Evidence map›Paper›PMID 11296287›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Candidate tumor suppressor HYAL2 is a glycosylphosphatidylinositol (GPI)-anchored cell-surface receptor for jaagsiekte sheep retrovirus, the envelope protein of which mediates oncogenic transformation.

S K Rai, F M Duh, V Vigdorovich, A Danilkovitch-Miagkova, M I Lerman, A D Miller

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
33.3field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 328 citations in OpenAlex.

  1. Article
  2. The association between blood-basedLung cancer management · 2025
    Article
  3. Hyaluronan: An Architect and Integrator for Cancer and Neural Diseases.International journal of molecular sciences · 2025
    Review
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  14. Elucidating the clinical spectrum and molecular basis of HYAL2 deficiency.Genetics in medicine : official journal of the American College of Medical Genetics · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

85 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

S K RaiFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
F M Duh
V Vigdorovich
A Danilkovitch-Miagkova
M I Lerman
A D Miller
Science Applications International Corporation (United States) · USCancer Research Center · USFred Hutch Cancer Center · US

Funding

OPERATIONS &TECHNICAL SUPPORTN01CO056000 · CO · SCIENCE APPLICATIONS INTERNATIONAL CORP · PI FISCHINGER, PETER J · 1995 to 2000
$95.0M
TRANSDUCTION OF BABOON HEMATOPOIETIC STEM CELLSP50HL054881 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BERNSTEIN, IRWIN · 1995 to 2004
$11.0M
PILOT STUDY--RETROVIRUS MEDIATED TRANSFER OF HUMAN GLUCOCEREBROSIDASE GENEP30DK047754 · NIDDK · UNIVERSITY OF WASHINGTON · PI WILSON, CHRISTOPHER B. · 1994 to 2008
$8.4M
NCI NIH HHS CO56000NHLBI NIH HHS HL54881NHLBI NIH HHS P50 HL054881NIDDK NIH HHS DK47754NIDDK NIH HHS P30 DK047754
6 · The paper itself

Abstract

Jaagsiekte sheep retrovirus (JSRV) can induce rapid, multifocal lung cancer, but JSRV is a simple retrovirus having no known oncogenes. Here we show that the envelope (env) gene of JSRV has the unusual property that it can induce transformation in rat fibroblasts, and thus is likely to be responsible for oncogenesis in animals. Retrovirus entry into cells is mediated by Env interaction with particular cell-surface receptors, and we have used phenotypic screening of radiation hybrid cell lines to identify the candidate lung cancer tumor suppressor HYAL2/LUCA2 as the receptor for JSRV. HYAL2 was previously described as a lysosomal hyaluronidase, but we show that HYAL2 is actually a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein. Furthermore, we could not detect hyaluronidase activity associated with or secreted by cells expressing HYAL2, whereas we could easily detect such activity from cells expressing the related serum hyaluronidase HYAL1. Although the function of HYAL2 is currently unknown, other GPI-anchored proteins are involved in signal transduction, and some mediate mitogenic responses, suggesting a potential role of HYAL2 in JSRV Env-mediated oncogenesis. Lung cancer induced by JSRV closely resembles human bronchiolo-alveolar carcinoma, a disease that is increasing in frequency and now accounts for approximately 25% of all lung cancer. The finding that JSRV env is oncogenic and the identification of HYAL2 as the JSRV receptor provide tools for further investigation of the mechanism of JSRV oncogenesis and its relationship to human bronchiolo-alveolar carcinoma.

Indexed as

Cell Transformation, NeoplasticGenes, Tumor SuppressorMembrane FusionCarcinoma, Small CellCell Transformation, ViralGenes, envGlycosylphosphatidylinositolsHumansHyaluronoglucosaminidaseJaagsiekte sheep retrovirusLung NeoplasmsPhosphatidylinositol Diacylglycerol-LyaseTumor Cells, CulturedType C PhospholipasesGlycosylphosphatidylinositolsHyaluronoglucosaminidasePhosphatidylinositol Diacylglycerol-LyaseType C Phospholipases

Identifiers

PMID11296287
PMCPMC31854
OpenAlexW2107214690

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.