ReviewBest practice & research. Clinical endocrinology & metabolism2010
Mouse models of endocrine tumours.
Review in Best practice & research. Clinical endocrinology & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 10 citations in OpenAlex.
- Carney complex: an update.European journal of endocrinology · 2015Review
- Follicular thyroid cancers demonstrate dual activation of PKA and mTOR as modeled by thyroid-specific deletion of Prkar1a and Pten in mice.The Journal of clinical endocrinology and metabolism · 2014Article
- cAMP/PKA signaling defects in tumors: genetics and tissue-specific pluripotential cell-derived lesions in human and mouse.Molecular and cellular endocrinology · 2013Review
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 1 institution in 1 country.
Funding
Abstract
Since the onset of the genomic era, there has been tremendous progress in identifying the genetic causes of endocrine tumours. Although this knowledge is valuable in its own right, understanding the molecular basis of tumourigenesis allows the development of new therapies targeted at the causative defects. Understanding the connection between genotype and phenotype is a complex process, which can only be partially understood from the analysis of primary tumours or from the studies of cells in vitro. To bridge this gap, genetically modified mice have been developed to allow molecular dissection of the relevant defects in an intact organism. In this article, we discuss the status of genetic modelling for hereditary and sporadic endocrine tumourigenesis with a goal towards providing a view of how this technology will be of future benefit to clinicians developing specifically targeted therapies for endocrine tumours.
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.