Multiple myeloma (MM) is one of the most common hematological malignancies and remains incurable. However, the survival of multiple myeloma patients has significantly increased due to the implementation of novel therapies along with autologous stem cell transplantation, changing the natural history of the disease. Consequently, there is an unmet need for more sensitive response assessment techniques capable of quantifying minimal tumor burden to identify patients at higher risk of early relapse. Multiparameter flow cytometry (MFC) is an essential tool for diagnosing and monitoring patients with various hematological conditions and has recently gained prominence in identifying, characterizing, and monitoring malignant plasma cells. The implementation of Next-Generation Flow (NGF) by EuroFlow aims to overcome the pitfalls of conventional MFC, including lack of standardization and lower sensitivity, by offering standardized and optimized protocols for evaluating response depth. Both MFC and NGF have wide-ranging applications in MM for diagnosis and measurable residual disease (MRD) monitoring. Plasma cell identification and clonality evaluation through MFC and NGF assist in diagnostic workup and are routinely used to assess therapeutic response through MRD analysis. Additionally, flow cytometry is applied for circulating tumor plasma cell (CTPC) enumeration, which has demonstrated significant prognostic value. Immune composition studies through MFC may provide better understanding of disease biology. Furthermore, MFC provides additional information about other bone marrow cell populations, assessing cellularity, immunophenotypic characteristics of plasma cells, and possible hemodilution. This review explores the applications of MFC and NGF in MM, highlighting their roles in diagnosis, response assessment, and prognosis. Beyond their established use in MRD monitoring, flow cytometry-derived immunophenotypic profiles show strong potential as cost-effective prognostic tools. We advocate for future studies to validate and integrate these markers into risk stratification models, complementing cytogenetic analyses and guiding individualized treatment strategies.

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired clonal hematologic disorder caused by somatic mutations in the PIGA gene of hematopoietic stem cells, leading to the absence of GPI-anchored proteins, including the complement regulators CD55 and CD59. This deficiency results in uncontrolled complement activation, causing intravascular and extravascular hemolysis, thrombosis, and bone marrow failure. Historically associated with substantial morbidity, PNH management has been transformed by the advent of complement inhibitors. Eculizumab, the first approved C5 inhibitor, significantly reduced thrombotic risk and improved survival but did not eliminate anemia due to extravascular hemolysis. Newer agents now target proximal complement components, offering broader control and improved convenience. This review summarizes the pathophysiology of PNH, evaluates established and emerging complement inhibitors, and discusses ongoing therapeutic challenges and future directions.

Acute myeloid leukemia (AML) continues to pose significant therapeutic challenges, with high relapse rates driven largely by leukemic stem cells (LSCs), a rare, therapy-resistant population with self-renewal capacity, niche adaptation, and the ability to re-initiate disease. In this state-of-the-art review, we synthesize recent advances in LSC biology, addressing (i) how LSCs differ functionally and phenotypically from normal hematopoietic stem cells (HSCs), (ii) practical approaches for LSC quantification using multiparameter flow cytometry and LSC-enriched marker panels, (iii) the dysregulated signaling, metabolic and epigenetic programs that enable LSC persistence under chemotherapy and contribute to measurable residual disease, and (iv) current therapeutic strategies targeting LSC eradication, including antibody-based therapies, apoptosis and metabolic inhibitors, and emerging epigenetic agents. We also examine the key translational barriers, particularly antigen overlap with normal progenitors, microenvironmental protection, and the need for assay harmonization, while proposing a practical framework for integrating LSC assessment into risk stratification and therapeutic development.

Background/Objectives: Haloperidol is a typical antipsychotic drug widely used for acute confusional state, psychotic disorders, agitation, delirium, and aggressive behavior. Methods: The toxicity of haloperidol was studied using zebrafish (ZF) embryos as a model organism. Dechorionated embryos were exposed to various concentrations of haloperidol (0.5–6.0 mg/L). The lethal dose concentration was estimated and was found to be 1.941 mg/L. Results: The impact of haloperidol was dose-dependent and significant from 0.25 mg/L. Haloperidol induced several deformities at sublethal doses, including abnormal somites, yolk sac edema, and skeletal deformities. Haloperidol significantly affected heart rate and blood flow and induced pericardial edema and hyperemia in a dose-dependent manner, suggesting its influence on heart development and function. Embryos exposed to haloperidol during their ontogenetic development had smaller body length and eye surface area than non-exposed ones in a dose-dependent manner. Conclusions: It was found that haloperidol significantly affects the behavior of the experimental organisms in terms of mobility, reflexes to stimuli, and adaptation to dark/light conditions.

Multiple myeloma (MM) is one of the most common hematological malignancies and remains incurable. However, survival of multiple myeloma patients has significantly increased due to the implementation of novel therapies along with autologous stem cell transplantation, changing the natural history of the disease. Consequently, there is an unmet need for more sensitive response assessment techniques capable of quantifying minimal tumor burden to identify patients at higher risk of early relapse. Multiparameter flow cytometry (MFC) is an essential tool for diagnosing and monitoring patients with various hematological conditions and has recently gained prominence in identifying, characterizing, and monitoring malignant plasma cells. The implementation of Next Generation Flow (NGF) by EuroFlow aims to overcome the pitfalls of conventional MFC, including lack of standardization and lower sensitivity, by offering standardized and optimized protocols for evaluating response depth. Both MFC and NGF have wide-ranging applications in MM for diagnosis and minimal residual disease (MRD) monitoring. Plasma cell identification and clonality evaluation through MFC and NGF assist in diagnostic workup and are routinely used to assess therapeutic response through MRD analysis. Additionally, flow cytometry is applied for circulating tumor plasma cell (CTPC) enumeration, which has demonstrated significant prognostic value. Immune composition studies through MFC may provide better understanding of disease biology. Furthermore, MFC provides additional information about other bone marrow cell populations, assessing cellularity, immunophenotypic characteristics of plasma cells, and possible hemodilution. This review explores the applications of MFC and NGF in MM, highlighting their roles in diagnosis, response assessment, and prognosis, and underscores the importance of incorporating these techniques into routine clinical practice for enhanced patient monitoring.

Acute myeloid leukemia (AML) continues to pose significant therapeutic challenges, with high relapse rates driven largely by leukemic stem cells (LSCs), a rare, therapy-resistant population with self-renewal capacity, niche adaptation, and the ability to re-initiate disease. In this state-of-the-art review, we synthesize recent advances in LSC biology, addressing (i) how LSCs differ functionally and phenotypically from normal hemato-poietic stem cells, (ii) practical approaches for LSC quantification using multiparameter flow cytometry and LSC-enriched marker panels, (iii) the metabolic and epigenetic programs that enable LSC persistence under chemotherapy and contribute to measurable residual disease, and (iv) current therapeutic strategies targeting LSC eradication, in-cluding antibody-based therapies, apoptosis and metabolic inhibitors, and emerging epigenetic agents. We also examine the key translational barriers, particularly antigen overlap with normal progenitors, microenvironmental protection, and the need for assay harmonization, and propose a practical framework for integrating LSC assessment into risk stratification and therapeutic development.