Evidence map›Paper›PMID 19920201›Full record

ArticleCancer research2009

Glioblastoma proto-oncogene SEC61gamma is required for tumor cell survival and response to endoplasmic reticulum stress.

Zheming Lu, Lei Zhou, Patrick Killela, Ahmed B Rasheed, Chunhui Di, William E Poe, Roger E McLendon, Darell D Bigner, Christopher Nicchitta, Hai Yan

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
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  6. Article
  7. HighOpen medicine (Warsaw, Poland) · 2024
    Article
  8. Article
  9. SEC61G assistsProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  11. Article
  12. Article
  13. 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

10 authors at 5 institutions in 2 countries.

Zheming LuDepartment of Pathology, The Pediatric Brain Tumor Foundation Institute, Duke University Medical Center, Durham, North Carolina 27710, USA.
Lei Zhou
Patrick Killela
Ahmed B Rasheed
Chunhui Di
William E Poe
Roger E McLendon
Darell D Bigner
Christopher Nicchitta
Hai Yan
Pediatric Brain Tumor Foundation · USDuke University Hospital · USPeking University · CNPeking University Cancer Hospital · CNUniversity of Florida · US

Funding

TUMOR SUPPRESSOR GENES IN HUMAN MEDULLOBLASTOMAP50NS020023 · NINDS · DUKE UNIVERSITY · PI BIGNER, DARELL D · 1985 to 2013
$17.3M
TEMODAR RESISTANCE IN CENTRAL NERVOUS SYSTEMP50CA108786 · NCI · DUKE UNIVERSITY · PI BIGNER, DARELL D · 2004 to 2009
$12.3M
BRAIN TUMORS: IMMUNOLOGICAL AND BIOLOGICAL STUDIESR37CA011898 · NCI · DUKE UNIVERSITY · PI BIGNER, DARELL D · 1988 to 2012
$8.1M
The Role of OTX2 in Molecular Pathogenesis of MedulloblastomaR01CA118822 · NCI · DUKE UNIVERSITY · PI YAN, HAI · 2006 to 2010
$1.2M
NCI NIH HHS 5P50 CA108786NCI NIH HHS P50 CA108786NCI NIH HHS R01 CA118822NCI NIH HHS R01CA118822NCI NIH HHS R37 CA 011898NCI NIH HHS R37 CA011898NINDS NIH HHS 5P50 NS20023NINDS NIH HHS P50 NS020023
6 · The paper itself

Abstract

Glioblastoma multiforme is the most prevalent type of adult brain tumor and one of the deadliest tumors known to mankind. The genetic understanding of glioblastoma multiforme is, however, limited, and the molecular mechanisms that facilitate glioblastoma multiforme cell survival and growth within the tumor microenvironment are largely unknown. We applied digital karyotyping and single nucleotide polymorphism arrays to screen for copy-number changes in glioblastoma multiforme samples and found that the most frequently amplified region is at chromosome 7p11.2. The high resolution of digital karyotyping and single nucleotide polymorphism arrays permits the precise delineation of amplicon boundaries and has enabled identification of the minimal region of amplification at chromosome 7p11.2, which contains two genes, EGFR and SEC61gamma. SEC61gamma encodes a subunit of a heterotrimeric protein channel located in the endoplasmic reticulum (ER). In addition to its high frequency of gene amplification in glioblastoma multiforme, SEC61gamma is also remarkably overexpressed in 77% of glioblastoma multiforme but not in lower-grade gliomas. The small interfering RNA-mediated knockdown of SEC61gamma expression in tumor cells led to growth suppression and apoptosis. Furthermore, we showed that pharmacologic ER stress agents induce SEC61gamma expression in glioblastoma multiforme cells. Together, these results indicate that aberrant expression of SEC61gamma serves significant roles in glioblastoma multiforme cell survival likely via a mechanism that is involved in the cytoprotective ER stress-adaptive response to the tumor microenvironment.

Indexed as

Brain NeoplasmsCell Growth ProcessesEndoplasmic ReticulumErbB ReceptorsGene AmplificationGenes, erbB-1GlioblastomaHeLa CellsHumansMembrane ProteinsProto-Oncogene MasRNA, Small InterferingSEC Translocation ChannelsTunicamycinErbB ReceptorsMAS1 protein, humanMembrane ProteinsProto-Oncogene MasRNA, Small InterferingSEC61G protein, humanSEC Translocation ChannelsTunicamycin

Identifiers

PMID19920201
PMCPMC2789175
OpenAlexW2152095920

What OpenQuestion holds

Textmetadata
LicenceTDM
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.