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TEST:
PredicineHEME™

Company:
Predicine
Type:
Laboratory Developed Test
Related tests:
Evidence

News

2ms
Predicine to present 15 liquid biopsy studies at AACR 2024 (Predicine Press Release)
"Predicine...announced today that it will present data from 15 ctDNA studies at AACR 2024, spotlighting the clinical utility of Predicine’s genomic and epigenomic liquid biopsy solutions for patient selection, disease monitoring, and disease mechanism studies."
Clinical data
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PredicineALERT™ • PredicineBEACON™ • PredicineCARE™ • PredicineCOMPLETE™ • PredicineHEME™
3ms
Extending and analytical validation of a hematological cancer panel for simultaneous detection of driver mutations, copy number variations and translocations in tissue and blood samples (AACR 2024)
Chromosome arm level CNVs reported in the validation materials were detected with 100% sensitivity and specificity.Conclusions The expansion of the PredicineHEME panel underwent analytical validation, meeting design expectations. With this extension, the assay can effectively detect driver mutations (SNVs/INDELs), CNVs at gene and chromosomal levels, and targeted large translocations in major hematological cancers.
PredicineHEME™
7ms
Genomic Landscape of Ibrutinib- and/or Acalabrutinib-intolerant Patients with B-cell Malignancies Treated with Zanubrutinib in a Phase 2 Study (ASH 2023)
This is the first study to describe the genomic landscape of patients with B-cell malignancies who were intolerant to ibrutinib and/or acalabrutinib. Here we show that the gene mutational profile of these patients at baseline or at/after disease progression is comparable with patients with relapse/refractory disease who tolerate ibrutinib and, consistent with other studies, patients with mutations in TP53, SF3B1 or ATM genes had less favorable prognosis on BTKi. Further, intolerant patients who progressed on zanubrutinib acquired new BTK mutations and/or had an increase in the frequency of BTK mutations.
P2 data • Clinical
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TP53 (Tumor protein P53) • ATM (ATM serine/threonine kinase) • NOTCH1 (Notch 1) • SF3B1 (Splicing Factor 3b Subunit 1)
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TP53 mutation • ATM mutation • SF3B1 mutation • SF3B1 K700E • BTK mutation • BTK C481
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PredicineHEME™
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Imbruvica (ibrutinib) • Brukinsa (zanubrutinib) • Calquence (acalabrutinib)
8ms
Acquired Mutations in Patients (Pts) with Relapsed/Refractory (R/R) Chronic Lymphocytic Leukemia (CLL) That Progressed in the ALPINE Study (ASH 2023)
To gain further insight into the genetic mechanisms of cBTKi resistance in a randomized population of pts with CLL, we performed next-generation sequencing (NGS) on samples from pts who had progression on zanubrutinib (zanu) or ibrutinib (ibr) in the phase 3 ALPINE study (NCT03734016; Brown et al. Of the 52 pts, most (82.6%) did not have acquired BTK or PLCG2 mutations. Among the zanu pts, 3/24 (12.5%) developed non-C481 BTK mutations. This rate was lower than that reported by Woyach et al (ICML 2023); shorter follow-up and fewer prior therapies in the ALPINE study may explain this discrepancy.
Clinical
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NOTCH1 (Notch 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • IGH (Immunoglobulin Heavy Locus) • KMT2D (Lysine Methyltransferase 2D) • BIRC3 (Baculoviral IAP repeat containing 3) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • PLCG2 (Phospholipase C Gamma 2) • CCND2 (Cyclin D2) • CDKN1B (Cyclin dependent kinase inhibitor 1B)
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Chr del(11q) • IGH mutation • PLCG2 mutation • BTK mutation • BTK C481 • Chr del(17p) + Chr del(11q) • TS 12
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PredicineHEME™
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Imbruvica (ibrutinib) • Brukinsa (zanubrutinib)
over1year
Genomic Characterization of Patients in a Phase 2 Study of Zanubrutinib in BTK Inhibitor–Intolerant Patients with Relapsed/Refractory B-Cell Malignancies (ASH 2022)
However, some patients (pts) have experienced toxicities to BTK inhibitors ibrutinib (ibr) and acalabrutinib (acala), which lead to dose reduction or treatment discontinuation. Exploratory analysis results confirmed that cell cycle, DNA damage, and NOTCH1 pathway genes were frequently mutated in pts with B-cell malignancies on study BGB-3111-215 (pts intolerant to ibr and/or acala). Pts with mutations associated with poor prognosis at baseline were more likely to develop PD.
P2 data • Clinical
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • RB1 (RB Transcriptional Corepressor 1) • NOTCH1 (Notch 1) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • SF3B1 (Splicing Factor 3b Subunit 1) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • CHEK2 (Checkpoint kinase 2) • BIRC3 (Baculoviral IAP repeat containing 3) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • PLCG2 (Phospholipase C Gamma 2) • CCND2 (Cyclin D2)
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TP53 mutation • ATM mutation • NOTCH1 mutation • MYD88 mutation • SF3B1 mutation • MYD88 L265P • ATM deletion • RB1 deletion • CHEK2 mutation • CXCR4 mutation • FBXW7 mutation • PLCG2 mutation • KRAS deletion • MYD88 wild-type
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PredicineHEME™
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Imbruvica (ibrutinib) • Brukinsa (zanubrutinib) • Calquence (acalabrutinib)