ArticleThe Journal of clinical investigation2007
The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancer.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.
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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
120 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.
- Defining the Molecular Intricacies of Human Papillomavirus-Associated Tonsillar Carcinoma.Cancer control : journal of the Moffitt Cancer CenterPooled it
- Impact of aromatase inhibitor treatment on global gene expression and its association with antiproliferative response in ER+ breast cancer in postmenopausal patients.Breast cancer research : BCR · 2019Trial
- Neoadjuvant palbociclib on ER+ breast cancer (N007): clinical response and EndoPredict's value.Endocrine-related cancer · 2018Trial
- The effects of Palbociclib and Ferulic acid combination on cellular processes in breast cancer.Discover oncology · 2026Article
- Genetic and epigenetic contribution to tamoxifen resistance in breast cancer, concepts to drive therapeutic strategies.Discover oncology · 2025Review
- 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
- Using bioinformatics and artificial intelligence to map the cyclin-dependent kinase 4/6 inhibitor biomarker landscape in breast cancer.Future oncology (London, England) · 2024Review
- Preclinical evaluation of CDK4 phosphorylation predicts high sensitivity of pleural mesotheliomas to CDK4/6 inhibition.Molecular oncology · 2024Article
- Review
- Determinants of response to CDK4/6 inhibitors in the real-world setting.NPJ precision oncology · 2023Article
- Significance of RB Loss in Unlocking Phenotypic Plasticity in Advanced Cancers.Molecular cancer research : MCR · 2023Article
- RB1-deficient prostate tumor growth and metastasis are vulnerable to ferroptosis induction via the E2F/ACSL4 axis.The Journal of clinical investigation · 2023Article
- Radiosensitization of Breast Cancer Cells with a 2-Methoxyestradiol Analogue Affects DNA Damage and Repair Signaling In Vitro.International journal of molecular sciences · 2023Article
- CDK4 phosphorylation status and rational use for combining CDK4/6 and BRAF/MEK inhibition in advanced thyroid carcinomas.Frontiers in endocrinology · 2023Article
- Integrated DNA and RNA Sequencing Reveals Drivers of Endocrine Resistance in Estrogen Receptor-Positive Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- ENDORSE: a prognostic model for endocrine therapy in estrogen-receptor-positive breast cancers.Molecular systems biology · 2022Article
- Relevance of pRB Loss in Human Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Review
- Novel Oncogenic Transcription Factor Cooperation in RB-Deficient Cancer.Cancer research · 2022Article
- RB/E2F1 as a Master Regulator of Cancer Cell Metabolism in Advanced Disease.Cancer discovery · 2021Article
- Co-targeting CDK4/6 and AKT with endocrine therapy prevents progression in CDK4/6 inhibitor and endocrine therapy-resistant breast cancer.Nature communications · 2021Article
60 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
The retinoblastoma tumor suppressor (RB) protein is functionally inactivated in the majority of human cancers and is aberrant in one-third of all breast cancers. RB regulates G(1)/S-phase cell-cycle progression and is a critical mediator of antiproliferative signaling. Here the specific impact of RB deficiency on E2F-regulated gene expression, tumorigenic proliferation, and the response to 2 distinct lines of therapy was investigated in breast cancer cells. RB knockdown resulted in RB/E2F target gene deregulation and accelerated tumorigenic proliferation, thereby demonstrating that even in the context of a complex tumor cell genome, RB status exerts significant control over proliferation. Furthermore, the RB deficiency compromised the short-term cell-cycle inhibition following cisplatin, ionizing radiation, and antiestrogen therapy. In the context of DNA-damaging agents, this bypass resulted in increased sensitivity to these agents in cell culture and xenograft models. In contrast, the bypass of antiestrogen signaling resulted in continued proliferation and xenograft tumor growth in the presence of tamoxifen. These effects of aberrations in RB function were recapitulated by ectopic E2F expression, indicating that control of downstream target genes was an important determinant of the observed responses. Specific analyses of an RB gene expression signature in 60 human patients indicated that deregulation of this pathway was associated with early recurrence following tamoxifen monotherapy. Thus, because the RB pathway is a critical determinant of tumorigenic proliferation and differential therapeutic response, it may represent a critical basis for directing therapy in the treatment of breast cancer.
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.