ReviewCancers2024
Triple-Negative Breast Cancer and Emerging Therapeutic Strategies: ATR and CHK1/2 as Promising Targets.
Review in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Integrated network pharmacology reveal new key curcumin-binding targets in triple-negative breast cancer.Discover oncology · 2026Article
- Breast cancer: taxonomy, distribution analysis, risk factors, predictive biomarkers, and modern treatment method.Apoptosis : an international journal on programmed cell death · 2026Review
- Transcriptomics-driven identification of CDK1 as a central oncogenic driver in TNBC: anFrontiers in bioinformatics · 2026Article
- Translational Aspects of DNA Damage Repair in Optimizing Cancer Chemotherapy.Advanced genetics (Hoboken, N.J.) · 2025Review
- Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA Damage.Cells · 2025Review
- Dual Disruption of DNA Repair by a Novel CHK2 Inhibitor, ART-446, and Olaparib is a Promising Strategy for Triple-Negative Breast Cancer Therapy.Biomolecules & therapeutics · 2025Article
- Tendomodulin in pan-cancer analysis: exploring its impact on immune modulation and uncovering functional insights in colorectal cancer.BMC cancer · 2025Article
- Efficacy of Wee1 G2 Checkpoint Kinase and Mouse Double Minute 2 Homolog Inhibitors in Gastrointestinal Stromal Tumors Determined by p53 Status.Oncology research · 2025Article
- Emerging opportunities to treat drug-resistant breast cancer: Discovery of novel small-molecule inhibitors against different targets.Frontiers in pharmacology · 2025Review
- Latest Therapeutical Approaches for Triple-Negative Breast Cancer: From Preclinical to Clinical Research.International journal of molecular sciences · 2024Review
- Multifaceted role of phytoconstituents based nano drug delivery systems in combating TNBC: A paradigm shift from chemical to natural.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- An Antagonist Antibody That Inhibits Cancer Cell Growth In Vitro through RACK1.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Advances in siRNA Drug Delivery Strategies for Targeted TNBC Therapy.Bioengineering (Basel, Switzerland) · 2024Review
- Correlation between Molecular Docking and the Stabilizing Interaction of HOMO-LUMO: Spirostans in CHK1 and CHK2, an In Silico Cancer Approach.International journal of molecular sciences · 2024Article
- Tumor Mutational Landscape and Its Correlation With Histopathological Characteristics in Breast Cancer.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Worldwide, breast cancer is the most frequently diagnosed malignancy in women, with triple-negative breast cancer (TNBC) being the most aggressive molecular subtype. Due to the dearth of effective therapeutic options for TNBC, novel agents targeting key mechanisms and pathways in cancer cells are continuously explored; these include ATR inhibitors, which target the ATR kinase involved in the DNA damage response (DDR) pathway, and CHK1/2 inhibitors, which target the Checkpoint Kinase 1/2 (CHK1/2) involved in cell cycle arrest and DNA repair. ATR and CHK1/2 inhibitors show potential as prospective treatments for TNBC by focusing on the DDR and interfering with cell cycle regulation in cancer cells. Preliminary preclinical and clinical findings suggest that when combined with chemotherapy, ATR and CHK1/2 inhibitors demonstrate significant anti-proliferative efficacy against TNBC. In this article, we introduce ATR and CHK1/2 inhibitors as promising therapeutic approaches for the management of TNBC. Preclinical and clinical studies performed evaluating ATR and CHK1/2 inhibitors for the treatment of TNBC and associated challenges encountered in this context to date are reviewed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.