Evidence map›Paper›PMID 14973384›Full record

ReviewJournal of mammary gland biology and neoplasia2000

The preneoplastic phenotype in murine mammary tumorigenesis.

D Medina

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. A novel and cost-effectiveBiology open · 2020
    Article
  3. Modeling Human Ductal Carcinoma In Situ in the Mouse.Journal of mammary gland biology and neoplasia · 2018
    Review
  4. Review
  5. Article
  6. Review
  7. Mouse models for efficacy testing of agents against radiation carcinogenesis—a literature review.International journal of environmental research and public health · 2012
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Common integration sites for MMTV in viral induced mouse mammary tumors.Journal of mammary gland biology and neoplasia · 2008
    Review
  14. Mus tales: a hands-on view.Journal of mammary gland biology and neoplasia · 2008
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

D MedinaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. dmedina@bcm.tmc.edu
Baylor College of Medicine · US

Funding

SELENIUM AND MAMMARY TUMORIGENESISR01CA011944 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MEDINA, DANIEL NONE · 1985 to 2003
$1.2M
EARLY EVENTS IN MULTIPLE-STAGE MAMMARY TUMORIGENESISR01CA047112 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MEDINA, DANIEL NONE · 1988 to 1998
–
NCI NIH HHS CA11944NCI NIH HHS CA47112NCI NIH HHS CA84230
6 · The paper itself

Abstract

Preneoplastic lesions in murine mammary tumorigenesis have been extensively investigated over the past 50 years. The two general types of lesion that have malignant potential are the alveolar hyperplasias represented by the classical hyperplastic alveolar nodule and the ductal hyperplasias. The former type of lesion is induced by viral, chemical and hormonal agents; the latter by chemical agents and specific genetic alterations. Individual animal models have been utilized to elucidate the basic biological properties of the lesions and some of the basic molecular alterations. The biological phenotype of the two types of lesions include immortalization and epithelial hyperplasia. The ductal hyperplasias are distinguished from the alveolar hyperplasias by their pattern of epithelial hyperplasia and their extent of aneuploidy. The molecular alterations underlying epithelial hyperplasia are numerous and dependent on the particular animal model. An important issue for future studies is how faithfully any of these models mimic human premalignant progression. A minimal set of criteria is proposed that includes morphological progression, hormone dependence and genetic instability. It is likely that hyperplasias from a specific mouse model will represent a subset of the lesions found in human disease. Analogous hyperplasias from several defined genetic models, adequately characterized at the biological and molecular levels, would provide appropriate models for testing chemopreventive agents.

Indexed as

Cell Transformation, NeoplasticPrecancerous ConditionsAnimalsDisease Models, AnimalHumansHyperplasiaMammary Neoplasms, AnimalMiceMice, TransgenicModels, BiologicalPhenotype

Identifiers

PMID14973384
OpenAlexW1605652585

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.