Evidence map›Paper›PMID 24676140›Full record

ArticleNeuro-oncology2014

Survivin transcript variant 2 drives angiogenesis and malignant progression in proneural gliomas.

Tiffany Doucette, Khatri Latha, Yuhui Yang, Gregory N Fuller, Arvind Rao, Ganesh Rao

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Survivin: a unique target for tumor therapy.Cancer cell international · 2016
    Review
  8. Article
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 1 institution in 1 country.

Tiffany DoucetteDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
Khatri LathaDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
Yuhui YangDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
Gregory N FullerDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
Arvind RaoDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
Ganesh RaoDepartment of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, Texas (T.D., L.K., Y.Y., G.R.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (G.N.F.); Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas (A.R.).
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Modeling Apoptotic Suppression in a Mouse Model of Brain TumorsK08NS070928 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RAO, GANESH · 2011 to 2015
$913k
NCI NIH HHS P30 CA016672NINDS NIH HHS K08 NS070928
6 · The paper itself

Abstract

backgroundThe influence of survivin isoforms on outcome in glioblastoma is poorly understood. We analyzed the dominant anti-apoptotic transcript variants of survivin using expression data and modeled them in vivo to determine their impact on glioma formation and progression.

methodsUsing data from low- and high-grade glioma knowledge bases, we expressed the anti-apoptotic isoforms of survivin (transcript variants 1 and 2) in vivo using the RCAS/Ntv-a model of murine glioma.

resultsIn low-grade gliomas, survivin RNA expression was increased in 22 of 167 (13.2%) of cases and was associated with shortened survival (P = .005). Survivin RNA was preferentially expressed in proneural (PN) relative to mesenchymal high-grade gliomas (P < .0001). In proneural gliomas, survivin was expressed in 94 of 141 (67%) of cases and was associated with shorter disease-free survival (P = .04). In a platelet-derived growth factor subunit B-dependent murine model of PN glioma, ectopic expression of variant 1 yielded tumors in 28 of 30 (93%) of mice, of which 25% were high-grade tumors, whereas ectopic expression of variant 2 yielded tumors in 27 of 28 (96%), of which 81% were high-grade tumors (P < .0001). Microvascular proliferation was significantly more prominent (P < .0001), and tumor-free survival was shorter in mice with variant 2 than variant 1-derived tumors (P = .01).

conclusionsSurvivin expression in low-grade gliomas is associated with poor survival and is preferentially expressed in PN gliomas. Compared with variant 1, variant 2 was associated with poorer survival and promoted malignant progression, angiogenesis, and shorter tumor-free survival in the PN murine model. Inhibiting survivin transcript variant 2, rather than variant 1 (the common isoform), may be an effective treatment strategy for glioma.

Indexed as

Disease ProgressionNeovascularization, PathologicAnimalsBrain NeoplasmsDatabases, FactualGliomaHumansInhibitor of Apoptosis ProteinsKaplan-Meier EstimateMiceMice, TransgenicProtein IsoformsSurvivinBIRC5 protein, humanInhibitor of Apoptosis ProteinsProtein IsoformsSurvivinangiogenesisapoptosisgliomasurvivin

Identifiers

PMID24676140
PMCPMC4136894
OpenAlexW2161210227

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.