Evidence map›Paper›PMID 1833772›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1991

Antioncogenic effect of adenovirus E1A in human tumor cells.

S M Frisch

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-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

40 citing papers in PubMed, 109 citations in OpenAlex.

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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.

S M FrischDepartment of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Washington University in St. Louis · US

Funding

EIA CONTROL OF PROTEASE GENE TRANSCRIPTIONR29GM044573 · NIGMS · WASHINGTON UNIVERSITY · PI FRISCH, STEVEN MILES · 1990 to 1994
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NIGMS NIH HHS R29 GM 44573
6 · The paper itself

Abstract

Stable expression of the adenovirus 5 E1A gene reduced anchorage-independent growth and tumorigenic potential, caused cytoskeletal reorganization, induced flat morphology, and restored contact inhibition in three human tumor cell lines. By these criteria, E1A appears to be functionally indistinguishable from a tumor suppressor gene in this context. The apparent paradox accorded by the observations of the ability of E1A to transform rodent cells in cooperation with other oncogenes suggests that E1A may be the prototype of a class of growth-regulatory proteins having context-specific transforming and antioncogenic activities.

Indexed as

Antineoplastic AgentsGenes, Tumor SuppressorAdenovirus Early ProteinsAdenoviruses, HumanAnimalsAntigens, Viral, TumorCell DivisionCell LineFibrosarcomaGenes, ViralHeLa CellsHumansMelanomaMiceMice, NudeNeoplasm TransplantationAdenovirus Early ProteinsAntigens, Viral, TumorAntineoplastic AgentsOncogene Proteins, ViralRecombinant Proteins

Identifiers

PMID1833772
PMCPMC52655
OpenAlexW2092124718

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.