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Introduction Oxidative stress caused by elevated ROS, as a novel therapeutic mechanism, has been implicated in various tumors including AML. AML cells are chronically under oxidative stress, yet overreliance on ROS production makes tumor cells increasingly vulnerable to further damage. Reducing the cytotoxic effect of ROS on normal cells while killing leukemia stem cell (LSC) with high levels of reactive oxygen species is a new challenge for oxidative stress therapy in leukemia. Methods By searching literature databases, we summarized recent relevant studies. The relationship of ROS on AML genes, signaling pathways, and transcription factors, and the correlation of ROS with AML bone marrow microenvironment and autophagy were summarized. In addition, we summarize the current status of research on ROS and AML therapeutics. Finally, we discuss the research progress on redox resistance in AML. Results This review discusses the evidence showing the link between redox reactions and the progression of AML and compiles the latest research findings that will facilitate future biological studies of redox effects associated with AML treatment. Conclusion We believe that exploiting this unique oxidative stress property of AML cells may provide a new way to prevent relapse and drug resistance.

Immune thrombocytopenia (ITP) is a prevalent hemorrhage condition that causes notable immune-related abnormalities. Recently discovered data has shown that the intestinal flora plays a crucial role in maintaining a balanced immune system. Furthermore, an imbalance in gut flora has the potential to increase the possibility of developing ITP. Moreover, some studies reported a strong link between inflammatory bowel disease (IBD) and ITP. In this review, we described the significance of gut immunity in ITP. In addition, we explored the associations between gut flora and ITP as well as IBD and ITP. Finally, we examined the effectiveness of existing therapies that regulate gut homeostasis and their impact on the prognosis of patients with ITP.

Background Osteoporosis (OP) is a complex skeletal disorder characterized by reduced bone mass, microarchitectural deterioration of bone tissue, and increased susceptibility to fractures. Bone mineral density (BMD), as the best indicator of bone mineral content per unit area of bone, is one of the key diagnostic factors for OP. Platelets (PLT), serving as important immune cells and components of the coagulation system, have been demonstrated to be associated with bone formation, resorption, and remodeling processes. However, no research has established the relationship between BMD and platelet count (PC) in the American population thus far. This study aims to investigate the correlation between BMD and PC among the American population, and to appraise the effects of additional risk factors on this association. Methods This investigation examined the relationship between BMD and PC by analyzing data from the National Health and Nutrition Examination Survey (NHANES) between 2011 and 2018. A weighted multivariate logistic regression analysis was employed to assess this correlation. Additionally, subgroup and smooth curve analyses were conducted to delve deeper into the BMD-PC relationship and to identify other potential determinants of PC. Results This study reveals a significant negative correlation between BMD and PC in the American adult population (β=-15.05, 95% CI: -22.07 to -8.03, p  < 0.0001). Subgroup analysis highlights notable differences in this correlation between genders and various racial groups. Smooth curve fitting and generalized additive models were applied to further explore the relationship between BMD and PC, considering the influence of multiple factors. Conclusion The present study investigated the correlation between BMD and PC in adults, with a particular focus on the potential risk factors for thrombocytopenia. This negative correlation was found to be markedly pronounced in males, an association not observed in females. Additionally, a potential inverse relationship between BMD and hemoglobin (HGB) levels was identified. Consequently, for individuals with elevated bone mass or osteoporosis (OP), we advocate for routine complete blood count monitoring to identify hematological irregularities. Considering the significant variations by sex, age, and race, special vigilance is advised for changes in PC among non-Hispanic white males under the age of 55.

Given the adverse impact of deep vein thrombosis (DVT) on the prognosis of multiple myeloma (MM) patients, identifying biomarkers for DVT is crucial for improving MM patient clinical outcomes. Therefore, this study aimed to evaluate the predictive value of miR-503-5p for DVT in MM, and explored the underlying mechanisms. Serum samples were collected from MM patients with and without DVT to measure miR-503-5p expression levels. ROC and Kaplan-Meier curves were employed to examine the predictive potential of miR-503-5p in MM-related DVT. MM serum-cultured human umbilical vein endothelial cells (HUVECs) were used to investigate the mechanisms of miR-503-5p in influencing the disease. Cell viability, oxidative stress status, and IL-6, TNF-α, TF, and TM levels were evaluated by CCK-8, antioxidant activity assay, and qRT-PCR. MiR-503-5p was upregulated in MM patients with DVT. The upregulation of miR-503-5p was a risk factor that demonstrated a high predictive value for DVT in MM patients. MiR-503-5p upregulation mediated the promotive effect of MM serum on HUVEC viability reduction, IL-6, TNF-α, and TF expression, and oxidative stress, and the inhibitory effect of MM serum on HUVEC TM expression. Moreover, WNT3A was a potential target of miR-503-5p in MM-related DVT. WNT3A downregulation mediated the effect of miR-503-5p on HUVECs. MiR-503-5p might be a promising biomarker for predicting DVT development in MM patients. MiR-503-5p might promote thrombosis in MM by affecting vein endothelial cells (VECs) through targeting WNT3A.

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.

Recent studies have confirmed that metabolites and immunocyte phenotype may be associated with the risk of lymphoma. However, the bidirectional causality between metabolites, immunocyte phenotype, disease risk, and whether immunity is an intermediate mediator between metabolism and lymphoma causality is still unclear. To elucidate the causal relationship between metabolites, immune cell phenotypes, and lymphomas, we used two-sample Mendelian randomization (MR) and two-step MR analysis. Applying large-scale genome-wide association studies (GWAS) pooled data, we selected 1400 metabolites and 731 immunocyte phenotypes with eight lymphoma subtypes for two-sample bi-directional MR analysis. In addition, we used two-step MR to quantify the proportion of metabolite effects on lymphomas mediated by immunocyte phenotype. This study yielded a bidirectional causal relationship between 17 metabolites and lymphoma and a bidirectional causal relationship between 12 immunocyte phenotypes and lymphoma. In addition, we found causal associations between metabolites and lymphomas, three groups of which were mediated by immunocyte phenotypes. Among them, CD27 on plasmablast/plasma cell (PB/PC) was a mediator of the positive association of arginine to glutamate ratio with chronic lymphocytic leukemia, with a mediator ratio of 14.60% (95% CI=1.29-28.00%, P=3.17 × 10-2). Natural killer (NK) cells as a percentage of all lymphocytes(NK %lymphocyte) was a mediator of the negative association of X-18922(unknown metabolite) levels with diffuse large B-cell lymphoma, with a mediation proportion of -8.940% (95% CI=-0.063-(-17.800) %, P=4.84 × 10-2). CD25 on IgD- CD24- B cell was the mediator of the positive association between X-24531(unknown metabolite) levels and diffuse large B-cell lymphoma, with a mediation proportion of 13.200% (95% CI=-0.156-26.200%, P=4.73 × 10-2). In the present study, we identified a causal relationship between metabolites and lymphoma, in which immunocyte phenotypes as mediators are involved in only a minor part. The mediators by which most metabolites affect the risk of lymphoma development remain unclear and require further exploration in the future.

Background Atypical chronic myeloid leukemia (aCML) is a highly aggressive type of blood cancer that falls under the category of myelodysplastic/myeloproliferative neoplasms (MDS/MPN). In the fifth edition of the WHO classification of tumors, this category has been renamed MDS/MPN with neutrophilia. Although eosinophilia is commonly observed in blood cancers, it is rarely seen in aCML. Case presentation This study presents a case of aCML that was diagnosed six years after the patient developed eosinophilia. The patient had undergone tests to rule out other primary and secondary diseases, but the eosinophilia remained unexplained. Treatment with corticosteroids and hydroxyurea had proven ineffective. Six years later, the patient experienced an increase in white blood cells, primarily neutrophils. After ruling out other possible diagnoses, a combination of morphologic and molecular genetic findings led to the diagnosis of aCML. The patient responded well to treatment with azacitidine. Conclusions This study summarizes the current state of aCML diagnosis and management and discusses the possible connection between eosinophilia and aCML.

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.

Multiple myeloma (MM) is a malignant tumor originating from plasma cells, and in recent years, its incidence has shown a significant upward trend in our country. Venous thromboembolism (VTE) is a relatively common complication in multiple myeloma (MM) patients. Venous thromboembolism includes deep vein thrombosis (DVT) and pulmonary embolism (PE), with patients facing a high risk of DVT during treatment. Studies have shown that the procoagulant state of MM, inflammatory response, and the therapeutic drugs used significantly increase the incidence of DVT. However, the exact mechanisms behind the increased risk of venous thrombosis are not yet fully understood. The occurrence of DVT not only has a severely negative impact on patient survival rates but also leads to adjustments in treatment plans and a reduction in patients' quality of life. This article analyzes the relationship between risk factors for DVT and MM, exploring current diagnostic methods, risk assessment tools, and personalized preventive treatment strategies, ultimately proposing future research directions. Through a review and analysis of relevant literature, it aims to enhance the understanding of multiple myeloma and deep vein thrombosis, providing references for clinical diagnosis and treatment.

Multiple myeloma has become the second most common hematologic malignancy threatening human health with the increasing incidence in the population, and the emergence of drug resistance in its treatment has become a problem that needs to be solved urgently. Recent studies have shown that the immune system is closely related to the development of multiple myeloma, and immune senescence plays an extremely critical role in MM treatment resistance. In this paper, we review the connection between immune senescence and the development of MM and its possible role in the drug resistance of MM treatment, to provide new research ideas for the in-depth study of the mechanism of immune senescence and the search for new immunotherapeutic targets to overcome the phenomenon of drug resistance in the immunotherapy of MM patients.