ReviewJournal of neuro-oncology2001
Molecular pathology of pituitary adenomas.
Review in Journal of neuro-oncology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 38 citations in OpenAlex.
- Lower PRDM2 expression is associated with dopamine-agonist resistance and tumor recurrence in prolactinomas.BMC cancer · 2015Article
- Brain tumor senescence might be mediated by downregulation of S-phase kinase-associated protein 2 via butylidenephthalide leading to decreased cell viability.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Promoter hypermethylation profile of cell cycle regulator genes in pituitary adenomas.Journal of neuro-oncology · 2007Article
- Article
- DNA microarrays: recent developments and applications to the study of pituitary tissues.Endocrine · 2005Review
- Prognostic indicators in pituitary tumors.Endocrine pathology · 2005Review
- Best Practice No 172: pituitary gland pathology.Journal of clinical pathology · 2003Review
- Inactivation of the p16 gene in human pituitary nonfunctioning tumors by hypermethylation is more common in null cell adenomas.Endocrine pathology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A great deal of knowledge about anterior pituitary development, the pathogenesis of pituitary tumor and pituitary tumor progression has accumulated during the past decade. The role of multiple genes and gene products in pituitary development and the relationship of these genes to postnatal pituitary function and pituitary tumor development are being actively explored. Recent studies indicate that genes important in pituitary development do not contribute to pituitary tumorigenesis. However, mutations and other genetic alterations in these genes often lead to pituitary hypofunction. Many oncogenes and tumor suppressor genes that contribute to pituitary tumorigenesis have been described. There is a growing body of evidence showing that cellular and molecular changes in cyclins and cyclin-dependent kinase inhibitors contribute to pituitary tumorigenesis. Finally, recent comparative genomic hybridization studies show that many more genes that are important in pituitary tumorigenesis and tumor progression have yet to be discovered.
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.