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    BIOMARKER:

    KIT translocation

    i
    Other names: KIT, C-Kit, CD117, PBT, SCFR, Stem Cell Factor Receptor, V-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog
    Entrez ID:
    3815
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    9ms
    A Dose Escalation and Cohort Expansion Study of KB-0742 in Participants With Relapsed or Refractory Solid Tumors or Non-Hodgkin Lymphoma (clinicaltrials.gov)
    P1/2, N=280, Recruiting, Kronos Bio | N=170 --> 280
    Enrollment change
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    MYC translocation • KIT translocation
    |
    istisociclib (KB-0742)
    1year
    Evaluation of Potential Role of R-Loop and G-quadruplex DNA in the Fragility of c-MYC during Chromosomal Translocation Associated with Burkitt's Lymphoma. (PubMed, J Biol Chem)
    The formation of R-loop and G-quadruplex was found to be mutually exclusive. Therefore, our results suggest that AID can bind to the single-stranded region of the R-loop and G4 DNA, leading to the deamination of cytosines to uracil and induction of DNA breaks in one of the DNA strands, leading to double-strand break, which could culminate in t(8;14) chromosomal translocation.
    Journal
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    KIT translocation
    over1year
    A Dose Escalation and Cohort Expansion Study of KB-0742 in Participants With Relapsed or Refractory Solid Tumors or Non-Hodgkin Lymphoma (clinicaltrials.gov)
    P1/2, N=170, Recruiting, Kronos Bio | Phase classification: P1 --> P1/2 | N=120 --> 170 | Trial completion date: Mar 2024 --> Dec 2025 | Trial primary completion date: Nov 2023 --> Dec 2025
    Phase classification • Enrollment change • Trial completion date • Trial primary completion date
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    MYC translocation • KIT translocation
    |
    istisociclib (KB-0742)
    over2years
    Enhancer RNA AL928768.3 from the IGH Locus Regulates MYC Expression and Controls the Proliferation and Chemoresistance of Burkitt Lymphoma Cells with IGH/MYC Translocation. (PubMed, Int J Mol Sci)
    Significant effects were observed only in cell lines bearing IGH/MYC abnormality but not in B-cell lines without this translocation nor primary B-cells. Our results indicate that AL928768.3 plays an important role in the development of Burkitt's lymphoma and suggest it and similar, yet undiscovered eRNAs as potential tissue-specific targets for cancer treatment.
    Journal
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    MYC expression • MYC translocation • KIT translocation
    4years
    A Diagnostic Approach to the Identification of Burkitt-like Lymphoma With 11q Aberration in Aggressive B-Cell Lymphomas. (PubMed, Am J Surg Pathol)
    In 2 DLBCL-BL, a dual MYC translocation/11q aberration pattern was detected. As a diagnostic algorithm, we, therefore, propose analysis of 11q status in MYC-negative high-grade lymphomas with features of BL, especially showing BCL2 negativity and a conspicuous coarse apoptotic debris in starry sky macrophages.
    Journal
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • BCL2 (B-cell CLL/lymphoma 2)
    |
    KIT translocation
    4years
    Development and Survival of MYC-driven Lymphomas Requires MYC-Antagonist MNT to Curb MYC-induced Apoptosis. (PubMed, Blood)
    Strikingly, by inducing Mnt deletion within transplanted fully-malignant Em-Myc lymphoma cells, we significantly extended transplant recipient survival. The dependency of lymphomas on MNT for survival suggests that drugs inhibiting MNT could significantly boost therapy of MYC-driven tumors by enhancing intrinsic MYC-driven apoptosis.
    Journal
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog)
    |
    MYC overexpression • KIT translocation
    4years
    Physiological levels of the PTEN-PI3K-AKT axis activity are required for maintenance of Burkitt lymphoma. (PubMed, Leukemia)
    In contrast to GCB-DLBCL, PTEN overexpression was tolerated by BL cell lines. We conclude that the molecular mechanisms instrumental to guarantee the survival of normal DZ B cells, including the tight regulation of the PTEN-PI3K-AKT axis, also operate in the survival/proliferation of BL.
    Clinical • Journal
    |
    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CXCR4 (Chemokine (C-X-C motif) receptor 4)
    |
    KIT translocation