Leukemia

Leukemia publishes high quality, peer reviewed research that covers all aspects of the research and treatment of leukemia and allied diseases. Studies of normal hemopoiesis are covered because of their comparative relevance. Topics of interest include oncogenes, growth factors, stem cells, leukemia genomics, cell cycle, signal transduction, molecular targets for therapy and more. We publish a range of content types including original research articles, reviews, letters, correspondence and comments that elaborate on significant advances in the field and cover topical issues.

List of Papers (Total 6,231)

Organelle proteomics reveals novel metabolic vulnerabilities in FLT3-ITD cells

In acute myeloid leukemia (AML), the insertion site of internal tandem duplications (ITDs) within the FLT3 gene critically determines the sensitivity to tyrosine kinase inhibitors (TKIs). Despite recent advances, patients harboring ITDs in the tyrosine kinase domain (TKD) still lack effective therapeutic options. To elucidate the molecular basis underlying the differential TKI...

A novel CD7-directed antibody-drug conjugate targeting BCL-XL with potent anti-leukemic activity in T-cell acute lymphoblastic leukemia

Current treatments of T-cell acute lymphoblastic leukemia (T-ALL) are based on intensive chemotherapy regimens which provide overall survival rates of ~85% in children and <50% in adults. Therefore, there is an unmet need for novel therapeutic options in T-ALL. Pre-clinical studies and clinical trials have demonstrated that inhibitors of BCL-XL and/or BCL-2, two anti-apoptotic...

Artificial intelligence-enhancement of flow cytometry data accelerates the identification of measurable residual chronic lymphocytic leukemia

Flow cytometry (FC) is essential for detecting measurable residual disease (MRD) in chronic lymphocytic leukemia (CLL), but its use is limited by the expertise and time required for manual analysis. We developed an artificial intelligence (AI) pipeline, Clustering/Classification of All Events, Dimensionality reduction, Downsampling, and Aberrancy Scaling (CCADDAS), to...

From fatal disease to functional cure: 25 years of tyrosine kinase inhibition in chronic myeloid leukemia

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome, which results from a translocation between chromosomes 9 and 22. This alteration gives rise to the BCR::ABL1 fusion oncogene, whose constitutive tyrosine kinase activity promotes uncontrolled proliferation and survival of leukemic cells. The discovery of...

Local oxygen tension dictates hematopoietic cell growth and potency

Hematopoietic stem and progenitor cells support a lifetime supply of blood and immune cells and constitute a powerful cell therapy platform for hematologic diseases. In this study, we define oxygen-dependent activities of hematopoietic stem and progenitor cells. We found that lineage-defined progenitor cells from umbilical cord blood, bone marrow, and mobilized peripheral blood...

CAR T-cells targeting CD117 effectively eliminate mast cells in preclinical models of advanced systemic mastocytosis

Systemic mastocytosis (SM) is characterized by uncontrolled expansion of neoplastic mast cells (MCs) and their accumulation in various tissues and organs, ranging from indolent variants to more advanced forms (advSM). Although several MC- and SM-expressed cell surface antigens have been identified, no immune therapy has been developed for advSM so far. The receptor tyrosine...

MDM2 inhibitors in myeloid cancers: from basic biology to clinical use in myeloproliferative neoplasms

Pharmacologic targeting of murine double minute 2 (MDM2) represents one of the most compelling strategies for therapeutic reactivation of wild-type p53 in hematologic malignancies. The MDM2–p53 autoregulatory loop is a central regulator of cellular stress responses, and in myeloid neoplasms—including acute myeloid leukemia (AML) and myeloproliferative neoplasms (MPN)—p53 is...

MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2

MECOM is a transcription factor critical for the maintenance of hematopoietic stem cells (HSCs) and the pathogenesis of myeloid leukemia. Germline mutations clustered in the C-terminal zinc finger domain (ZFD) of MECOM are known to cause MECOM-associated syndromes, involving bone marrow failure and skeletal anomalies. However, the molecular consequences of these mutations and the...

Smoldering multiple myeloma in transition: redefining early myeloma in the modern era

Smoldering multiple myeloma (SMM) has long been viewed as an intermediate precursor state, monitored until symptoms or organ dysfunction signaled the transition to active multiple myeloma (MM). Over the past decade, however, major advances in molecular biology, modern imaging, and immunotherapy have reshaped our understanding of early plasma cell disorders. The recent FDA...

Development and validation of the predictive aplastic score system (PASS): a simplified tool to diagnose acquired aplastic anemia in adults

Acquired aplastic anemia (AA) can present similarly to inherited bone marrow failure syndromes (IBMFS) but treatment differs. AA diagnosis relies on excluding IBMFS; however, genetic testing is not always available, may delay care or be inconclusive. We developed the Predictive Aplastic Score System (PASS), a clinical tool using readily available data to distinguish AA from IBMFS...

The spectrum of immunoglobulin heavy chain enhancer hijacking in chronic lymphocytic leukemia

Activation of oncogenes by hijacking immunoglobulin gene loci (IG) enhancers via chromosomal translocation is a common pathogenetic mechanism in B-cell malignancies, affecting 5–10% of chronic lymphocytic leukemia (CLL). The oncogenic partners in many of these cases remain unidentified. Therefore, we conducted a comprehensive analysis of 144 CLL samples with IGH-translocation...

ASC4OPT: asciminib treatment optimization study in patients with chronic myeloid leukemia in chronic phase previously treated with two or more tyrosine kinase inhibitors

The ASC4OPT non-comparative phase 3b study (NCT04948333) evaluates asciminib once daily (QD) or twice daily (BID) in chronic myeloid leukemia in chronic phase (CML-CP) treated with ≥2 tyrosine kinase inhibitors (TKIs). This study enrolled 169 patients not in major molecular response (MMR), with unsatisfactory response (intolerant, warning or failure) as defined by European...

A targeted circulating tumor DNA landscape of copy number aberrations in large B-cell lymphomas

The utility of circulating tumor DNA (ctDNA) for mutational genotyping, pretreatment prognostication, and assessment of molecular response is well established in patients with aggressive large B-cell lymphoma (LBCL). Here, we have applied targeted panel and duplex sequencing of plasma ctDNA to study copy number aberrations (CNAs) along with mutational landscapes in 123 uniformly...

Imputing causality and clonal dynamics from single-cell transcriptomics in paroxysmal nocturnal hemoglobinuria

Paroxysmal nocturnal hemoglobinuria (PNH) originates from hematopoietic stem cells (HSCs) harboring somatic mutations in the phosphatidylinositol glycan class A (PIGA) gene. Clonal expansion of PIGA-mutated cells occurs uniquely in the setting of bone marrow (BM) failure, but specific pathophysiologic mechanisms remain unclear. We performed single-cell RNA sequencing (scRNA-seq...

HDAC8 inhibition targets STAT3–MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia

KMT2A-rearranged (KMT2A-r) acute myeloid leukemia (AML) is an aggressive AML subtype characterized by 11q23 chromosomal rearrangements involving KMT2A gene and clinically associated with poor prognosis. Herein, we show that HDAC8 is upregulated in KMT2A-r AML and high HDAC8 is associated with poor overall survival in KMT2A-r AML patients. Using a KMT2A::MLLT3 mouse model, we...

A velocity-informed framework for resolving functional stratification in rare human stem cells

Single-cell transcriptomics has transformed our understanding of stem cell biology; however, the analysis of extremely rare and quiescent populations remains limited by the low cell numbers and functional inaccessibility. Here, we present a velocity-informed framework to resolve transcriptional stratification in ultra-rare stem cells, using very small embryonic-like stem cells...

Genomic fusion breakpoints for DNA-based measurable residual disease monitoring in pediatric acute lymphoblastic leukemia

Measurable residual disease (MRD) is a key prognostic factor in pediatric acute lymphoblastic leukemia (ALL), but current gold-standard methods based on immunoglobulin/T-cell receptor (IG/TCR) rearrangements are complex and not informative in a subset of patients. Genomic breakpoints of oncogenic fusions (GFBs) are stable, biologically grounded markers that may overcome these...

Intracellular IL-23R is necessary for mitotic spindle formation and viability in AML

Interleukin-23 receptor (IL-23R) is a cell surface cytokine receptor classically expressed on T cells, where it regulates T cell activation. Here, we discovered a novel intracellular localization and function for IL-23R in Acute Myeloid Leukemia (AML). Compared to normal hematopoietic cells, IL-23R was increased in primary AML samples. IL-23R was predominantly localized...

PRMT5 inhibition sensitizes B-cell lymphoma cells to ferroptosis

Protein arginine methyltransferase 5 (PRMT5) is overexpressed in B-cell lymphomas, including diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL). While PRMT5 is known to regulate multiple oncogenic pathways, including PI3K-AKT signaling, its role in lipid metabolism and ferroptosis, a regulated, iron-dependent cell death driven by lipid peroxidation, remains...