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    TEST:
    MI Tumor Seek™

    Company:
    Caris Life Sci
    Type:
    Laboratory Developed Test
    Related tests:
    Details
    Evidence

    News

    4ms
    Optimizing immunotherapy in mismatch repair-deficient colorectal cancer through tailored, subtype-specific treatment approaches (ESMO 2025)
    "The CheckMate 8HW trial reported longer progression-free survival with Ipilimumab/Nivolumab (Ipi/Nivo) compared to Nivo monotherapy, but it remains unclear if all dMMR CRC patients should be offered ipi/nivo. Here, we investigated the survival benefit of Ipi/Nivo compared to Pembrolizumab (pembro) according to MutS vs. MutL co-loss...Assessment of mutS vs. mutL status provides a novel stratification that can further refine treatment algorithms for selection of specific ICI regimens in this patient population. Legal entity responsible for the study The authors."
    BRAF (B-raf proto-oncogene) • STK11 (Serine/threonine kinase 11) • MLH1 (MutL homolog 1) • MSH6 (MutS homolog 6) • MSH2 (MutS Homolog 2) • PMS2 (PMS1 protein homolog 2)
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    MI Tumor Seek™
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    Keytruda (pembrolizumab) • Opdivo (nivolumab) • Yervoy (ipilimumab)
    6ms
    Targeting anti-apoptosis as a therapeutic strategy in neuroendocrine neoplasms. (PubMed, Endocr Relat Cancer)
    We report the first known case of a pancreatic NET with response to venetoclax. BCL2 expression correlated with high MKI67 expression, worse survival, and a highly immune-enriched microenvironment.
    Journal • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • RB1 (RB Transcriptional Corepressor 1) • MKI67 (Marker of proliferation Ki-67)
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    RB1 mutation
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    MI Tumor Seek™
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    Venclexta (venetoclax)
    7ms
    Multiomic Characterization of RCC1 and RCC2 Expression and Their Association With Molecular Alterations, Immune Phenotypes, and Cancer Outcomes. (PubMed, JCO Oncol Adv)
    RCC1 and RCC2 expression is a negative prognostic marker in NSCLC, PC, and CRC. Further studies to investigate RCC1 and RCC2 function at the molecular level may provide opportunities for novel targeted drug development.
    Journal • Tumor mutational burden
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    TMB (Tumor Mutational Burden)
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    TMB-H
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    MI Tumor Seek™
    10ms
    Comprehensive molecular profiling of squamous non-small cell lung cancer reveals high incidence of actionable genomic alterations among patients with no history of smoking. (PubMed, Lung Cancer)
    A high frequency of AGAs were detected in never-smokers with sqNSCLC, with significantly increased prevalence of actionable EGFR and MET alterations compared to ever-smokers. Our findings indicate that, analogous to the diagnostic algorithm for non-squamous NSCLC, NGS testing to inform frontline treatment decision-making is critical for never-smokers with sqNSCLC.
    Journal • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
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    EGFR (Epidermal growth factor receptor) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • IFNG (Interferon, gamma) • IL6 (Interleukin 6)
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    EGFR mutation
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    MI Tumor Seek™
    10ms
    Human Epidermal Growth Factor Receptor 2 Alterations and Prognostic Implications in All Subtypes of Breast Cancers. (PubMed, JCO Precis Oncol)
    ERBB2-mut and fusions were observed in all breast cancer subtypes-more commonly in HER2+/low, metastatic, and lobular histology tumors-and associated with poorer prognosis.
    Retrospective data • Journal
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    HER-2 (Human epidermal growth factor receptor 2) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • CDH1 (Cadherin 1)
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    HER-2 positive • HER-2 amplification • HER-2 mutation
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    MI Tumor Seek™
    12ms
    Genomic Landscape of Malignant Phyllodes Tumors Identifies Subsets for Targeted Therapy. (PubMed)
    Considering the occurrence of several actionable alterations including a TPM4:NTRK1 fusion reported herein, these results support the use of next-generation sequencing (NGS) including RNA analysis for fusion detection to identify such alterations in patients with MPTs. These findings highlight the importance of comprehensive NGS in MPT research to uncover potential targeted treatment options for these patients.
    Journal • PD(L)-1 Biomarker • IO biomarker
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    MI Tumor Seek™
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    Vitrakvi (larotrectinib)
    1year
    Evidence for Unified Assessment Criteria of HER2 IHC in Colorectal Carcinoma. (PubMed, Mod Pathol)
    Among 22 HER2-positive/heterogenous cases with successful ISH testing, 100% (22/22) demonstrated amplification via ISH. Because the classification of tumors as HER2-positive/heterogenous by IHC correlated very closely with ISH positivity, our results suggest that ISH is likely unnecessary for CRCs with 3+ HER2 overexpression in 10-49% of neoplastic cells.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2)
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    HER-2 positive • HER-2 overexpression • RAS wild-type • HER-2 positive + HER-2 overexpression • HER-2 positive + RAS wild-type
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    PATHWAY antiHer2/neu (4B5) Rabbit Monoclonal Primary Antibody • MI Tumor Seek™
    1year
    Detection of Novel Fusion Events in Gastric Carcinoma Involving the ARHGAP Gene Family (AMP 2024)
    Our study documents novel fusions in MSS gastric carcinoma involving the ARHGAP family. Patients with these tumors usually lack eligibility for targeted therapies, such as those directed against HER2 and involving immune checkpoint inhibition, and could ultimately benefit from new treatment avenues modulating RHOA activity as a result of ARHGAP fusions.
    Tumor mutational burden • IO biomarker
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    HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ARID1A (AT-rich interaction domain 1A) • CLDN18 (Claudin 18) • PBRM1 (Polybromo 1) • KMT2D (Lysine Methyltransferase 2D) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • KDM6A (Lysine Demethylase 6A) • RHOA (Ras homolog family member A) • SOX9 (SRY-Box Transcription Factor 9) • ELF3 (E74 Like ETS Transcription Factor 3) • ARHGAP • CDKN1B (Cyclin dependent kinase inhibitor 1B) • CTNND1 (Catenin Delta 1) • ARHGAP42 (Rho GTPase Activating Protein 42)
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    TMB-H • HER-2 amplification • PBRM1 mutation
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    MI Tumor Seek™
    1year
    COMPREHENSIVE EVALUATION OF DNA DAMAGE RESPONSE PATHWAY ALTERATIONS AND ASSOCIATED IMMUNOTHERAPY-RESPONSE BIOMARKERS IN SARCOMAS (CTOS 2024)
    DDR pathway alterations are present in numerous histologic subtypes of sarcoma. In many subtypes, DDR pathway-altered tumors were found to have increased rates of PD-L1+, dMMR/MSI-high, and TMB-high biomarkers commonly used to identify patients who may benefit from immunotherapy. Further studies to validate these associations are needed associations and could lead to a novel clinical trial exploring the use of immune checkpoint inhibitors in DDR-mutated sarcoma.
    Tumor mutational burden • PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
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    TMB (Tumor Mutational Burden)
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    TMB-H • MSI-H/dMMR
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    VENTANA PD-L1 (SP142) Assay • MI Tumor Seek™
    1year
    Fusion transcriptome landscape in Glioblastoma (SNO 2024)
    Comprehensive molecular profiling reveals that approximately 10% of IDH WT GBMs carry oncogenic fusions that may be therapeutic targets. Broad spectrum of observed fusions underscores the need for novel clinical trial designs to allow efficient enrollment for prospective testing of potential targeted agents.
    EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR3 (Fibroblast growth factor receptor 3) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • RB1 (RB Transcriptional Corepressor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDK4 (Cyclin-dependent kinase 4) • CAPZA2 (Capping Actin Protein Of Muscle Z-Line Subunit Alpha 2) • SEC61G (SEC61 Translocon Subunit Gamma) • PTPRZ1 (Protein Tyrosine Phosphatase Receptor Type Z1)
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    TP53 mutation • EGFR mutation • NTRK1 fusion • NTRK2 fusion • MET amplification • EGFR amplification • ALK fusion • ROS1 fusion • MET mutation • EGFRvIII mutation • FGFR3 fusion • IDH wild-type • EGFR fusion
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    MI Tumor Seek™
    1year
    Comprehensive characterization of the androgen receptor in male breast cancer (SABCS 2024)
    Our analysis suggests a strong association between AR expression and TP53 mutations, TMB-H, and PD-L1 positivity, immune cell infiltration, immune checkpoint and stem cell-related gene. Also, T cell inflamed and IFNy score were inversely related. Further exploration of specific alterations and immune-oncology markers associated with AR expression may help in clinical trial design for male patients with BC.
    Tumor mutational burden • PD(L)-1 Biomarker • BRCA Biomarker • IO biomarker
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    PD-L1 (Programmed death ligand 1) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • AR (Androgen receptor) • IFNG (Interferon, gamma) • LAG3 (Lymphocyte Activating 3) • CHEK2 (Checkpoint kinase 2) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • CD34 (CD34 molecule) • KLF4 (Kruppel-like factor 4) • POU5F1 (POU Class 5 Homeobox 1) • ALDH2 (Aldehyde Dehydrogenase 2 Family Member) • FOXP3 (Forkhead Box P3)
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    TP53 mutation • TMB-H • TP53 wild-type • AR overexpression • AR expression • TP53 expression • FOXP3 expression
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    MI Tumor Seek™
    1year
    Identifying regulators of MHC repression and therapeutic targets to overcome immune evasion in SCLC (SITC 2024)
    Moreover, our study identifies the direct role of DNAPKCs as a therapeutic target that can augment the anti-tumor immune response of PD-L1-blockade by induction of MHC-I expression in SCLC. Our findings have important implications for harnessing NHEJ regulators for immunotherapy in SCLC, a cancer in critical need of better therapeutic options.
    PD(L)-1 Biomarker • IO biomarker
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    HLA-A (Major Histocompatibility Complex, Class I, A) • HLA-B (Major Histocompatibility Complex, Class I, B) • PRKDC (Protein Kinase, DNA-Activated, Catalytic Subunit) • TAP1 (Transporter 1) • HLA-C (Major Histocompatibility Complex, Class I, C)
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    MI Tumor Seek™