ArticleThe American journal of pathology2009
Genetic ablation of caveolin-1 drives estrogen-hypersensitivity and the development of DCIS-like mammary lesions.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 60 citations in OpenAlex.
- Expression of cyclin D1a and D1b as predictive factors for treatment response in colorectal cancer.British journal of cancer · 2012Trial
- Genomic mapping reveals cisplatin disruption of protein phosphorylation signalling genome-wide.Metallomics : integrated biometal science · 2026Article
- RNA-binding proteins as therapeutic targets in cancer.RNA biology · 2025Review
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- RBM39 Functions as a Potential Oncogene Through the NF-κB Signaling Pathway in Colorectal Cancer Cells.Journal of Cancer · 2025Article
- RNA-binding protein 39: a promising therapeutic target for cancer.Cell death discovery · 2021Review
- Biology of the mRNA Splicing Machinery and Its Dysregulation in Cancer Providing Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- Article
- RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020Review
- Cancer the'RBP'eutics-RNA-binding proteins as therapeutic targets for cancer.Pharmacology & therapeutics · 2019Review
- CAPER as a therapeutic target for triple negative breast cancer.Oncotarget · 2018Article
- Genomic and expression profiling reveal molecular heterogeneity of disseminated tumor cells in bone marrow of early breast cancer.NPJ breast cancer · 2018Article
- Effect of estrogen receptor β agonists on proliferation and gene expression of ovarian cancer cells.BMC cancer · 2017Article
- Synergistic drug combinations from electronic health records and gene expression.Journal of the American Medical Informatics Association : JAMIA · 2017Article
- UHM-ULM interactions in the RBM39-U2AF65 splicing-factor complex.Acta crystallographica. Section D, Structural biology · 2016Article
- Clinical significance of SPRR1A expression in progesterone receptor-positive breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- CAPER is vital for energy and redox homeostasis by integrating glucose-induced mitochondrial functions via ERR-α-Gabpa and stress-induced adaptive responses via NF-κB-cMYC.PLoS genetics · 2015Article
- Targeted protein destabilization reveals an estrogen-mediated ER stress response.Nature chemical biology · 2014Article
- Overexpression of HCC1/CAPERα may play a role in lung cancer carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Caveolin-1 regulates genomic action of the glucocorticoid receptor in neural stem cells.Molecular and cellular biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 1 institution in 2 countries.
Funding
Abstract
Caveolin-1 (Cav-1) loss-of-function mutations are exclusively associated with estrogen receptor-positive (ER(+)) human breast cancers. To dissect the role of Cav-1 loss-of-function in the pathogenesis of human breast cancers, we used Cav-1(-/-) null mice as a model system. First, we demonstrated that Cav-1(-/-) mammary epithelia overexpress two well-established ER co-activator genes, CAPER and Foxa1, in addition to ER-alpha. Thus, the functional loss of Cav-1 may be sufficient to confer estrogen-hypersensitivity in the mammary gland. To test this hypothesis directly, we subjected Cav-1(-/-) mice to ovariectomy and estrogen supplementation. As predicted, Cav-1(-/-) mammary glands were hyper-responsive to estrogen and developed dysplastic mammary lesions with adjacent stromal angiogenesis that resemble human ductal carcinoma in situ. Based on an extensive biomarker analysis, these Cav-1(-/-) mammary lesions contain cells that are hyperproliferative and stain positively with nucleolar (B23/nucleophosmin) and stem/progenitor cell markers (SPRR1A and beta-catenin). Genome-wide transcriptional profiling identified many estrogen-related genes that were over-expressed in Cav-1(-/-) mammary glands, including CAPER--an ER co-activator gene and putative stem/progenitor cell marker. Analysis of human breast cancer samples revealed that CAPER is overexpressed and undergoes a cytoplasmic-to-nuclear shift during the transition from pre-malignancy to ductal carcinoma in situ. Thus, Cav-1(-/-) null mice are a new preclinical model for studying the molecular paradigm of estrogen hypersensitivity and the development of estrogen-dependent ductal carcinoma in situ lesions.
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.