tamoxifen / Generic mfg. - LARVOL DELTA

Prolyl-tRNA synthetase inhibition disrupts oncogenic translation in T-cell acute lymphoblastic leukemia (ASH 2025) - "Primary leukemia was then secondary transplanted in wildtype recipients, which were treated with either vehicle or tamoxifen to induce Cre-mediated deletion of Eprs1...These findings were corroborated in vivo , where hemizygous Eprs1 deletion delayed leukemia progression and extended survival. Together, our findings identify enhanced proline tRNA biogenesis as a critical adaptation in T-ALL pathogenesis and provide a strong molecular and preclinical rationale for therapeutically targeting ProRS in T-ALL."

Acute Lymphocytic Leukemia • Hematological Malignancies • Leukemia • Multiple Myeloma • T Acute Lymphoblastic Leukemia • T-cell Acute Lymphoblastic Lymphoma • CCND3 • EPRS1 • HES1 • MYC • NOTCH1

Endothelial SRSF1 regulates hematopoietic stem cell function in the bone marrow microenvironment (ASH 2025) - "Tamoxifen-induced EC-specific Srsf1 knockout mice(Srsf1iECKO) displayed a significant increase in white blood cells (WBCs) and a decrease in red blood cellsand platelets...These findings suggest an instructive role forendothelial SRSF1-regulated spliced isoforms in modulating HSC homeostasis and localization. Geneexpression and alternative splicing analysis of in vivo and in vitro sources of Srsf1iECKO BMECs areongoing and will be the focus of understanding the SRSF1 alternative splicing regulons that instructhematopoiesis in the BM microenvironment."

Hematological Malignancies • CDH5 • CXCL12 • JAG1

Risk of venous thromboembolism associated with CDK 4/6 inhibitors and adjuvant hormonal therapy in non-metastatic breast cancer: A systematic review and meta-analysis (ASH 2025) - "More recently, the Introduction of cyclin-dependentkinase 4 and 6 (CDK 4/6) inhibitors, Abemaciclib, Palbociclib, and Ribociclib, has led to new treatment forhigh-risk patients...The comparator group in thisanalysis consisted of patients treated with endocrine therapy alone with aromatase inhibitors (AI),tamoxifen, or fulvestrant... Results from this study show that for adult patients with local and locally advanced breastcancer, there is increased risk of VTE development when treated with CDK 4/6 inhibitors compared totreatment with endocrine therapy alone. Limitations to this analysis include exclusion of metastaticdisease, limited data available on mortality associated with VTE incidence, and varying degrees of patient-specific thromboembolic risk factors. As the use of CDK 4/6 inhibitors in the treatment of breast cancergrows, this information will provide further information for conversations about risks and benefits whenselecting treatment plans."

Metastases • Retrospective data • Review • Breast Cancer • Chronic Kidney Disease • Genetic Disorders • HER2 Breast Cancer • HER2 Negative Breast Cancer • HER2 Positive Breast Cancer • Hormone Receptor Breast Cancer • Hormone Receptor Positive Breast Cancer • Oncology • Respiratory Diseases • Solid Tumor • Venous Thromboembolism • HER-2

Adaptive rebalancing of ROS composition averts LSD1 inhibitor–induced oxidative stress in AML (ASH 2025) - "Importantly, ATRA's efficacy enhances significantly when combined with arsenictrioxide (ATO), which elevates reactive oxygen species (ROS), a group of reactive oxygen-containingmolecules including superoxide anions that collectively contribute to oxidative stress.To examine the role of ROS during LSD1 inhibition, we treated primary patient-derived AML samples andcell lines with LSD1i (GSK-LSD1) and monitored ROS dynamics using selective intracellular biosensors andROS type-specific fluorescent probes...Notably, scavenging ROSwith N-acetylcysteine (NAC) significantly impairs differentiation, indicating that ROS plays a critical role inmediating the pro-differentiation effects of LSD1i. To validate that LSD1 regulates ROS, we developed amurine leukemogenic model by transducing hematopoietic stem and progenitor cells (HSPCs) fromLsd1fl/fl conditional knockout mice with the MLL-AF9 oncogene and tamoxifen-inducible Crerecombinase...Rather than decreasing overall ROS..."

Oxidative stress • Acute Myelogenous Leukemia • Acute Promyelocytic Leukemia • Hematological Malignancies • Leukemia • CYBB • KDM1A • MPO

Synergistic correction of polycythemia vera phenotype via dual targeting of JAK2 and Gas6 in Jak2 exon 12 mutant mice (ASH 2025) - "Despite treatments like phlebotomy,cytoreduction, and JAK2 inhibitors (e.g., ruxolitinib, RUX), disease control is often insufficient...PV was induced at 5–7 weeks of age withtamoxifen... Gas6 deletion mitigates PV, supporting its role in controlling disease proliferation.Batiraxcept plus RUX reversed splenomegaly and normalized erythroid differentiation. Persistent highhematocrit despite normalized reticulocytes suggests longer treatment is needed. Preliminary datasuggest Gas6 also contributes to clotting abnormalities."

Preclinical • Hematological Disorders • Hematological Malignancies • Leukemia • Myelofibrosis • Myeloproliferative Neoplasm • Polycythemia Vera • Solid Tumor • Thrombosis • ABL1 • AXL • BCR • GAS6 • JAK2 • MERTK • TFRC

Harnessing repressive LEF1/β-catenin complexes to overcome drug resistance in chronic lymphocytic leukemia (ASH 2025) - "In aconverse experiment, tamoxifen induced stabilization of β-catenin (Mb1-Cre-ERT2 x Ctnnb1ex3/+)subverted leukemogenesis: while 7 out of 11 wildtype littermates developed CLL (median survival=426days), none of 11 mice with B-cell-specific β-catenin stabilization succumbed to CLL (P=0.02).Interestingly, β-catenin stabilization in B-cells resulted in selective depletion of CD5+ CD19+ CLL cells,which express high levels of nuclear LEF1 (intracellular FACS) and spared CD5- CD19+ normal B-cells thatlack LEF1 expression. Three GSK3B inhibitors LY2090314, AZD1080 and CHIR99021 achieved favorable safety and PK/PDprofiles in previous clinical trials for solid tumors and neurological disorders. Our results provide arationale for repurposing GSK3B-inhibitors for the treatment of refractory and RT CLL."

Chronic Lymphocytic Leukemia • CNS Disorders • Hematological Malignancies • Leukemia • Richter's Syndrome • Solid Tumor • CD5 • CTNNB1 • IKZF1 • LEF1 • MYC

Pulmonary Embolism–Attributable mortality among patients with breast cancer in the United States, 1999-2021 (ASH 2025) - "In addition to chemotherapy and tamoxifen, the Introduction of new therapeutic agents,including cyclin-dependent kinase 4/6 inhibitors, antibody-drug conjugates, poly(ADP-ribose) polymeraseinhibitors, and immune checkpoint inhibitors, has been associated with venous thromboembolism risk.We analyzed trends in PE-related mortality from 1999 to 2021 among U.S. patients with breast cancer,stratified by age, sex, race and ethnicity, and U.S. Census region. Mortality data were obtained from the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) Multiple Cause of Death database... Age-adjusted PE–attributable mortality among individuals with breast cancer was stableuntil 2017, then rose significantly through 2021. The increase was observed overall, in females, acrossage groups, racial/ethnic subgroups, and regions (except the Northeast), despite stable breast cancerincidence. Continued elevation in 2022-2023 suggests..."

Clinical • Breast Cancer • Infectious Disease • Oncology • Pulmonary Embolism • Respiratory Diseases • Solid Tumor • Venous Thromboembolism

Real world evidence of treatment patterns in hereditary hemorrhagic telangiectasia (ASH 2025) - "Treatment examinedincluded bevacizumab, pazopanib, pomalidomide, aminocaproate, tranexamic acid (TXA), octreotide,lanreotide, thalidomide, tacrolimus, sirolimus, tamoxifen and raloxifene...The majority of HHT patients were treated withferrous sulfate (n=910), followed by iron sucrose, ferrous gluconate, ferric carboxymaltose, iron dextran,and ferric derisomaltose...While 8% of patients treated with TXA had VTE, the data does not support a definitiveconclusion of increased VTE in patients treated with anti-fibrinolytics. To further elucidate treatmentpractices in HHT, a multi-center approach incorporating review of medical records would providevaluable insights into real-world practices."

Clinical • HEOR • Real-world • Real-world evidence • Anemia • Aplastic Anemia • Cardiovascular • Cerebral Hemorrhage • CNS Disorders • Gastrointestinal Disorder • Hematological Disorders • Hypertension • Renal Disease • Venous Thromboembolism

HEXIM1 is a critical regulator of cell cycle progression and terminal maturation during steady-state and stress erythropoiesis (ASH 2025) - "At steady-state, Hexim1 deletion – achieved via intraperitoneal injection of tamoxifen –resulted in impaired terminal erythroid maturation, in-vivo... Our collective published and preliminary data strongly position HEXIM1 as a critical,multifaceted regulator essential for early progenitor expansion and late-stage erythroid maturation. Ourrecent studies position HEXIM1 as an essential cell cycle regulator in erythropoiesis. Future work aims todissect the definitive physiological roles and downstream molecular consequences of Hexim1 deletion inadult mice under both steady-state and anemic stress conditions, aiming to clarify its contribution toerythropoiesis in health and disease."

Hematological Disorders • CD34 • GATA1 • HEXIM1 • TFRC

Bone marrow adipocytes fuel hematopoietic regeneration via fatty acid release (ASH 2025) - "Pharmacologic modulation of bone marrowadipocytes using rosiglitazone (which increases adipocytes) and bisphenol A diglycidyl ether (BADGE,which decreases adipocytes) did not affect steady-state hematopoiesis or HSC frequency and function.However, these treatments significantly impacted hematopoietic regeneration after bone marrowtransplantation, with rosiglitazone promoting and BADGE inhibiting recovery...Conditional deletion of these genes in HSCs did not affect steady-state hematopoiesis butsignificantly impaired regeneration, highlighting the critical role of FA oxidation in HSCs during stress.To identify the source of FA, we generated Lepr-CreER; Pnpla2fl/fl mice, in which Pnpla2 (encodingadipose triglyceride lipase, ATGL) was conditionally deleted in LEPR+ cells and their adipocyte progeny.Following tamoxifen induction, these mice exhibited normal steady-state hematopoiesis but impairedregeneration, with reduced FA levels in HSPCs...Next, we developed a dual..."

Bone Marrow Transplantation • Hematological Disorders • CD36 • LEPR • SCARB1

Aberrant cell cycle regulation and osteoblastic differentiation in diamond-blackfan anemia (DBA) mesenchymal stem cells (ASH 2025) - "MouseDBA MSCs were derived from RPL11+/fl carrying Cre-ERt2 and Mx1-Cre, in which the Rpl11 gene is deletedupon injecting tamoxifen or polyinosinic:polycytidylic acid (poly(I:C)), respectively...In addition, the LATS inhibitorrestored the lamellipodia formation and stellate morphology of DBA MSCs in a dose-dependent manner.In conclusion, we characterized and identified the impaired YAP signaling pathway of bone marrowmesenchymal stem cells in DBA. Results from this study will lay the groundwork for understanding thebone marrow microenvironment of DBA and identifying potential targets for more effective treatment inDBA."

Anemia • Genetic Disorders • Hematological Disorders • Sarcoma • Solid Tumor • Targeted Protein Degradation • CCNA2 • CDK1 • GATA1 • LATS1 • RPL11 • RPS26 • RUNX2

Temporal control of CAR expression enables thymic generation of autoreactive T cells targeting tumor-associated antigens (ASH 2025) - "Constructs that were tested included CARs with decreasedcostimulation, CARs under the control of a distal LCK promoter (distal LCK activity is restricted to the laterstages of thymic T cell development), and a Cre-dependent tamoxifen-inducible CAR. We demonstrate that CD19 CAR expression can be successfully induced months afterintrathymic delivery of Cre-dependent, CAR-transduced HSPCs; however, as anticipated, thymic negativeselection eliminates a subset of CAR-expressing single positive thymocytes. Future directions will focus ondeveloping clinically translatable strategies for thymic CAR T cell generation, including the use oftetracycline-inducible expression systems or the design of CARs specific for truly tumor-restricted, non-self-antigens, thereby circumventing central tolerance barriers imposed by autoreactivity."

IO biomarker • Oncology • CD19

STAG2 mutation preserves a stem cell phenotype in FLT3-ITD-mediated MDS to leukemia transformation (ASH 2025) - "Here wepresent a sequential mutagenesis murine model of co-Stag2/Flt3ITD mutation, using pIpC-inducibleMx1Cre and tamoxifen-inducible Flpo recombinase...Overall, our data highlights how pre-existing Stag2 mutation alters the cellular composition and behaviorpost transformation. This model will not only shed light on the AML-MRC pathogenesis but also create apre-clinical testing platform with potential therapeutic relevance."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • FLT3 • PROCR • STAG2

RAS G12 and Q61 codon mutations confer distinct disease characteristics in Acute Myeloid Leukemia and exhibit differential response to RAS(ON) inhibitor RMC-7977. (ASH 2025) - "There is growing interest in understanding and targeting RASmutations in AML, owing to studies indicating that RAS mutations are associated with relapse aftermultiple novel targeted therapy agents, including azacitidine/venetoclax, and FLT3 and IDH1/2 inhibitors.In addition, the advent of novel RAS(ON) inhibitors showing promise in solid cancers offers a therapeuticstrategy that could be deployed to target these mutations. Our group has previously described the use oftamoxifen inducible, Cre-recombinant single- and double-mutant mouse models harboring Npm1c,NrasG12D, and NrasQ61R mutant alleles and shown that there are distinct codon specific phenotypedifferences in RAS-mutant AML...RMC-7977 was shown to ablate MAPK signaling and have high potency across a range of RAS-mutated AML cell lines, with highest potency observed in THP1 (G12D, IC50 585pM), compared to OCI-AML3 (Q61L, IC50 5.85pM) and HL60 (Q61L, IC50 2.78nM). RMC-7977 induced a variable degree ofapoptosis and..."

Acute Myelogenous Leukemia • Developmental Disorders • Hematological Malignancies • Leukemia • Solid Tumor • Thrombocytopenia • ANXA5 • FLT3 • GLI2 • IDH1 • IDH2 • NRAS

Examining the role of U2AF1 and TET2 mutations in a myeloid malignancy mouse model (ASH 2025) - "To address this, we crossed the same U2AF1 S34F transgeneinto HSC-SCL Cre-ER, which is activated by tamoxifen specifically in hematopoietic stem cells [Gothert J, etal...Furthermore, additional work canbe done to explain the mechanism through which these mutations produce the observed phenotypes,such as through altered expression of specific genes. Finally, further studies are necessary to betterunderstand why splicing factor mutations are drivers of myeloid malignancies despite providing acompetitive disadvantage in mouse models."

Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • RUNX1 • TET2 • U2AF1

Galectin-3 in host murine models lessens the severity of graft-versus-host disease by preserving intestinal stem cells irrespective of gut microbiota composition (ASH 2025) - "4)We made selective Gal-3-/- in LGR5+Intestinal stem cells (ISCs) by crossing Gal-3fl/fl mice with LGR5Cre mice, leading to Gal-3fl/flLGR5Cre mice.To induce Gal-3-/- in LGR5+ ISCs, Gal-3fl/flLGR5Cre mice were given Tamoxifen...This studyshowed that Gal-3 protects ISCs, sustaining gut integrity post allo-HCT. Future studies aimed at strategiesto enhance the effect of Gal-3 in non-hematopoietic gut cells may improve preclinical GvHD with thepotential to translate to clinical trials to decrease GvHD severity without affecting GvL."

Gut Microbiota • Preclinical • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • CD4 • IFNG • IL17A • LGALS3 • MUC2 • THY1 • TNFA

Enhanced FLI1 accessibility mediates STAG2-mutant leukemogenesis (ASH 2025) - "We then performed FLI1 Cut&Runand showed FLI1 binds to cis-regulatory elements and more accessible region of the KO cells.Functionally, FLI1 knock down led to decreased CD34 cell surface markers in the KO cells, which confirmsthat FLI1 mediates phenotype changes.We next generated dual Stag2ΔNpm1c/+ murine models with tamoxifen inducible UbcCreERT2 to establishthe functional effects on hematopoiesis...We determined that the abnormalchromatin remodeling driven by STAG2 mutation occurs in HSPCs and hyperactivity of FLI1 is the keydysfunction in Stag2/Npm1c co-mutant. Further studies include determining the phenotypic andchromatin response of FLI1 inhibition in STAG2 mutant models, which will pave the way to highlight newtherapeutic potentials of cohesin mutant leukemia."

Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • CD34 • CD48 • FLI1 • FLT3 • HOXA9 • MECOM • STAG2

Bone marrow microenvironment retinoic acid receptor signaling represses multipotential progenitor dependent B cell lymphopoiesis through secretion of resistin (ASH 2025) - "To investigatehow RXRs regulate the lymphopoietic potential of BMA, we generated tamoxifen-inducible, BMA-specificRXRα/β deficient mice (AdipoQCre-ERT2; RXRα/βΔ/Δ)...These results highlight the BMA RXR–Resistin axis as amodifiable niche pathway that selectively controls MPP-derived lymphopoiesis without compromisingmyeloid or T-cell reconstitution. Modulating this axis may offer novel therapeutic strategies to enhanceimmune recovery post-HSCT."

Bone Marrow Transplantation • Hematological Disorders • Infectious Disease • RETN • TNFA

Clonal persistence of BRAFV600E under MEK inhibition in histiocytosis (ASH 2025) - P=N/A | "Ten CD34⁺ samples were profiled using the TAPESTRI platform for single-cell DNA and protein analysis and/or PromethION Nanopore long-read sequencing.In parallel, we used a conditional BRAFV600Ehet-SclCre+ murine model induced by tamoxifen (200mg/kg/day for 4 days) and treated with trametinib (0.3 mg/kg/day) for one month. Residualdisease persists in hematopoietic progenitors and displays a therapy-induced shift from monocytes to Bcells, suggesting lineage plasticity and identifying B cells as a potential reservoir. Our BRAFV600E murinemodel faithfully recapitulates clonal persistence under MEKi, underscoring the need for combinatorialstrategies to achieve complete molecular remission."

Langerhans Cell Histiocytosis • Rare Diseases • Solid Tumor • CD1C • CD34 • MME • TET2

Atypical hemolytic uremic Syndrome Triggered by malignancy and drug exposure: A systematic review and meta-analysis (ASH 2025) - "Tacrolimus was the mostreported drug trigger (n=6)followed by gemcitabine (n=5), vincristine (n=5), bevacizumab (n=3), carfilzomib (n=3), 6-mercaptopurine(n=2), methotrexate (n=2), and mitomycin (n=2). Aflibercept, bactrim, bleomycin, capecitabine, cisplatin, cyclophosphamide, cytarabine,dasatinib, deferasirox, dinutuximab, estarylla, ketoprofen, L-asparaginase, modakafusp alfa, PEG-asparaginase, sunitinib, syntheticpsychoactive drugs, tamoxifen, and topotecan were reported as potential triggers for aHUS in one patient each...The pooled rate of treatment with eculizumab was 74% (95% CI, 0.629-0.842, p < 0.01, I2 = 72%),and the pooled rate of renal recovery was 65% (95% CI, 0.525-0.761, p < 0.01, I2 = 55%)...AKI and hematological abnormalities in these patients should prompt an emergent work-up and treatment. Current evidenceis primarily derived from case reports, so prospective trials are necessary to establish the incidence, associations, triggers, and outcomes..."

Retrospective data • Review • Acute Kidney Injury • Acute Lymphocytic Leukemia • Anemia • Atypical Hemolytic Uremic Syndrome • B Acute Lymphoblastic Leukemia • Biliary Cancer • Breast Cancer • Cholangiocarcinoma • Complement-mediated Rare Disorders • Genito-urinary Cancer • Hematological Malignancies • Hepatocellular Cancer • Hodgkin Lymphoma • Leukemia • Lung Cancer • Lymphoma • Multiple Myeloma • Nephrology • Neuroblastoma • Oncology • Ovarian Cancer • Pancreatic Cancer • Prostate Cancer • Renal Cell Carcinoma • Renal Disease • Solid Tumor • Thrombocytopenia • Urothelial Cancer

U2AF1S34F mutant HSPCs have a fitness advantage in aged and inflamed bone marrow (ASH 2025) - "The recipient mice were pre-conditioned with low dose busulfan and CD4 and CD8 cell-depletingantibodies to clear HSPCs and remove T-lymphocytes, respectively...Tamoxifen-inducible HSC specific Cre mice (hScl-CreERT) werecrossed to our Rosa26EYFP/+; U2af1S34F/+ or U2af1+/+ conditional knock-in mice for in-vivo inflammationand single cell RNA sequencing (scRNA-seq) studies.Results...These studies show how context dependentselection can contribute to malignant clonal evolution that manifests primarily in the elderly. In all, ourfindings support the value of implementing lifestyle changes aimed at reducing inflammation with age,along with targeted monitoring, to mitigate clonal expansion and lower the risk of associated adverseoutcomes including MDS and AML."

Acute Myelogenous Leukemia • Hematological Malignancies • CD4 • CD8 • IL1B • TET2 • U2AF1

Loss of endothelial mir-126 drives age-related reduction of hematopoietic activity (ASH 2025) - "Similar results were obtained in geneticallymodified mice carrying tamoxifen-induced double-fluorescent reporter [Tie2-CreER/TdTomato/Tg(Ly6a-GFP)] that allowed to track ECs...Finally, aged HSCs co-cultured with aged ECs had lower levels of miR-126 and reduced long-term engraftment in congenicrecipient mice compared with aged HSCs co-cultured with young ECs (engraftment at 16 weeks: 46.2% vs65.7%, P=0.0003); this reduction could be rescued by co-treatment with miR-126 mimic (16 weeks: 46.2%vs 57.2%, P=0.03).In summary, we uncover a crucial role of inflammaging-mediated loss of EC miR-126 that lead to agingBM vascular remodeling with decreased density of arterioles and EC-miR-126 supply to HSCs, thatexpand, but lose regenerative capacity. Targeting miR-126 loss with miR-126 mimic restores miR-126levels and reconstitution capacities in aged HSCs, therefore representing a potential therapeuticapproach to mitigate aging-related HSC dysfunction and rejuvenate hematopoiesis."

Hematological Disorders • Inflammation • CD31 • CD48 • MIR126 • PECAM1 • PTPRC • TNFA

Erythroid-specific, inducible CDAN1∆/∆ mouse model phenocopies congenital dyserythropoietic anemia type-la (ASH 2025) - "We assayed liver nonheme iron content via a colorimetricassay (Torrance J.D. & Bothwell T.H., 1980, Churchill Livingstone) and observed an increase in livernonheme iron stores, suggesting the onset of secondary iron loading. After flow sorting for the differentpopulations of BM erythroblasts, we performed assay for transposase accessible chromatin (ATAC) withhigh-throughput sequencing per each erythroblast population in CDAN1∆/∆ versus CDAN1WT/WT micewhile on long-term tamoxifen induction; our preliminary analysis suggests differential gene accessibilitybetween control and CDAN1∆/∆ EBs.In conclusion, we have generated a reliable model of CDA-Ia which we use as a platform to investigatethe role of Codanin-1 in chromatin organization and condensation during erythropoiesis and how IFN-αmay exert a therapeutic effect on patients with CDA-Ia."

Preclinical • Anemia • Genetic Disorders • Hematological Disorders • ERFE • IFNA1

IFNγ-driven MHC class II expression by intestinal epithelial cells dictates local cytolytic Th1 cell differentiation and intestinal stem cell loss (ASH 2025) - "However, the molecular cues by which CD4+ T cells areinvoked to mediate lethal gut GVHD at the epithelial interface after allogeneic BMT is unclear.We compared GVHD induced by male antigen (H-Y) reactive TCR-transgenic CD4+ T cells (Marilyn T) inwhich MHC-II was deleted prior to or shortly after BMT by tamoxifen injection (day -10 to -6 versus day +4to +8, respectively) in Villin CreERT2 IAb fl/fl male recipient mice...This effect required the induction of MHC II-expression onISC by IFNg. In sum, direct IFNg-signaling in IEC is critical for the MHC-II-dependent early local generationof cytolytic Th1 differentiation that thereafter mediate MHC-II-dependent ISC deletion, demonstrating acritical interferon–MHC-II feed forward axis in the initiation of cytolytic Th1-dependent gut disease."

Acute Graft versus Host Disease • Bone Marrow Transplantation • Gastrointestinal Disorder • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • CD4 • CD69 • CD8 • GZMB • IFNG • PRF1

Sox11-induced reprogramming of B2 cells to a B1a-like phenotype promotes Mantle Cell Lymphoma in mice (ASH 2025) - "We found that elevated levels of SOX11 in B-cells are sufficient to drive MCL-like lymphomas in mice.Moreover, SOX11 expression synergized with loss of p53 and overexpression of Ccnd2 to form aggressiveMCL-like CD19+CD5+CD23-IgM+IgD+ lymphomas, with a median survival of 314 (p53Mb1; n=11), 165(SOX11/p53Mb1; n=19), and 134 (SOX11/Ccnd2/p53Mb1; n=15) days. These SOX11-driven lymphomasshow transcriptional, immunophenotypic and functional similarities with both murine B1a cells and MCLpatients. scRNAseq analysis shows that SOX11 overexpression from CLP stage blocks T-cell developmentand skews B-cell development towards the B1a and marginal zone B-cell (MZB) lineage."

Preclinical • B Cell Lymphoma • Hematological Malignancies • Lymphoma • Mantle Cell Lymphoma • Non-Hodgkin’s Lymphoma • CCND2 • CD5 • FCER2 • MALT1 • SOX11 • TP53