ReviewOncogene2000
The mammary pathology of genetically engineered mice: the consensus report and recommendations from the Annapolis meeting.
Review in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 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
252 citing papers in PubMed, 490 citations in OpenAlex.
- Trial
- CDK12 promotes tumorigenesis but induces vulnerability to therapies inhibiting folate one-carbon metabolism in breast cancer.Nature communications · 2022Trial
- Rat somatic genome editing enables ER+ breast cancer modeling.bioRxiv : the preprint server for biology · 2025Article
- DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications.Life science alliance · 2025Article
- Precision preclinical modeling to advance cancer treatment.Journal of the National Cancer Institute · 2025Review
- Knock-out of CD73 delays the onset of HR-negative breast cancer by reprogramming lipid metabolism and is associated with increased tumor mutational burden.Molecular metabolism · 2024Article
- Different Oncogenes and Reproductive Histories Shape the Progression of Distinct Premalignant Clones in Multistage Mouse Breast Cancer Models.The American journal of pathology · 2024Article
- Benzophenone-3 alters expression of genes encoding vascularization and epithelial-mesenchymal transition functions during Trp53-null mammary tumorigenesis.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024Article
- MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer.The Journal of experimental medicine · 2023Article
- Review
- Α Humanized RANKL Transgenic Mouse Model of Progestin-Induced Mammary Carcinogenesis for Evaluation of Novel Therapeutics.Cancers · 2023Article
- Exploring the link between viruses and cancer in companion animals: a comprehensive and comparative analysis.Infectious agents and cancer · 2023Review
- Molecular Characterization and Landscape of Breast cancer Models from a multi-omics Perspective.Journal of mammary gland biology and neoplasia · 2023Review
- Article
- New C3H KitScientific reports · 2022Article
- Loss of RPTPγ primes breast tissue for acid extrusion, promotes malignant transformation and results in early tumour recurrence and shortened survival.British journal of cancer · 2022Article
- Ecdysoneless Overexpression Drives Mammary Tumorigenesis through Upregulation of C-MYC and Glucose Metabolism.Molecular cancer research : MCR · 2022Article
- Article
- Molecular signatures of in situ to invasive progression for basal-like breast cancers: An integrated mouse model and human DCIS study.NPJ breast cancer · 2022Article
- Identification of early biomarkers in saliva in genetically engineered mouse model C(3)1-TAg of breast cancer.Scientific reports · 2022Article
192 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 10 institutions in 2 countries.
Funding
Abstract
NIH sponsored a meeting of medical and veterinary pathologists with mammary gland expertise in Annapolis in March 1999. Rapid development of mouse mammary models has accentuated the need for definitions of the mammary lesions in genetically engineered mice (GEM) and to assess their usefulness as models of human breast disease. The panel of nine pathologists independently reviewed material representing over 90% of the published systems. The GEM tumors were found to have: (1) phenotypes similar to those of non-GEM; (2) signature phenotypes specific to the transgene; and (3) some morphological similarities to the human disease. The current mouse mammary and human breast tumor classifications describe the majority of GEM lesions but unique morphologic lesions are found in many GEM. Since little information is available on the natural history of GEM lesions, a simple morphologic nomenclature is proposed that allows direct comparisons between models. Future progress requires rigorous application of guidelines covering pathologic examination of the mammary gland and the whole animal. Since the phenotype of the lesions is an essential component of their molecular pathology, funding agencies should adopt policies ensuring careful morphological evaluation of any funded research involving animal models. A pathologist should be part of each research team.
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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.