ReviewPituitary2009
The molecular biology of pituitary tumors: a personal perspective.
Review in Pituitary, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 28 citations in OpenAlex.
- SFRP2 is a Novel Diagnostic Biomarker and Suppresses the Proliferation of Pituitary Adenoma.Journal of oncology · 2022Article
- Identification of gene co-expression modules and hub genes associated with the invasiveness of pituitary adenoma.Endocrine · 2020Article
- Acromegaly: a Latin American perspective.Pituitary · 2014Article
- Should aip gene screening be recommended in family members of FIPA patients with R16H variant?Pituitary · 2013Article
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
No grant is acknowledged in the PubMed record.
Abstract
Oncogenes and tumor suppressor genes involved in most common cancers are not involved in the great majority of pituitary adenomas. Similarly, there is little evidence to suggest that the mutations involved in genetic syndromes associated with pituitary tumors (such as the gsp, MEN1, PKAR1A or AIP mutations) are common in sporadic tumors. A novel pituitary tumor transforming gene (PTTG, securin) has been identified which is over-expressed in most tumors--but it is unclear as to its causal role in oncogenesis. Cell signaling abnormalities have been identified in pituitary tumors but their genetic basis is unknown. However, both the Akt pathway and the MAPK pathway are over-expressed in many pituitary tumors, which results in the inhibition of cell cycle inhibitors. These pathways share a common root in the tyrosine kinase receptor, and a change to these receptors or their relationship to membrane matrix-related proteins may be an early event in tumorigenesis.
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.