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A Pituitary-Derived MEG3 Isoform Functions as a Growth Suppressor in Tumor Cells

2003· article· en· 448 citations· W2164252048 on OpenAlex· 10.1210/jc.2003-030222

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.023
GPT teacher head0.310
Teacher spread
0.287 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

Human pituitary adenomas are the most common intracranial neoplasm. Typically monoclonal in origin, a somatic mutation is a prerequisite event in tumor development. To identify underlying pathogenetic mechanisms in tumor formation, we compared the difference in gene expression between normal human pituitary tissue and clinically nonfunctioning pituitary adenomas by cDNA-representational difference analysis. We cloned a cDNA, the expression of which was absent in these tumors, that represents a novel transcript from the previously described MEG3, a maternal imprinting gene with unknown function. It was expressed in normal human gonadotrophs, from which clinically nonfunctioning pituitary adenomas are derived. Additional investigation by Northern blot and RT-PCR demonstrated that this gene was also not expressed in functioning pituitary tumors as well as many human cancer cell lines. Moreover, ectopic expression of this gene inhibits growth in human cancer cells including HeLa, MCF-7, and H4. Genomic analysis revealed that MEG3 is located on chromosome 14q32.3, a site that has been predicted to contain a tumor suppressor gene involved in the pathogenesis of meningiomas. Taken together, our data suggest that MEG3 may represent a novel growth suppressor, which may play an important role in the development of human pituitary adenomas.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
The Journal of Clinical Endocrinology & Metabolism
Topic
Genetic Syndromes and Imprinting
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
Funders
U.S. Public Health ServiceNational Institutes of HealthJarislowsky FoundationNational Institute of Diabetes and Digestive and Kidney DiseasesMassachusetts General Hospital
Keywords
Pituitary tumorsBiologyTumor suppressor geneCorticotropic cellPituitary adenomaGene isoformCancer researchEctopic expressionMEG3GeneGene expressionSomatic cellPituitary glandAdenomaMolecular biologyCarcinogenesisGeneticsEndocrinologyDownregulation and upregulationHormone
Has abstract in OpenAlex
yes