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    GENE:

    AFDN (Afadin, Adherens Junction Formation Factor)

    i
    Other names: AFDN, Afadin, Adherens Junction Formation Factor, AF6, MLLT4, Myeloid/Lymphoid Or Mixed-Lineage Leukemia; Translocated To, 4, ALL1-Fused Gene From Chromosome 6 Protein, Protein AF-6, Afadin, AF-6, Myeloid/Lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila); Translocated To, 4, Afadin Adherens Junction Formation Factor, L-Afadin, MLL-AF6
    Associations

    News

    Trials
    2ms
    Assessing t(6;11)(q27;q23) and Tetrasomy 21 in Down Syndrome Patient: Cytogenetic Implications in Acute Myeloid Leukemia Pathogenesis. (PubMed, J Assoc Genet Technol)
    Conventional cytogenetic analysis revealed the presence of an additional chromosome 21 and a translocation between chromosomes 6 and 11, which were further confirmed by FISH. This case highlights the significance of cytogenetic techniques in identifying complex chromosomal disorders and provides insights into the clinical implications of such abnormalities.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • AFDN (Afadin, Adherens Junction Formation Factor)
    3ms
    Deciphering the oncogenic role of key genes in HNSC: insights from multi-omics and functional studies. (PubMed, Discov Oncol)
    In conclusion, MAPK3, MLLT4, PLAU, and SERPINE1 emerge as promising biomarkers and therapeutic targets for HNSC.
    Journal
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    SERPINE1 (Serpin Family E Member 1) • AFDN (Afadin, Adherens Junction Formation Factor) • MAPK3 (Mitogen-Activated Protein Kinase 3) • PLAU (Plasminogen Activator)
    3ms
    Gene Expression Profiling Provides an Improved Characterization of CD79B-Mutated Diffuse Large B-Cell Lymphomas. (PubMed, J Pers Med)
    TP53 mutation showed an association with poorer overall survival in a secondary analysis, consistent with prior reports, while survival by CD79B/MYD88 mutation status and the differentially expressed genes showed no significant differences in this cohort. In conclusion, the current study identified novel up-regulated genes in CD79B-mutated DLBCLs beyond NF-κB pathway signaling, which may contribute to a better definition of potential therapeutic targets and further improves the characterization of this distinct and aggressive DLBCL subgroup.
    Journal
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    TP53 (Tumor protein P53) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • RUNX1 (RUNX Family Transcription Factor 1) • CD79B (CD79b Molecule) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CARD11 (Caspase Recruitment Domain Family Member 11) • IL10 (Interleukin 10) • CD14 (CD14 Molecule) • PIM1 (Pim-1 Proto-Oncogene) • BCL2A1 (BCL2 Related Protein A1) • GZMB (Granzyme B) • IL7 (Interleukin 7) • RASGRF1 (Ras Protein Specific Guanine Nucleotide Releasing Factor 1) • AFDN (Afadin, Adherens Junction Formation Factor) • HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1) • WNT11 (Wnt Family Member 11)
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    TP53 mutation
    4ms
    Age-specific mutation profiles and their prognostic implications in pediatric KMT2A-rearranged acute myeloid leukemia. (PubMed, Haematologica)
    Multivariate analysis identified older age, a high white blood cell count, KMT2A::MLLT4, and KRAS mutations as independent adverse prognostic factors for both EFS and OS. These age-specific mutation profiles suggest distinct disease mechanisms across age groups and may help refine risk stratification and treatment strategies for pediatric KMT2A-r AML.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • KMT2A (Lysine Methyltransferase 2A) • AFDN (Afadin, Adherens Junction Formation Factor)
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    KRAS mutation • KMT2A mutation • MLL mutation
    5ms
    Upfront Menin-inhibitor resistance in multiply pretreated leukemias. (PubMed, Exp Hematol)
    Future studies will need to clarify more broadly which genomic/epigenomic alterations drive upfront resistance. Regardless of mechanism, our data supports using Menin-inhibitors upfront or in early lines of therapy before substantial genomic or epigenomic evolution has occurred.
    Journal
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    TP53 (Tumor protein P53) • KMT2A (Lysine Methyltransferase 2A) • KMT2C (Lysine Methyltransferase 2C) • AFF1 (AF4/FMR2 Family Member 1) • AFDN (Afadin, Adherens Junction Formation Factor) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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    TP53 mutation
    6ms
    Haploidentical Hematopoietic Stem Cell Transplantation With Ex Vivo TCR Alpha/Beta and CD19 Depletion in Pediatric Hematologic Malignancies (clinicaltrials.gov)
    P1, N=50, Recruiting, Washington University School of Medicine | N=32 --> 50 | Trial completion date: Nov 2027 --> May 2029 | Trial primary completion date: Nov 2027 --> May 2029
    Enrollment change • Trial completion date • Trial primary completion date
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • CD38 (CD38 Molecule) • CREBBP (CREB binding protein) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • AFF1 (AF4/FMR2 Family Member 1) • HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • HLA-DQB1 (Major Histocompatibility Complex, Class II, DQ Beta 1) • MECOM (MDS1 And EVI1 Complex Locus) • NCAM1 (Neural cell adhesion molecule 1) • NUP214 (Nucleoporin 214) • TCF3 (Transcription Factor 3) • FUS (FUS RNA Binding Protein) • HLA-B (Major Histocompatibility Complex, Class I, B) • KAT6A (Lysine Acetyltransferase 6A) • DEK (DEK Proto-Oncogene) • AFDN (Afadin, Adherens Junction Formation Factor) • EGR1 (Early Growth Response 1) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
    8ms
    KRAS mutation status critically determines the clinical outcome of patients with KMT2A-rearranged acute myeloid leukemia. (PubMed, Cancer)
    These results demonstrate the independent prognostic value of KRAS mutations across treatment modalities, including both conventional chemotherapy and hematopoietic stem cell transplantation.
    Clinical data • Journal
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    KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KMT2A (Lysine Methyltransferase 2A) • AFDN (Afadin, Adherens Junction Formation Factor)
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    KRAS mutation • NRAS mutation • KRAS wild-type • RAS wild-type
    9ms
    Screening of MLL fusion genes and rare breakpoint cases in patients with acute myeloid leukemia (PubMed, Zhonghua Xue Ye Xue Za Zhi)
    After two cycles, eight patients achieved CR, with 50% of them experiencing recurrence within 2 months. RNA seq technology is useful for screening fusion genes with unconventional or novel cleavage sites, and patients with positive MLL fusion genes demonstrated a poorer prognosis.
    Journal
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    AFDN (Afadin, Adherens Junction Formation Factor)
    9ms
    Magrolimab Therapy in Conjunction with Conventional Chemotherapeutics Slows Disease Progression in Pediatric Acute Myeloid Leukemia Patient-Derived Xenograft Models. (PubMed, Cancers (Basel))
    To evaluate its preclinical efficacy in vivo, Magro was tested as a single agent and in combination with conventional chemotherapy drugs, Cytarabine (Ara-C) or Azacitidine (Aza), in three pediatric AML (pAML) patient-derived xenograft (PDX) models-AML006 (KMT2A::MLLT1), AML010 (+10, WT1), and AML013 (KMT2A::MLLT4). Interestingly, the two models that demonstrated improvement in survival with Magro harbored KMT2A rearrangements, suggesting a subset of patients that may be more responsive to the effects of CD47 blockade. As this drug is being evaluated for use in other malignancies, future studies may focus on investigating the importance of biomarker-based patient selection.
    Preclinical • Journal
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    KMT2A (Lysine Methyltransferase 2A) • WT1 (WT1 Transcription Factor) • AFDN (Afadin, Adherens Junction Formation Factor) • SIRPA (Signal Regulatory Protein Alpha)
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    KMT2A rearrangement
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    cytarabine • azacitidine • magrolimab (ONO-7913)
    11ms
    Cryptic KMT2A::AFDN Fusion Due to AFDN Insertion into KMT2A in a Patient with Acute Monoblastic Leukemia. (PubMed, Genes (Basel))
    This case highlights the importance of integrating multiple testing modalities with expert review when there is a discrepancy. Our findings emphasize the need for a comprehensive approach to genomic assessment to enhance diagnostic accuracy and guide therapeutic decision-making.
    Journal
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    KMT2A (Lysine Methyltransferase 2A) • AFDN (Afadin, Adherens Junction Formation Factor)
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    KMT2A rearrangement
    12ms
    Afadin loss induces breast cancer metastasis through destabilisation of E-cadherin to F-actin linkage. (PubMed, J Pathol)
    © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland
    Journal
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    CDH1 (Cadherin 1) • AFDN (Afadin, Adherens Junction Formation Factor)