birabresib (OTX015) / Merck (MSD) - LARVOL DELTA

Preclinical Studies Demonstrating Efficacy of Tasquinimod in Models of Advanced Myeloproliferative Neoplasm (MPN) in Blastic Phase (ASH 2023) - "Additionally, our findings showed that co-treatment with TM (5 to 30 µM) and ruxolitinib (250 to 1000 nM), BET inhibitor OTX015 (50 to 250 nM) or pelabresib (CPI-0610) (100 to 500 nM), or BCL2/Bcl-xL inhibitor navitoclax induced synergistic lethality in advanced MPN-BP cells exhibiting delta synergy scores of >1.0 (by the ZIP method). In a separate experiment on the same PDX model, treatment with TM (30 mg/kg/day) also induced significantly greater survival advantage than treatment with ruxolitinib (30 mg/kg/day) or OTX015 (30 mg/kg/day) by oral gavage. These findings clearly demonstrate preclinical efficacy of TM in advanced MPN-BP cellular models and create the rationale to further interrogate the efficacy of TM alone and in combinations with current, front-line therapies for advanced MPN with excess blasts."

IO biomarker • Metastases • Preclinical • Fibrosis • Immunology • Inflammation • Myelofibrosis • Myeloproliferative Neoplasm • Oncology • BCL2 • BCL2L1 • CALR • CCND1 • CD123 • CD33 • CD34 • CD99 • CDK6 • CDKN1A • CLEC12A • CXCR4 • IL3RA • IL6 • ITGAM • JAK2 • MPO • MYC • NLRP3 • S100A8 • S100A9 • TERT • TLR4 • TNFA

Notable Efficacy of Co-Treatment with FHD-286, a Dual BRG1/BRM ATP-Ase Inhibitor, and Menin or BET Inhibitor, Decitabine or Venetoclax Against AML with MLL-r or Mutant NPM1 (ASH 2023) - "BRG1 (SMARCA4) and BRM (SMARCA2) are the core ATPase within the multi-protein, ATP-dependent, chromatin remodeling BAF complexes that regulate gene transcription. Finally, co-treatment with FHD-286 and OTX015 or SNDX-5613 (oral gavage) was significantly more effective than each drug alone in reducing the AML burden and overall survival of mice engrafted with a separate PDX model of AML cells with mtNPM1 and FLT3-ITD, without significant toxicity. These findings demonstrate the pre-clinical efficacy of FHD-286-based rational combinations and underscore their promise against AML with MLL1r or mtNPM1."

Clinical • IO biomarker • Acute Myelogenous Leukemia • BCL2 • BRD4 • CASP3 • CD123 • CD33 • CD99 • CDK4 • CDKN1A • CEBPA • CLEC12A • FLT3 • HEXIM1 • IL3RA • ITGAM • MCL1 • MEF2C • MYC • NPM1 • PBX3 • PLK1 • SMARCA2 • SMARCA4

Superior Preclinical Efficacy of BRG1/BRM Inhibitor Combined With BET Inhibitor or Decitabine Against MECOM-rearranged (MECOM-r) Acute Myeloid Leukemia (AML) (SOHO 2025) - "Taken together, these findings highlight the promise of FHD-286– based rational combinations, especially with BETi, navitoclax, or decitabine, in exerting significant anti-AML efficacy against cellular models of MECOM-r AML."

Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BCL2L1 • CD93 • CDK4 • GATA2 • ITGAM • KIT • MECOM • MYC • PLK1 • SMARCA4

Pre-Clinical Efficacy of CDK7 Inhibitor-Based Combinations in Cellular Models of Advanced Myeloproliferative Neoplasms (MPN) Transformed to AML (ASH 2023) - "Treatment with JAK inhibitor (JAKi), e.g., ruxolitinib, venetoclax or hypomethylating agents alone or in combination are ineffective in improving the poor survival in MPN-sAML...Present studies demonstrate that treatment with ATP-competitive, covalent CDK7 inhibitors (CDK7i) SY-1365, and clinical grade SY-5609, dose-dependently (20 to 250 nM) increased % G1 while reducing the % of cell-cycle S phase SET2 and HEL cells...SY-5609 treatment also exerted synergistic lethality with the BETi pelabresib or BD2-selective BETi ABBV-744 or the CBP/p300 inhibitor GNE-049 in MPN-sAML cells...Additionally, compared to each drug or vehicle control, co-treatment with SY-5609 and OTX015 (30 mg/kg/day by oral gavage) reduced more MPN-sAML burden and significantly improved survival in a HEL-Luc/GFP xenograft model without inducing toxicity. These findings demonstrate promising preclinical activity of CDK7 inhibition against the cellular models of MPN-sAML, supporting the rationale to..."

Metastases • Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myeloproliferative Neoplasm • Oncology • ASXL1 • AURKA • BCL2L1 • BRD4 • CALR • CASP9 • CCND1 • CD123 • CD34 • CD99 • CDK1 • CDK4 • CDK6 • CDK9 • CDKN1A • CLEC12A • HEXIM1 • IL3RA • ITGAM • JAK2 • MCL1 • MYC • PIM1 • PLK1 • RUNX1 • SRSF2 • STAT5 • TET2 • TGFB1

Evaluation of the Lethal Activity and Its Mechanism of Tasquinimod in Advanced Myeloproliferative Neoplasm (MPN) in Blastic Phase (ASH 2024) - "Importantly, cotreatment with TQ (5 to 30 µM) and ruxolitinib (250 to 1000 nM), BET inhibitor OTX015 (50 to 250 nM) or pelabresib (CPI-0610) (100 to 500 nM), or BCL2/Bcl-xL inhibitor navitoclax, induced synergistic lethality in advanced MPN-BP cells, represented by delta synergy scores of >1.0 (by the ZIP method)...Co-treatment with TQ and RGFP966 (HDAC3i) induced synergistic lethality in post-MPN sAML cells...These findings demonstrate the pre-clinical efficacy of TQ and/or JAKi or BETi or with novel agents identified here in advanced MPN and MPN-AML cells. They also create the rationale to further interrogate the pre-clinical efficacy of the TQ-based combinations against cellular models of advanced MPN."

IO biomarker • Metastases • Fibrosis • Hematological Malignancies • Immunology • Leukemia • Myelofibrosis • Myeloproliferative Neoplasm • Oncology • BCL2 • BCL2L1 • CALR • CCL2 • CCND1 • CD123 • CD33 • CD34 • CD99 • CDK6 • CDKN1A • CLEC12A • CXCL12 • CXCL8 • CXCR4 • HDAC3 • IL1A • IL3RA • IL6 • ITGAM • JAK2 • MPO • MYC • NLRP3 • NSD2 • S100A8 • S100A9 • TERT • TLR4 • TNFA • TP53

DUAL BET/HAT INHIBITOR–BASED COMBINATIONS EXERT SYNERGISTIC LETHALITY AGAINST MYELOPROLIFERATIVE NEOPLASMS (MPN) TRANSFORMED TO AML (EHA 2026) - "Additionally, treatment with BETi (e.g., birabresib) reduced leukemia burden and induced clinical remissions...Results In present studies, we elucidated the gene-expression alterations and lethal activity of dual BET/HAT inhibitor EP31670 alone and in combination with other targeted agents to achieve superior preclinical efficacy in post-MPN sAML cells that are sensitive or resistant to JAKi or BETi...Notably, co-treatment with EP and ruxolitinib induced synergistic lethality in cultured and patient-derived (PD) post-MPN sAML...We also determined that co-treatment with EP and CDK7i SY-5609 (SY) was synergistically lethal in sAML cell lines including those resistant to JAKi or BETi, as well as PD MPN-sAML cells...Co-treatment with EP and SY resulted in significantly greater reduction in leukemia burden and further improved the overall survival of the mice than treatment with each agent alone (p < 0.05). Summary/Conclusion These findings demonstrate promising..."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myeloproliferative Neoplasm • BCL2 • BRD4 • CALR • CDK6 • CDKN1A • EP300 • HEXIM1 • JAK2 • MYC • PIM1

ASXL1 mutations in AML are associated with a distinct epigenetic state that results in vulnerabilities to epigenetic-targeted agents (AACR 2025) - "Notably, compared to parental cells, OCIAML3 ASXL1 Y591* cells exhibited reduced sensitivity to standard anti-AML, chemotherapeutic agents, including cytarabine, etoposide and daunorubicin. Our findings confirm the previously published discovery that the presence of mtASXL1 confers an increased sensitivity to BETi inhibitors, e.g., pelabresib or birabresib...Importantly, in the NSG mice engrafted with OCIAML3 ASXL1 Y591*, monotherapy with NEO2734, pelabresib or SEL120 significantly reduced AML burden. Collectively these findings highlight previously uncharacterized biologic effects of the presence of mtASXL1 and support the rationale for further evaluating AML therapies incorporating BETi, HAT-BETi or mediator-kinase inhibitor."

Acute Myelogenous Leukemia • Hematological Malignancies • Oncology • ASXL1 • AURKA • BAP1 • CDK9 • E2F1 • EP300 • FZD5 • HOXA9 • MEIS1 • MYC • PLK1 • SPI1 • TCF7L2

ASXL1 Mutations in AML Are Associated with a Distinct Epigenetic State Which Highlights Vulnerabilities to Specific Epigenetic-Targeted Agents (ASH 2024) - "Notably, compared to parental cells, OCIAML3 ASXL1 Y591* cells exhibited reduced sensitivity to standard anti-AML chemotherapeutic agents, including cytarabine, etoposide and daunorubicin...Our findings also demonstrate and confirm that mtASXL1-expressing AML cells exhibited increased sensitivity to BETi (pelabresib or birabresib)...Importantly, in the NSG mice engrafted with luciferized OCIAML3 ASXL1 Y591*, monotherapy with NEO2734 (5 mg/kg QD), pelabresib (30 mg/kg QD) or SEL120-34A (40 mg/kg QD), compared to vehicle control, significantly reduced AML burden. Collectively these findings highlight previously uncharacterized biologic effects of the presence of mtASXL1 and support the rationale for further evaluating AML therapies incorporating BETi, HAT-BETi or inhibitor of mediator kinase."

Acute Myelogenous Leukemia • Hematological Malignancies • Immunology • Oncology • Targeted Protein Degradation • ASXL1 • AURKA • BAP1 • BRD4 • CD14 • CDK9 • E2F1 • FZD5 • HOXA9 • MEIS1 • MYC • NDUFA2 • PLK1 • SPI1 • TCF7L2

ASXL1 Mutations in AML Are Associated With a Distinct Epigenetic State That Results in Vulnerabilities to Epigenetic-Targeted Agents (SOHO 2025) - " Notably, compared with parental cells, OCIAML3 ASXL1 Y591* cells exhibited reduced sensitivity to chemotherapeutic agents, including cytarabine, etoposide, and daunorubicin. In contrast, mtASXL1-expressing AML cells exhibited increased sensitivity to bromodomain and extraterminal inhibitors (BETi; pelabresib or birabresib)... These findings highlight that rationally targeted agents including NEO2734, pelabresib, and SEL120 or their combinations can potentially exert significant anti-AML efficacy against AML cells with mtASXL1."

Acute Myelogenous Leukemia • Hematological Malignancies • Oncology • ASXL1 • BAP1 • BCL9L • DVL1 • HOXA9 • MEIS1 • MYC • SPI1 • TCF7L2 • WNT5B • WNT7B

Novel combination therapies to overcome non-genetic/adaptive menin inhibitor resistance in AML with MLL1r or mtNPM1 (AACR 2024) - "In vivo treatment with FHD-286 and OTX015 or SNDX-5613 significantly reduced the AML burden in mice bearing OCI-AML3-MITR xenografts. These findings underscore preclinical activity of epigenetically-targeted agent-based combinations and highlight their promise in overcoming MI resistance in AML with MLL1r or mtNPM1."

Combination therapy • IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BCL2 • BRD4 • CDK6 • CLEC12A • CREBBP • EP300 • FLT3 • HOXA9 • IGF2BP2 • MEF2C • MEIS1 • NPM1 • PBX3 • SMARCA2 • SMARCA4

Identifying ’Druggable’ Targets and Preclinically Overcoming Non-Genetic/Adaptive Resistance to Menin Inhibitors in AML with MLL1r or mtNPM1 (ASH 2024) - "These MITR cells exhibited cross-resistance to other MIs, including ziftomenib and DS1594b...Notably, in a luciferized MLL1r MITR AML PDX model, compared to treatment with each agent alone, co-treatment with FHD-286 and SNDX-5613 or OTX015 for 8-weeks yielded significantly superior survival of the NSG mice (p < 0.05). These findings demonstrate that co-treatment with FHD-286 overcomes in vitro and in vivo MI-resistance, while significantly improving in vivo efficacy of BETi in the cell-line xenograft and PDX models of MITR AML cells. They also show that combinations of epigenetically targeted agents may be effective in MI-sensitive or -resistant AML with MLL1r or mtNPM1."

IO biomarker • Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BCL2 • BRD4 • CDK6 • CLEC12A • CREBBP • EP300 • FLT3 • HOXA9 • IGF2BP2 • MEF2C • MEIS1 • NPM1 • PBX3 • SMARCA4

Superior preclinical efficacy of BRG1/BRM inhibitor combined with BET inhibitor or decitabine against MECOM-rearranged AML (AACR 2025) - "Finally, as compared to treatment with each drug alone or vehicle control, in PD xenograft (PDX) models of AML cells with MECOM-r, co-treatment with FHD-286 and decitabine or OTX015 significantly reduced AML burden and improved overall survival of the NSG mice, without inducing significant toxicity. Taken together, these findings highlight the promise of FHD-286 treatment alone and in rational combinations in exerting significant anti-AML efficacy against cellular models of AML, especially those with MECOM-r and EVI1 overexpression."

Preclinical • Acute Myelogenous Leukemia • Oncology • CD93 • CDK4 • GATA2 • ITGAM • KIT • MECOM • MYC • PLK1 • SMARCA2 • SMARCA4

Preclinical efficacy of dual BET/HAT inhibitor–based combinations against post myeloproliferative neoplasm secondary AML cells (ASH 2025) - "Notably, treatment with BETi (e.g., OTX015) wasshown to reduce leukemia burden and improve survival in xenograft models of post-MPN sAML cells.However, BETi resistance and BETi-refractory disease develop uniformly...Compared to pan-BET inhibitor INCB057643,treatment with EP31670 induced significantly greater in vitro lethality in HEL92.1.7 and SET2 cells.Notably, in vitro treatment of cell lines and PD post-MPN sAML cells with EP31670 in combination withruxolitinib, for 72 to 96 hours induced synergistic lethality, as determined by SynergyFinder...Notably, co-treatment with EP31670 and SY-5609resulted in significantly greater reduction in leukemia burden and overall survival of the mice thantreatment with each agent alone (p < 0.05). These findings demonstrate promising preclinical activity ofEP31670 against cellular models of MPN-sAML and strongly support the rationale to further evaluate thein vivo efficacy of EP31670-based combinations against advanced MPN with..."

IO biomarker • Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Myeloproliferative Neoplasm • ASXL1 • BCL2 • BRD4 • CALR • CDK6 • CDKN1A • DNMT3A • EP300 • HEXIM1 • IL6 • JAK2 • MYC • PIM1 • RUNX1 • STAT5 • STAT5AWqe • TP53

BET inhibition unmasks a targetable glycolytic dependency through a HIF1α stabilization and driven transcriptional program in a defined subset of triple-negative breast Cancer. (PubMed, Cell Death Discov) - "Here, we investigated the responses to the BETi JQ1 and OTX015 across a heterogeneous panel of TNBC models...While the glycolysis inhibitor 2-deoxy-D-glucose (2-DG) is effective as a single agent in the glycolytic-prone setting, it has limited efficacy in other TNBC models...By mapping a transcriptional-metabolic axis that dictates BETi sensitivity, this study moves beyond the identification of a resistant subset of TNBC to reveal a deeper principle: targeted inhibition can actively reprogram cellular circuitry, thereby constructing its own unique therapeutic vulnerability. Thus, the path to overcoming resistance may lie not in evading this rewiring, but in strategically exploiting the alternative dependencies it creates."

Journal • Breast Cancer • Oncology • Solid Tumor • Triple Negative Breast Cancer • BRD4 • HIF1A • MYC

Combined inhibition of BETs and HDACs as a potential epigenetics-based therapy for malignant rhabdoid tumor. (PubMed, Cell Death Dis) - "Using a focused epigenetic compound screen across multiple MRT cell lines, we identified that the HDAC inhibitor panobinostat (LBH589) and the BET inhibitor birabresib (OTX015) act synergistically to inhibit cell proliferation, with combination index (CI) values consistently <1. In vivo, this dual-epigenetic targeting significantly attenuated tumor growth in MRT xenograft models, outperforming either monotherapy, and was associated with suppressed proliferation and E2F1 signaling. Our findings unveil a novel synergistic strategy that pharmacologically recapitulates a core SMARCB1-mediated tumor-suppressive circuit, nominating combined HDAC and BET inhibition as a promising therapeutic avenue for MRT."

Journal • Eye Cancer • Oncology • Pediatrics • Retinal Disorders • Rhabdoid Tumor • Sarcoma • Solid Tumor • CCNA2 • CCNB1 • CCND1 • CDK4 • E2F1 • SMARCB1

Repurposing Birabresib to target Gram‑positive bacteria. (PubMed, NPJ Antimicrob Resist) - "We identified Birabresib as a promising candidate using this approach. Here, we demonstrate that Birabresib effectively inhibits Gram-positive bacteria, exhibits synergy with the antibiotic rifampicin, and has limited cytotoxicity on the human cell line tested."

Journal • Infectious Disease • Targeted Protein Degradation

Strategic evolution of drug discovery modalities: Tanabe Pharma's approach to immunology and oncology (PubMed, Nihon Yakurigaku Zasshi) - "Leveraging insights from the BRD4 inhibitor Y-803, we has developed MT-4561, which demonstrates high degradation activity and antitumor efficacy and is currently in Phase I clinical trials. These efforts exemplify a modality-driven drug discovery approach tailored to disease-specific pathologies, aiming to provide new therapeutic options for intractable diseases through the integration of scientific knowledge and technological innovation."

Journal • Review • Oncology • Targeted Protein Degradation • BRD4 • IL2 • PSMB8

BET domain functions in IDH1R132H/p53mut/ATRXloss astrocytoma malignancy (AACR 2026) - "Consistently, the immunoblot analysis showed that BRD3 expression is induced by the triple-mut and further enhanced by ionizing radiation (IR) and temozolomide (TMZ) treatment. Functionally, inhibition of BET proteins using either pan-BET inhibitors (JQ1, OTX015) or bromodomain 1 (BD1)-selective inhibitor GSK778—but not bromodomain 2 (BD2)-selective inhibitor GSK620— markedly reduces triple-mut glioma cell growth and impairs neurosphere self-renewal, and enhances TMZ-induced cell death...These findings identify a BD1-dependent transcriptional network that regulates astrocytoma cell phenotype and contributes to an immunosuppressive microenvironment. Targeting BD1 represents a rational therapeutic strategy by simultaneously suppressing tumor cell-intrinsic oncogenic signaling (e.g.,YAP1/TAZ signaling) and reshaping the immunosuppressive microenvironment."

IO biomarker • P53mut • Astrocytoma • Brain Cancer • Glioblastoma • Glioma • Oncology • Solid Tumor • BRD2 • BRD3 • IDH1 • IFNG • TAFAZZIN • YAP1

A druggable genome screen identifies b-catenin transcription targets as desmoid cell vulnerabilities (AACR 2026) - "Inhibition of exportin-1 with selinexor or shRNA directed at XPO1 inhibited proliferation (by 51%, p<0.05), but failed to affect β-catenin subcellular localization as in other systems...Inhibition of MDM2 with milademetan or shRNA similarly increased p53 and p21 and reduced proliferation (by 60%, p<0.05)...BRD4 inhibition via shRNA or treatment with birabresib reduced proliferation (85%, p<0.01) but did not affect p53/p21 signaling... BRD4, MDM2 and XPO1 were identified as potential therapeutic targets in DT with gene products modulating p53/p21 or β-catenin activity. Both BRD4 and MDM2 represent direct transcriptional targets of β-catenin though negative regulation of MDM2 in the context of DT cell dependency on its protein product suggest secondary genetic events or environmental signaling may be necessary to counteract this potential tumor suppressive effect of β-catenin."

IO biomarker • Oncology • Sarcoma • Solid Tumor • BRD4 • CDKN1A • MDM2 • TERT • TGFBI • TP53 • XPO1

Sequential inhibition of PARP and BET as a rational therapeutic strategy for glioblastoma multiforme (AACR 2024) - "Through unbiased transcriptomic and proteomic sequencing, and employing Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA), and Transcriptome-Proteome Correlation Analysis, we discovered that the BET inhibitor (BETi) Birabresib profoundly alters the processes of DNA replication and cell cycle progression in GBM cells, extending beyond the previously known impact of BET inhibition on homologous recombination repair...Our findings provide a broader and deeper understanding of the synergistic interaction between BETi and PARPi than previously recognized. This study offers compelling preclinical evidence supporting the development of innovative drug administration strategies focusing on PARPi for GBM therapy."

Late-breaking abstract • Brain Cancer • CNS Tumor • Glioblastoma • Oncology • Solid Tumor • HRD

Hospital-Compounded Birabresib Capsules for NUT Carcinoma: A Quality- and Risk-Based CMC Strategy. (PubMed, Pharm Res) - "This risk-proportionate, CMC-oriented hospital framework enabled the first authorised therapeutic use of birabresib in NUT carcinoma and may be extended to other discontinued small molecules used in regulated access programmes for ultra-rare diseases."

Journal • Developmental Disorders • NUT Midline Carcinoma • Oncology • Rare Diseases

Early access program of birabresib in NUT carcinoma patients (Sarcoma-RC 2026) - P=N/A | "Legal entity responsible for the study The authors. Funding Has not received any funding."

Clinical • NUT Midline Carcinoma • Oncology • BRD4 • NUTM1 • STING

Single-cell transcriptomic signatures identify drug combinations to address platinum resistance in ovarian cancer (ESGO 2026) - "Among 64 predicted drugs, the NEDD8-activiating enzyme (NAE) inhibitor pevonedistat, the inhibitor of apoptosis (IAP) inhibitor LCL161 and the bromodomain (BRD2/3/4) inhibitor birabresib, exhibited a long-term inhibitory effect in two organoid models. Even though this combination treatment did not result in significant survival benefit, it reduced the tumour size, metastatic dissemination and staging of the disease. Conclusion We demonstrate that targeting transcriptional resistance signatures with selective inhibitors can partially reverse carboplatin resistance in clinically relevant organoid and PDX models, supporting their potential as combination strategies to improve therapeutic response."

Oncology • Ovarian Cancer • Solid Tumor • BRD2

Discovery of a potent thienodiazepine derivative as a novel BRD4 degrader. (PubMed, Bioorg Med Chem) - "We discovered bromodomain-containing protein 4 (BRD4) degraders as novel antitumor therapeutics leveraging our internal knowledge on Y-803 (birabresib, OTX015/MK-8628), which was discovered by our company as the first-in-class BRD4 inhibitor. Since we had obtained rich structure-activity relationship (SAR) information on its core skeleton, thienodiazepine, we designed and optimized Von Hippel-Lindau (VHL)-based BRD4 degraders based on the thienodiazepine scaffold. Here, we report that we obtained a novel, best-in-class BRD4 degrader, which showed a potent antitumor effect in a xenograft model of acute myeloid leukemia (AML)."

Journal • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • Targeted Protein Degradation • Von Hippel-Lindau Syndrome • BRD4

Overcoming Menin inhibitor resistance in AML cells with combinations including BET proteins and dual BRG1/BRM inhibitor. (PubMed, Blood) - "Compared to each drug alone, co-treatment with SNDX-5613 (revumenib) and FHD-286 or OTX015 and FHD-286 significantly reduced the in vivo AML burden and improved survival of the immune depleted mice, without inducing significant toxicity, in the xenograft models of MITR and MI-resistant PD MLL1-r AML cells. These findings highlight novel, targeted, drug combinations that overcome MI resistance in AML cells with MLL1-r or mtNPM1."

Journal • Acute Myelogenous Leukemia • BRD4 • CREBBP • HOXA9 • MEIS1 • NPM1 • SMARCA2 • SMARCA4