Evidence map›Paper›PMID 3155863›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1985

Identification of a single chromosome in the normal human genome essential for suppression of hamster cell transformation.

A Stoler, N Bouck

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1985. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 80 citations in OpenAlex.

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  7. Genetic mapping of tumor susceptibility genes involved in mouse plasmacytomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 1993
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  16. Loss of alleles from the distal short arm of chromosome 1 occurs late in melanoma tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 1989
    Article
  17. Recessive mechanisms of malignancy.British journal of cancer · 1988
    Review
  18. Article
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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

2 authors at 1 institution in 1 country.

A Stoler
N Bouck
Northwestern University · US

Funding

GENETIC ANALYSIS OF MALIGNANT TRANSFORMATIONR01CA027306 · NCI · NORTHWESTERN UNIVERSITY · PI BOUCK, NOEL P · 1985 to 1992
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NCI NIH HHS CA 27306
6 · The paper itself

Abstract

Normal human fibroblasts were fused to carcinogen-transformed baby hamster kidney (BHK) cells and found to be able to suppress the anchorage-independent transformed phenotype of the hamster cells. This suppression was not due to interspecies incompatibility, for transformation could be effectively expressed in hybrids if either the human or the BHK parent had initially been transformed by a dominantly acting viral genome. Upon growth of suppressed hybrids, loss of human chromosomes was accompanied by the re-expression of transformation. Karyotype analysis indicated that only human chromosome 1 was retained in all hybrids that were suppressed and was lost in all hybrids in which transformation was re-expressed. Cytological evidence for the presence or absence of chromosome 1 was confirmed by electrophoretic identification of the human isozyme for phosphoglucomutase 1. Clones re-expressing transformation were isolated from two suppressed hybrids and in both cases loss of suppression was accompanied by the loss of human chromosome 1. Thus, the maintenance of suppression in these cross-species hybrids appears to require the continued presence of normal human chromosome 1. These findings raise the possibility that the frequent involvement of human chromosome 1 in potentially inactivating aberrations in human tumors may reflect a suppressor role for this chromosome in human malignancy.

Indexed as

Cell FusionCell Transformation, NeoplasticChromosomes, Human, 1-3AnimalsCricetinaeHumansKaryotypingNeoplasmsPhenotypePhosphoglucomutasePhosphoglucomutase

Identifiers

PMID3155863
PMCPMC397082
OpenAlexW2026421952

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.