Evidence map›Paper›PMID 10702795›Full record

ArticleOncogene2000

HYAL1LUCA-1, a candidate tumor suppressor gene on chromosome 3p21.3, is inactivated in head and neck squamous cell carcinomas by aberrant splicing of pre-mRNA.

G I Frost, G Mohapatra, T M Wong, A B Csóka, J W Gray, R Stern

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. 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
2.6field-weighted citation impact, top 11% 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, 69 citations in OpenAlex.

  1. Hyaluronic Acid as a Modern Approach in Anticancer Therapy-Review.International journal of molecular sciences · 2022
    Review
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  6. A perspective on mammalian upstream open reading frame function.The international journal of biochemistry & cell biology · 2013
    Review
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  8. Article
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  13. Hyaluronan and hyaluronidase in genitourinary tumors.Frontiers in bioscience : a journal and virtual library · 2008
    Review
  14. Article
  15. Article
  16. Review
  17. Review
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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

6 authors at 2 institutions in 1 country.

G I FrostDepartment of Pathology, School of Medicine, University of California, San Francisco, California, CA 94143, USA.
G Mohapatra
T M Wong
A B Csóka
J W Gray
R Stern
University of California, San Francisco · USCancer Genetics (United States) · US

Funding

PILOT--TENASCIN AND ITS RECEPTOR IN ORAL CANCERP50DE011912 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI PALEFSKY, JOEL · 1996 to 2001
$1.3M
CELL AND MOLECULAR BASIS OF ORAL BIOLOGYT32DE007204 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI DAMSKY, CAROLINE H · 1989 to 2004
$818k
NIDCR NIH HHS P50 DE/CA11912NIDCR NIH HHS T32DE07204
6 · The paper itself

Abstract

The hyaluronidase first isolated from human plasma, Hyal-1, is expressed in many somatic tissues. The Hyal-1 gene, HYAL1, also known as LUCA-1, maps to chromosome 3p21.3 within a candidate tumor suppressor gene locus defined by homozygous deletions and by functional tumor suppressor activity. Hemizygosity in this region occurs in many malignancies, including squamous cell carcinomas of the head and neck. We have investigated whether cell lines derived from such malignancies expressed Hyal-1 activity, using normal human keratinocytes as controls. Hyal-1 enzyme activity and protein were absent or markedly reduced in six of seven carcinoma cell lines examined. Comparative genomic and fluorescence in situ hybridization identified chromosomal deletions of one allele of HYAL1 in six of seven cell lines. Initial RT - PCR analyses demonstrated marked discrepancies between levels of HYAL1 mRNA and protein. Despite repeated sequence analyses, no mutations were found. However, two species of transcripts were identified when primers were used that included the 5' untranslated region. The predominant mRNA species did not correlate with protein translation and contained a retained intron. A second spliced form lacking this intron was found only in cell lines that produced Hyal-1 protein. Inactivation of HYAL1 in these tumor lines is a result of incomplete splicing of its pre-mRNA that appears to be epigenetic in nature. Oncogene (2000) 19, 870 - 877.

Indexed as

Gene Expression Regulation, EnzymologicAlternative SplicingCarcinoma, Squamous CellCell LineChromosomes, Human, Pair 3DNA, ComplementaryEnzyme InductionExonsGene Expression RegulationGenes, Tumor SuppressorHead and Neck NeoplasmsHumansHyaluronoglucosaminidaseIntronsOpen Reading FramesPromoter Regions, GeneticDNA, ComplementaryHyaluronoglucosaminidaseRNA Precursors

Identifiers

PMID10702795
OpenAlexW2015736101

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.