leukemia in adults is acute myeloid leukemia (AML). While some individuals have had better effectiveness due to advancements in targeted medications, recurrence after remission and inadequate treatment specificity continue to be significant therapeutic problems. By controlling essential metabolic pathways and metabolites, metabolic reprogramming, a crucial strategy for cellular adaptability to energy needs, modifies cellular metabolic rhythms. In addition to being involved in immune cell proliferation, differentiation, and effector function, this pathway is also essential for leukemogenesis and survival signaling in AML. By altering the expression of immune molecules, the release of certain metabolites (such as lactate, ROS, glutamine, etc.) has a significant impact on the immune response to tumors. It is noteworthy that the metabolic interactions between immune cells and AML cells form a distinct pattern of energy competition in the tumor microenvironment. This study examined the new approach of targeting metabolic pathways to improve immunotherapy, systematically clarified the regulatory mechanism of metabolic reprogramming between AML cells and immune cells to counteract tumor immunity, and concentrated on the synergistic effect of current therapies and metabolic interventions. These findings offered a fresh perspective on how to fully realize the potential of metabolic therapy for AML.

Acute myeloid leukemia (AML) is a highly heterogeneous hematologic malignancy, characterized by complex molecular features and mechanisms of treatment resistance, which lead to a poor prognosis and high relapse rates. The complexity of multi-pathway interactions and the dysregulated dynamics of tumor cell death pathways may contribute to the wide range of clinical outcomes observed despite advancements in current therapies. Most current research focuses on a single form of cell death, neglecting the mechanisms of other death pathways and their synergistic interactions, which hinders the development of novel therapeutic approaches. The present review systematically integrates and compares the molecular features of key cell death modalities in AML, including autophagy, apoptosis, pyroptosis, necroptosis, ferroptosis and cuproptosis. The present review analyzes their specific triggers, signaling hubs and regulatory networks within the metabolic microenvironment, and discusses the dynamic crosstalk among these pathways. A key focus is the therapeutic potential of exploiting this crosstalk to design synergistic combination therapies. To overcome the limitations of conventional treatments and improve patient outcomes, it is essential to further investigate the transition mechanisms of various cell death modes in AML progression, drug resistance and relapse. Additionally, establishing a theoretical foundation for the development of innovative therapies that synergistically regulate multiple death pathways is crucial.

The STK11 gene mutation is a common genetic alteration in non-small cell lung cancer (NSCLC) and is significantly associated with poor responses to current immunotherapy regimens. Despite its prevalence, there is currently no established standard for front-line treatment in this subtype of NSCLC, underscoring the increasing need for personalized therapeutic strategies. In this report, we present a case of a patient with STK11-mutant NSCLC who was treated with first-line cadonilimab (10mg/kg) in combination with pemetrexed (500mg/m^2) plus carboplatin (AUC=5), resulting in a notable extension of progression-free survival (PFS). This case highlights the potential efficacy and feasibility of combining immunotherapy with chemotherapy in patients with STK11-mutant NSCLC. Additionally, we provide a review of recent advancements in research related to STK11 mutations in lung cancer as reported in the literature.