ArticleNeoplasia (New York, N.Y.)2011
Cdk2-null mice are resistant to ErbB-2-induced mammary tumorigenesis.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 54 citations in OpenAlex.
- Frontiers in Cell-Cycle-Targeting Therapies: Addressing the Heterogeneity of the Cancer Cell Cycle.Cancers · 2026Article
- Targeting CDKs in cancer therapy: advances in PROTACs and molecular glues.NPJ precision oncology · 2025Review
- Targeting cyclin-dependent kinase 2 (CDK2) interactions with cyclins and Speedy 1 (Spy1) for cancer and male contraception.Future medicinal chemistry · 2025Review
- Atypical cell cycle regulation promotes mammary stem cell expansion during mammary development and tumourigenesis.Breast cancer research : BCR · 2024Article
- DNASE1L3 inhibits hepatocellular carcinoma by delaying cell cycle progression through CDK2.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Article
- Cell cycle proteins as promising targets in cancer therapy.Nature reviews. Cancer · 2017Review
- CCNA2 facilitates epithelial-to-mesenchymal transition via the integrin αvβ3 signaling in NSCLC.International journal of clinical and experimental pathology · 2017Article
- Cyclin-Dependent Kinase Inhibitors as Anticancer Therapeutics.Molecular pharmacology · 2015Article
- Article
- Targeting cell cycle regulators in hematologic malignancies.Frontiers in cell and developmental biology · 2015Review
- Genetically engineered mice as experimental tools to dissect the critical events in breast cancer.Advances in cancer research · 2014Review
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Silencing CDK4 radiosensitizes breast cancer cells by promoting apoptosis.Cell division · 2013Article
- CDC25A protein stability represents a previously unrecognized target of HER2 signaling in human breast cancer: implication for a potential clinical relevance in trastuzumab treatment.Neoplasia (New York, N.Y.) · 2013Observational
- Assembly, activation, and substrate specificity of cyclin D1/Cdk2 complexes.Biochemistry · 2013Article
- A NIK-IKKα module expands ErbB2-induced tumor-initiating cells by stimulating nuclear export of p27/Kip1.Cancer cell · 2013Article
- Cdk4 and nek2 signal binucleation and centrosome amplification in a her2+ breast cancer model.PloS one · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- PES1 promotes breast cancer by differentially regulating ERα and ERβ.The Journal of clinical investigation · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
The concept of targeting G(1) cyclin-dependent kinases (CDKs) in breast cancer treatments is supported by the fact that the genetic ablation of Cdk4 had minimal impacts on normal cell proliferation in majority of cell types, resulting in near-normal mouse development, whereas such loss of Cdk4 completely abrogated ErbB-2/neu-induced mammary tumorigenesis in mice. In most human breast cancer tissues, another G(1)-regulatory CDK, CDK2, is also hyperactivated by various mechanisms and is believed to be an important therapeutic target. In this report, we provide genetic evidence that CDK2 is essential for proliferation and oncogenesis of murine mammary epithelial cells. We observed that 87% of Cdk2-null mice were protected from ErbB-2-induced mammary tumorigenesis. Mouse embryonic fibroblasts isolated from Cdk2-null mouse showed resistance to various oncogene-induced transformation. Previously, we have reported that hemizygous loss of Cdc25A, the major activator of CDK2, can also protect mice from ErbB-2-induced mammary tumorigenesis [Cancer Res (2007) 67(14): 6605-11]. Thus, we propose that CDC25A-CDK2 pathway is critical for the oncogenic action of ErbB-2 in mammary epithelial cells, in a manner similar to Cyclin D1/CDK4 pathway.
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.