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    GENE:

    CHEK1 (Checkpoint kinase 1)

    i
    Other names: CHEK1, CHK1, Checkpoint kinase 1
    2d
    KDM4D enhances radiosensitivity in esophageal squamous cell carcinoma through the SRBD1/RPL11/c-Myc/WIP1/CHK1 axis. (PubMed, Am J Transl Res)
    Rescue experiments and xenograft studies further verified this regulatory axis. KDM4D enhances ESCC radiosensitivity through the SRBD1/RPL11/c-Myc/WIP1/CHK1 pathway, highlighting its potential as both a diagnostic biomarker and a therapeutic target.
    Journal
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • CHEK1 (Checkpoint kinase 1) • PPM1D (Protein Phosphatase Mg2+/Mn2+ Dependent 1D) • KDM4D (Lysine Demethylase 4D) • RPL11 (Ribosomal Protein L11)
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    TP53 wild-type
    2d
    Free energy perturbation-assisted identification of checkpoint kinase 1 targeted small-molecule inhibitors for cancer therapy using AI- and physics-driven molecular design. (PubMed, Comput Biol Chem)
    The binding disrupted the intramolecular hydrogen-bond network in Chk1 and encouraged the formation of new hydrogen bonds. These results provide a strong foundation for optimizing and developing new Chk1 inhibitors as potential anticancer agents.
    Journal
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    CHEK1 (Checkpoint kinase 1) • CHD1 (Chromodomain Helicase DNA Binding Protein 1) • CHD2 (Chromodomain Helicase DNA Binding Protein 2)
    6d
    Therapy-Induced Cellular Senescence in Non-Hodgkin Lymphomas, with Emphasis on Aggressive B-Cell Subtypes: Molecular Mechanisms and Emerging Drug Targets. (PubMed, Curr Cancer Drug Targets)
    In lymphomas, TIS is a dynamic stress-adaptation state that can support persistence and relapse. Rational integration of senescence biomarkers, timing-based therapies, and targeted senolytic/senomorphic interventions may enhance long-term treatment efficacy; however, most senescence-targeted strategies remain investigational and require lymphoma-specific clinical validation.
    Journal • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • BCL2L1 (BCL2-like 1) • CHEK2 (Checkpoint kinase 2) • CHEK1 (Checkpoint kinase 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
    6d
    Dangerous liaisons: Promiscuous inhibition of CHK1 and AMPK is a lethal affair for cancer cells. (PubMed, Cell Chem Biol)
    In this issue of Cell Chemical Biology, Guo et al.1 reveal that the Checkpoint kinase 1 (CHK1) inhibitor Prexasertib moonlights as an AMP-activated protein kinase (AMPK) inhibitor that primes cancer cells for destruction. This off-target synergy highlights that serendipitous promiscuity can supercharge the efficacy of some "selective" kinase inhibitors.
    Journal
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    CHEK1 (Checkpoint kinase 1) • AMPK (Protein Kinase AMP-Activated Catalytic Subunit Alpha 1)
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    prexasertib (ACR-368)
    8d
    KPT-330-mediated XPO1 inhibition impairs homologous recombination and enhances radiosensitivity in extranodal NK/T-cell lymphoma. (PubMed, Br J Cancer)
    XPO1 inhibition impairs HR and enhances radiosensitivity by disrupting the c-Myc-RAD51/CHEK1 axis. These findings support prospective evaluation of KPT-330-based radiosensitization in R/R ENKTL.
    Journal • IO biomarker
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • RAD51 (RAD51 Homolog A) • CHEK1 (Checkpoint kinase 1) • XPO1 (Exportin 1)
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    Xpovio (selinexor)
    9d
    Molecular mechanisms of KMT2C alterations in gastrointestinal cancers: enhancer network destabilization, lineage plasticity, and clinical translation. (PubMed, Front Immunol)
    In this review, we integrate evidence from hepatocellular carcinoma, pancreatic ductal adenocarcinoma, cholangiocarcinoma, colorectal cancer, gastric cancer, esophageal cancer, and gallbladder cancer within a unified framework that links KMT2C domain architecture to enhancer-network destabilization, phenotypic state transitions, and clinical manifestations. We further propose a functional evaluation paradigm that reframes discrete KMT2C variants as graded states of epigenetic deficiency, coupled with a closed-loop validation strategy integrating tissue-based profiling, liquid biopsy monitoring, and spatial multi-omics analyses.
    Review • Journal • Tumor mutational burden • PARP Biomarker
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    TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • KMT2C (Lysine Methyltransferase 2C) • CHEK1 (Checkpoint kinase 1) • DRD (DNA Repair Deficiency)
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    DDR
    9d
    Uncovering the potential anti-cancer compounds from Strobilanthes cusia against colorectal cancer through network pharmacology and molecular docking. (PubMed, Sci Rep)
    In vitro validation demonstrated dose-dependent apoptosis and proliferation inhibition in both cell lines, with significantly lower IC50 values at 48 h (isolated: 10.52 ± 1.91µM; commercial: 8.96 ± 9.35µM) than at 24 h. These findings identify CHEK1 as a mechanistically relevant target and support further translational investigation of S. cusia-derived andrographolide in CRC therapy.
    Journal
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    CHEK1 (Checkpoint kinase 1)
    12d
    Clinical applications of PARP inhibitors in breast, ovarian, and prostate cancer: current insights and future directions. (PubMed, Clin Adv Hematol Oncol)
    Since the initial US Food Administration approval of olaparib in 2014, PARP inhibitors have shown efficacy across ovarian, breast, and prostate cancers, although differences in trial design and biomarker strategies have resulted in tumor-specific indications...Ongoing studies are evaluating rational combinations targeting complementary DNA damage response pathways (ATR/CHK1/WEE1, PI3K/AKT) and integrating immunotherapy or hormonal agents to extend benefit. Moving forward, harmonizing HRD testing across tumor types, accounting for germline, somatic, and liquid biopsy-derived alterations, and refining patient selection will be essential to maximize therapeutic efficacy and safely expand PARP inhibitor use beyond canonical BRCA-mutated cancers.
    Review • Journal • BRCA Biomarker • PARP Biomarker • IO biomarker
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    BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • HRD (Homologous Recombination Deficiency) • BRCA (Breast cancer early onset) • CHEK1 (Checkpoint kinase 1)
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    BRCA2 mutation • BRCA1 mutation • HRD
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    Lynparza (olaparib)
    12d
    Integrated network pharmacology reveal new key curcumin-binding targets in triple-negative breast cancer. (PubMed, Discov Oncol)
    Our integrated analysis suggests that curcumin exerts multitarget inhibitory effects in TNBC by concurrently modulating mitotic regulation (via AURKA), MAPK signaling (via BRAF (V600E)), and DNA damage checkpoints (via CHEK1). Among these, CHEK1 emerged as the most thermodynamically stable and conformationally favorable binding target for curcumin, indicating its potential as a crucial mediator of curcumin's antitumor activity.
    Journal
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    BRAF (B-raf proto-oncogene) • AURKA (Aurora kinase A) • CHEK1 (Checkpoint kinase 1)
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    BRAF V600E • BRAF V600
    13d
    NCI-2017-02296: Testing Olaparib in Patients With Advanced or Metastatic (Cancer That Has Spread) Bladder Cancer and Other Genitourinary Tumors With DNA-Repair Genetic Changes (clinicaltrials.gov)
    P2, N=60, Active, not recruiting, National Cancer Institute (NCI) | Suspended --> Active, not recruiting
    Enrollment closed • Tumor mutational burden
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    TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • ABL1 (ABL proto-oncogene 1) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • STK11 (Serine/threonine kinase 11) • NPM1 (Nucleophosmin 1) • POLE (DNA Polymerase Epsilon) • CCND1 (Cyclin D1) • BAP1 (BRCA1 Associated Protein 1) • MLH1 (MutL homolog 1) • MSH6 (MutS homolog 6) • MSH2 (MutS Homolog 2) • ATRX (ATRX Chromatin Remodeler) • CHEK2 (Checkpoint kinase 2) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • RAD51 (RAD51 Homolog A) • FANCA (FA Complementation Group A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • POLD1 (DNA Polymerase Delta 1) • CHEK1 (Checkpoint kinase 1) • BARD1 (BRCA1 Associated RING Domain 1) • FANCL (FA Complementation Group L) • BRD4 (Bromodomain Containing 4) • DOT1L (DOT1 Like Histone Lysine Methyltransferase) • FANCE (FA Complementation Group E) • FANCG (FA Complementation Group G) • IKBKE (Inhibitor Of Nuclear Factor Kappa B Kinase Subunit Epsilon) • FANCC (FA Complementation Group C)
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    PALB2 mutation • BRIP1 mutation
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    FoundationOne® CDx
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    Lynparza (olaparib)
    15d
    Multiomics integration prioritizes potential drug targets for lung cancer. (PubMed, Discov Oncol)
    This multi-omics MR framework identifies genes whose genetically predicted expression is associated with increased or decreased lung cancer risk and may help prioritize candidate targets for future lung cancer drug development.
    Journal
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    FLT4 (Fms-related tyrosine kinase 4) • CHEK1 (Checkpoint kinase 1)
    19d
    Differential DNA damage response to WRN inhibition identifies a targetable vulnerability in ARID1A-mutated cancers. (PubMed, Sci Adv)
    The antitumor efficacy of WRN inhibition alone and in combination with p21 inhibition was validated using cell line-based xenograft and patient-derived xenograft mouse models. Our findings define WRN as a selective therapeutic target in ARID1A-mutated cancers and suggest a combinatorial strategy of WRN and p21 inhibition as a therapeutic approach.
    Journal
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    ARID1A (AT-rich interaction domain 1A) • CHEK2 (Checkpoint kinase 2) • CHEK1 (Checkpoint kinase 1) • WRN (WRN RecQ Like Helicase) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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    ARID1A mutation