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    BIOMARKER:

    Chr del(10)

    9ms
    Acute Lymphoblastic Leukemia With Near-haploid Karyotype and Philadelphia Chromosome. (PubMed, Anticancer Res)
    The coexistence of the BCR::ABL1 chimera and near-haploidy in the same cytogenetic clone suggested a possible synergistic role in leukemogenesis, with the former activating signaling pathways and the latter disrupting gene dosage balance.
    Journal
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    ABL1 (ABL proto-oncogene 1)
    |
    Chr del(10)
    over2years
    Risk assessment with low pass whole genome sequencing of cell free DNA before CD19 CAR T-cells for large B-cell lymphoma. (PubMed, Blood)
    By combining FCS with traditional markers of increased tumor bulk (elevated LDH and >1 extranodal sites), we built a simple risk model that could reliably risk stratify patients. Thus, lpWGS of cfDNA is a minimally invasive assay that could rapidly identify high-risk patients and may guide patient selection for and targeted therapies to evaluate in future clinical trials.
    Journal • CAR T-Cell Therapy
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    CD19 (CD19 Molecule)
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    LDH elevation • Chr del(10)
    almost3years
    A COMPLETELY GENETIC PROGNOSTIC MODEL OVERCOMES CLINICAL PROGNOSTICATORS IN MANTLE CELL LYMPHOMA: RESULTS FROM THE MCL0208 TRIAL FROM THE FONDAZIONE ITALIANA LINFOMI (FIL) (SIE 2021)
    351 CNVs were identified in at least one patient. Besides TP53 deletion 10 further CNVs showed predictive by univariate analysis and were selected for multivariate Cox modelling. Actually, 4 CNVs maintained independent association with PFS: Loss@chr22 in 10/165 (6%) patients with a HR of 4.14 (p=0.028), LOH@chr17 in 5 (3%) with a HR of 4.79 (p=0.010), HDEL@chr9 in 3 (2%) with a HR of 18.1 (p=0.001) and CDKN2A loss in 30 (18%) with a HR of 2.6 (p=0.002).
    Clinical
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    TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CD19 (CD19 Molecule) • KMT2D (Lysine Methyltransferase 2D)
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    TP53 mutation • TP53 deletion • KMT2D mutation • Chr del(10)
    3years
    Malignant Glioma Subset from Actuate 1801 Phase 1/2 Study of 9-ING-41, a Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitor, as a Single Agent and Combined with Chemotherapy Refractory (SNO 2021)
    All received initial radiation and temozolomide (18/18), prior salvage therapies included nitrosoureas (15/18), bevacizumab (8/18), TTFields (6/18), checkpoint inhibitor (4/18). Median PFS and OS were 1.9 (0.3-11.1) and 6.0 (1.6-16.6) months, respectively. CONCLUSIONS 9-ING-41 plus/minus lomustine is safe and warrants further study in glioma patients.
    P1/2 data • PD(L)-1 Biomarker • IO biomarker
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    EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • PTEN (Phosphatase and tensin homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • RB1 (RB Transcriptional Corepressor 1) • NF1 (Neurofibromin 1) • MGMT (6-O-methylguanine-DNA methyltransferase) • TERT (Telomerase Reverse Transcriptase) • PALB2 (Partner and localizer of BRCA2) • LAG3 (Lymphocyte Activating 3) • ATRX (ATRX Chromatin Remodeler)
    |
    TP53 mutation • EGFR mutation • EGFR amplification • PALB2 mutation • NF1 mutation • CDKN2A deletion • CDKN2A mutation • RB1 deletion • TERT mutation • Chr del(10) • NF1 rearrangement
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    Avastin (bevacizumab) • temozolomide • lomustine • elraglusib (9-ING-41)