ArticleOncogene2010
Rb inactivation accelerates neoplastic growth and substitutes for recurrent amplification of cIAP1, cIAP2 and Yap1 in sporadic mammary carcinoma associated with p53 deficiency.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 42 citations in OpenAlex.
- A review of genetic variant databases and machine learning tools for predicting the pathogenicity of breast cancer.Briefings in bioinformatics · 2023Review
- Significance of RB Loss in Unlocking Phenotypic Plasticity in Advanced Cancers.Molecular cancer research : MCR · 2023Article
- Dietary phytochemicals/nutrients as promising protector of breast cancer development: a comprehensive analysis.Pharmacological reports : PR · 2022Review
- Cytoplasmic and Nuclear Functions of cIAP1.Biomolecules · 2022Review
- Review
- Molecular events in the pathogenesis of vulvar squamous cell carcinoma.Seminars in diagnostic pathology · 2021Review
- Article
- Recurrent genetic alterations and biomarker expression in primary and metastatic squamous cell carcinomas of the vulva.Human pathology · 2019Article
- Anti-apoptotic factor Birc3 is up-regulated by ELL2 knockdown and stimulates proliferation in LNCaP cells.American journal of clinical and experimental urology · 2019Article
- p53 shades of Hippo.Cell death and differentiation · 2018Review
- Induced p53 loss in mouse luminal cells causes clonal expansion and development of mammary tumours.Nature communications · 2017Article
- Risk Factors and Preventions of Breast Cancer.International journal of biological sciences · 2017Review
- RB1 deficiency in triple-negative breast cancer induces mitochondrial protein translation.The Journal of clinical investigation · 2016Article
- The Chromatin Remodeling Component Arid1a Is a Suppressor of Spontaneous Mammary Tumors in Mice.Genetics · 2016Article
- MicroRNA-34a promotes genomic instability by a broad suppression of genome maintenance mechanisms downstream of the oncogene KSHV-vGPCR.Oncotarget · 2016Article
- Report on the use of non-clinical studies in the regulatory evaluation of oncology drugs.Cancer science · 2016Review
- Control of Proliferation and Cancer Growth by the Hippo Signaling Pathway.Molecular cancer research : MCR · 2016Review
- Organ size control is dominant over Rb family inactivation to restrict proliferation in vivo.Cell reports · 2014Article
- IAP proteins as targets for drug development in oncology.OncoTargets and therapy · 2013Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Genetically defined mouse models offer an important tool to identify critical secondary genetic alterations with relevance to human cancer pathogenesis. We used newly generated MMTV-Cre105Ayn mice to inactivate p53 and/or Rb strictly in the mammary epithelium, and to determine recurrent genomic changes associated with deficiencies of these genes. p53 inactivation led to formation of estrogen receptor-positive raloxifene-responsive mammary carcinomas with features of luminal subtype B. Rb deficiency was insufficient to initiate carcinogenesis but promoted genomic instability and growth rate of neoplasms associated with p53 inactivation. Genome-wide analysis of mammary carcinomas identified a recurrent amplification at chromosome band 9A1, a locus orthologous to human 11q22, which contains protooncogenes cIAP1 (Birc2), cIAP2 (Birc3) and Yap1. It is interesting that this amplicon was preferentially detected in carcinomas carrying wild-type Rb. However, all three genes were overexpressed in carcinomas with p53 and Rb inactivation, likely due to E2F-mediated transactivation, and cooperated in carcinogenesis according to gene knockdown experiments. These findings establish a model of luminal subtype B mammary carcinoma, identify critical role of cIAP1, cIAP2 and Yap1 co-expression in mammary carcinogenesis and provide an explanation for the lack of recurrent amplifications of cIAP1, cIAP2 and Yap1 in some tumors with frequent Rb deficiency, such as mammary carcinoma.
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.