ArticleCell reports2018
Targeting the Vulnerability of RB Tumor Suppressor Loss in Triple-Negative Breast Cancer.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 104 citations in OpenAlex.
- Alternate actions of CDK4/6 inhibitors beyond cell cycle blockade: unexplored roles in therapy resistance.Cancer metastasis reviews · 2025Review
- Intrinsic RB activation induces tumoral and stromal anti-tumor responses that limit triple-negative breast cancer.NPJ breast cancer · 2025Article
- RB loss sensitizes triple-negative breast cancer to apoptosis induced by cellular stress.Cell death discovery · 2025Article
- Potential Loss of Imprinting of Tumor Suppressor Gene RB1 in Triple Negative Breast Cancer.Breast cancer research : BCR · 2025Article
- Article
- Article
- RSK1-driven TRIM28/E2F1 feedback loop promotes castration-resistant prostate cancer progression.The Journal of clinical investigation · 2025Article
- A novel CDK4 inhibitor for myeloid protection in chemotherapy-treated triple-negative breast Cancer.Investigational new drugs · 2025Article
- BH3 mimetics targeting BCL-XL have efficacy in solid tumors with RB1 loss and replication stress.Nature communications · 2025Article
- Transformation to Neuroendocrine Phenotype in Non-Small-Cell Lung Carcinoma: A Literature Review.International journal of molecular sciences · 2025Review
- Palmitoylation prevents B7-H4 lysosomal degradation sustaining tumor immune evasion.Nature communications · 2025Article
- Proteogenomic discovery ofScience advances · 2025Article
- Recent Advances in Pineoblastoma Research: Molecular Classification, Modelling and Targetable Vulnerabilities.Cancers · 2025Review
- The Landscape of Potential Targeted Treatments and Chemotherapy Efficacy Biomarkers for TNBC.Breast cancer (Dove Medical Press) · 2025Review
- Modulation of the cytoskeleton for cancer therapy.Frontiers in cell and developmental biology · 2025Article
- p16 Immunohistochemical Patterns in Triple-Negative Breast Cancer: Clinical and Genomic Similarities of the p16 Diffuse Pattern to pRB Deficiency.Pathobiology : journal of immunopathology, molecular and cellular biology · 2025Article
- Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025Article
- Loss of chromosome cytoband 13q14.2 orchestrates breast cancer pathogenesis and drug response.Breast cancer research : BCR · 2024Article
- Histological transformation in lung adenocarcinoma: Insights of mechanisms and therapeutic windows.Journal of translational internal medicine · 2024Article
- AKT Inhibition Sensitizes to Polo-Like Kinase 1 Inhibitor Onvansertib in Prostate Cancer.Molecular cancer therapeutics · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Approximately 30% of triple-negative breast cancers (TNBCs) exhibit functional loss of the RB tumor suppressor, suggesting a target for precision intervention. Here, we use drug screens to identify agents specifically antagonized by the retinoblastoma tumor suppressor (RB) using CDK4/6 inhibitors. A number of candidate RB-synthetic lethal small molecules were identified, including anti-helmenthics, chemotherapeutic agents, and small-molecule inhibitors targeting DNA-damage checkpoints (e.g., CHK) and chromosome segregation (e.g., PLK1). Counter-screens using isogenic TNBC tumor cell lines and cell panels with varying endogenous RB statuses confirmed that therapeutic effects were robust and selective for RB loss of function. By analyzing TNBC clinical specimens, RB-deficient tumors were found to express high levels of CHK1 and PLK1. Loss of RB specifically resulted in loss of checkpoint functions governing DNA replication, yielding increased drug sensitivity. Xenograft models demonstrated RB-selective efficacy of CHK inhibitors. This study supports the possibility of selectively targeting RB loss in the treatment of TNBC.
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.