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    GENE:

    H1-4 (H1.4 Linker Histone, Cluster Member)

    i
    Other names: H1-4, H1.4 Linker Histone, Cluster Member, HIST1H1E, H1s-4, H1.4, H1F4, Histone Cluster 1 H1 Family Member E, H1 Histone Family, Member 4, Histone Cluster 1, H1e, Histone 1, H1e, Histone H1s-4, Histone H1.4, Histone H1b, H1e, DJ221C16.5, RMNS, H1E
    2ms
    Study of Epcoritamab as a Consolidation Therapy in CLL/SLL (clinicaltrials.gov)
    P2, N=22, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting
    Enrollment open
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    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • SF3B1 (Splicing Factor 3b Subunit 1) • CD79B (CD79b Molecule) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • BIRC3 (Baculoviral IAP repeat containing 3) • CD5 (CD5 Molecule) • POT1 (Protection of telomeres 1) • H1-4 (H1.4 Linker Histone, Cluster Member) • NFKBIE (NFKB Inhibitor Epsilon) • ZMYM3 (Zinc Finger MYM-Type Containing 3) • CHD2 (Chromodomain Helicase DNA Binding Protein 2) • FCER2 (Fc Fragment Of IgE Receptor II)
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    Chr del(11q)
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    clonoSEQ
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    Gazyva (obinutuzumab) • Epkinly (epcoritamab-bysp)
    2ms
    ESR-23-22182: Intermittent Versus Continuous Venetoclax With Acalabrutinib for CLL/SLL (clinicaltrials.gov)
    P2, N=62, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting | Initiation date: Jun 2025 --> Dec 2025
    Enrollment open • Trial initiation date
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    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • SF3B1 (Splicing Factor 3b Subunit 1) • CD79B (CD79b Molecule) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • BIRC3 (Baculoviral IAP repeat containing 3) • CD5 (CD5 Molecule) • POT1 (Protection of telomeres 1) • H1-4 (H1.4 Linker Histone, Cluster Member) • NFKBIE (NFKB Inhibitor Epsilon) • ZMYM3 (Zinc Finger MYM-Type Containing 3) • CHD2 (Chromodomain Helicase DNA Binding Protein 2) • FCER2 (Fc Fragment Of IgE Receptor II)
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    Chr del(11q)
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    clonoSEQ
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    Venclexta (venetoclax) • Calquence (acalabrutinib)
    10ms
    Superior survival in diffuse large B cell lymphoma of the bone with immune rich tumor microenvironment. (PubMed, Blood Cancer J)
    Conclusively, PB-DLBCL and polyostotic-DLBCL share immune-molecular TME characteristics, supporting their classification as a unified bone-DLBCL entity. The distinct immune-rich TME profile of bone-DLBCL associated with superior survival potentially shapes emerging immunomodulatory strategies.
    Journal
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    FOXP3 (Forkhead Box P3) • H1-4 (H1.4 Linker Histone, Cluster Member)
    10ms
    Coupling deep phenotypic quantification with next-generation phenotyping for 192 individuals with germline histonopathies. (PubMed, HGG Adv)
    Notably, the community-wide cancer incidence is currently 1%, which falls below the recommended 5% cut off for routine surveillance. Ultimately, this works highlights the ways in which histonopathy-associated phenotypes change throughout the lifespan, necessitating longitudinal re-evaluation; that every identified individual shapes our understanding of these syndromes in a way that improves care for this community; and the value of ongoing translational work to address the outstanding question of cancer predisposition for individuals living with germline histonopathies.
    Journal
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    H1-4 (H1.4 Linker Histone, Cluster Member) • H3C1 (H3 Clustered Histone 1)
    1year
    Identification of IFI27 involvement in the progression of neuroblastoma through bioinformatics analysis and experimental assays. (PubMed, J Mol Histol)
    Conversely, in SK-N-AS cells, IFI27 overexpression inhibited cell proliferation, migration, and invasion. IFI27 was lowly expressed in NB and participated in the progression of NB, which provides a new insight into the pathogenic mechanism and novel therapeutic strategy for NB.
    Journal
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    H1-4 (H1.4 Linker Histone, Cluster Member) • IFI27 (Interferon Alpha Inducible Protein 27) • TNFSF10 (TNF Superfamily Member 10) • DDX58 (DExD/H-Box Helicase 58)
    over1year
    Efficacy and safety analysis of the OR-CHOP regimen for the treatment of MCD subtype diffuse large B cell lymphoma in the real-world setting (PubMed, Zhonghua Xue Ye Xue Za Zhi)
    Objective: To investigate the efficacy and safety of orelabrutinib combined with R-CHOP in the treatment of MCD subtype diffuse large B cell lymphoma (DLBCL)...All patients were treated with R-CHOP or R-miniCHOP in Course 1, OR-CHOP or OR-miniCHOP (21 days for one course) in Courses 2-6, and R-monotherapy in Courses 7-8...Furthermore, the OR-CHOP regimen was generally well tolerated during clinical use, with hematological toxicity being the main adverse effect. This study revealed that the OR-CHOP regimen can be used as an effective and safe first-line treatment for MCD subtype DLBCL.
    Retrospective data • Journal • Real-world evidence • Real-world
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    MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • ETV6 (ETS Variant Transcription Factor 6) • KMT2D (Lysine Methyltransferase 2D) • CD79B (CD79b Molecule) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • PIM1 (Pim-1 Proto-Oncogene) • CD58 (CD58 Molecule) • H1-4 (H1.4 Linker Histone, Cluster Member) • BTG2 (BTG Anti-Proliferation Factor 2)
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    Rituxan (rituximab) • vincristine • Inokai (orelabrutinib)
    over1year
    Somatic mutation phasing and haplotype extension using linked-reads in multiple myeloma. (PubMed, bioRxiv)
    For example, our analysis of one patient suggested that two NRAS hotspot mutations occurred on the same haplotype but were independent events in different subclones. Given sufficient tumor purity and data quality, our framework illustrates how haplotype-aware analysis of somatic mutations in cancer can be beneficial for some cancer cases.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • NRAS (Neuroblastoma RAS viral oncogene homolog) • H1-4 (H1.4 Linker Histone, Cluster Member)
    almost2years
    Generation and external validation of a histological transformation risk model for patients with follicular lymphoma. (PubMed, Mod Pathol)
    In conclusion, we propose a clinicogenetic risk model to predict FL HT to DLBLC, combining genetic alterations in HIST1H1E, KMT2D, and TNFRSF14 genes and clinical features (FLIPI) at diagnosis. This model could improve the management of FL patients and allow treatment strategies that would prevent or delay transformation.
    Journal
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    KMT2D (Lysine Methyltransferase 2D) • TNFRSF14 (TNF Receptor Superfamily Member 14) • H1-4 (H1.4 Linker Histone, Cluster Member)
    almost2years
    Mutation landscape in Chinese nodal diffuse large B-cell lymphoma by targeted next generation sequencing and their relationship with clinicopathological characteristics. (PubMed, BMC Med Genomics)
    This study presents the mutation landscape in Chinese nodal DLBCL, highlights the genetic heterogeneity of DLBCL and shows the role of panel-based NGS to prediction of prognosis and potential molecular targeted therapy in DLBCL. More precise genetic classification needs further investigations.
    Journal • Next-generation sequencing • IO biomarker
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    TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • KMT2D (Lysine Methyltransferase 2D) • CD79B (CD79b Molecule) • KMT2C (Lysine Methyltransferase 2C) • PIM1 (Pim-1 Proto-Oncogene) • SOCS1 (Suppressor Of Cytokine Signaling 1) • H1-4 (H1.4 Linker Histone, Cluster Member) • DDX3X (DEAD-Box Helicase 3 X-Linked)
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    TP53 mutation • MYD88 L265P
    almost2years
    Mutational, immune microenvironment, and clinicopathological profiles of diffuse large B-cell lymphoma and follicular lymphoma with BCL6 rearrangement. (PubMed, Virchows Arch)
    In conclusion, both BCL6-R-positive FL and BCL6-R-positive DLBCL had a common mutational profile; but also, differences. DLBCL cases had a higher density of microenvironment markers.
    Journal • PD(L)-1 Biomarker • IO biomarker
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    PD-L1 (Programmed death ligand 1) • BCL2 (B-cell CLL/lymphoma 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NOTCH1 (Notch 1) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • BCL6 (B-cell CLL/lymphoma 6) • KMT2D (Lysine Methyltransferase 2D) • NOTCH2 (Notch 2) • CREBBP (CREB binding protein) • CD163 (CD163 Molecule) • ARID1B (AT-Rich Interaction Domain 1B) • CD36 (thrombospondin receptor) • IL10 (Interleukin 10) • RHOA (Ras homolog family member A) • PIM1 (Pim-1 Proto-Oncogene) • CSF1R (Colony stimulating factor 1 receptor) • HLA-B (Major Histocompatibility Complex, Class I, B) • H1-4 (H1.4 Linker Histone, Cluster Member) • PLOD2 (procollagen-lysine,2-oxoglutarate 5-dioxygenase 2) • BTG2 (BTG Anti-Proliferation Factor 2) • LAIR1 (Leukocyte Associated Immunoglobulin Like Receptor 1)
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    ATM mutation • MYD88 L265P • BCL6 rearrangement • ARID1B mutation • IL10-L • PIM1 mutation • MYC negative
    2years
    Assessment of the Expression of Genes Related to Epigenetic and Chromatin Modifications in Diffuse Large B-Cell Lymphoma Patients Resistant to R-CHOP (ASH 2023)
    The mainstay of frontline therapy remains R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) or R-CHOP-like immunochemotherapy. Differences in gene expression may lead to chemoresistance, and higher expression levels are associated with a worse prognosis. This study sheds light on the importance of chromatin and epigenetic modifications in DLBCL progression, guiding the development of future therapies.
    Clinical
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    SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • KMT2C (Lysine Methyltransferase 2C) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • ARID1B (AT-Rich Interaction Domain 1B) • EP300 (E1A binding protein p300) • NCOR1 (Nuclear Receptor Corepressor 1) • CHD8 (Chromodomain Helicase DNA Binding Protein 8) • H1-4 (H1.4 Linker Histone, Cluster Member)
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    Rituxan (rituximab) • doxorubicin hydrochloride • cyclophosphamide • vincristine • prednisone