ArticleThe Journal of clinical investigation2010
Rb deletion in mouse mammary progenitors induces luminal-B or basal-like/EMT tumor subtypes depending on p53 status.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 143 citations in OpenAlex.
- TLR7 signature of tumour innervation reveals two distinct pathways of triple-negative breast cancer progression.British journal of cancer · 2026Article
- Involvement of KEAP1/NRF2 pathway in non-BRAF mutated squamous cell carcinoma of the thyroid.The Journal of pathology · 2025Article
- Reactivation of Multipotency in the Mammary Gland - a Ripple in the Pond and a Turn of the Tide.Journal of mammary gland biology and neoplasia · 2025Review
- Cells-of-Origin of Breast Cancer and Intertumoral Heterogeneity.Advances in experimental medicine and biology · 2025Review
- Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024Review
- Thinking (Metastasis) outside the (Primary Tumor) Box.Cancers · 2023Article
- Retinoblastoma: present scenario and future challenges.Cell communication and signaling : CCS · 2023Review
- Network modeling suggests HIV infection phenocopies PI3K-AKT pathway mutations to enhance HPV-associated cervical cancer.Molecular omics · 2023Article
- Distinct shared and compartment-enriched oncogenic networks drive primary versus metastatic breast cancer.Nature communications · 2023Article
- SPINOPHILIN: A multiplayer tumor suppressor.Genes & diseases · 2023Review
- Loss of Brca1 and Trp53 in adult mouse mammary ductal epithelium results in development of hormone receptor-positive or hormone receptor-negative tumors, depending on inactivation of Rb family proteins.Breast cancer research : BCR · 2022Article
- Ecdysoneless Overexpression Drives Mammary Tumorigenesis through Upregulation of C-MYC and Glucose Metabolism.Molecular cancer research : MCR · 2022Article
- Hippo-TAZ signaling is the master regulator of the onset of triple-negative basal-like breast cancers.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Loss of function of BRCA1 promotes EMT in mammary tumors through activation of TGFβR2 signaling pathway.Cell death & disease · 2022Article
- Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes.The EMBO journal · 2022Article
- Loss of function of GATA3 induces basal-like mammary tumors.Theranostics · 2022Article
- How Lineage Tracing Studies Can Unveil Tumor Heterogeneity in Breast Cancer.Biomedicines · 2021Review
- Transgenic mouse models of breast cancer.Cancer letters · 2021Article
- Article
- Role of the Holoenzyme PP1-SPN in the Dephosphorylation of the RB Family of Tumor Suppressors During Cell Cycle.Cancers · 2021Review
40 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
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Breast cancer is a highly heterogeneous disease, with several different subtypes being characterized by distinct histology, gene expression patterns, and genetic alterations. The tumor suppressor gene retinoblastoma 1 (RB1) is frequently lost in both luminal-B and triple-negative tumor (TNT; i.e., estrogen receptor-, progesterone receptor-, and human epidermal growth factor receptor 2-negative) breast cancer subtypes. However, a causal role for RB1 loss in different subtypes remains undefined. Here we report that deletion of Rb alone or together with its relative p107 in mouse mammary stem/bipotent progenitor cells induced focal acinar hyperplasia with squamous metaplasia. These lesions progressed into histologically diverse, transplantable mammary tumors with features of either luminal-B or TNT subtypes. The TNTs included basal-like tumors as well as tumors that exhibited epithelial-to-mesenchymal transition (EMT). The EMT-type tumors and a subset of the basal-like tumors, but not luminal-B-like tumors, expressed mutant forms of the tumor suppressor p53. Accordingly, targeted deletion of both Rb and p53 in stem/bipotent progenitors led to histologically uniform, aggressive, EMT-type tumors. Reintroduction of Rb into these tumor cells suppressed growth in vitro and tumor formation in vivo. These results establish a causal role for Rb loss in breast cancer in mice and demonstrate that cooperating oncogenic events, such as mutations in p53, dictate tumor subtype after Rb inactivation.
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.