Evidence map›Paper›PMID 22067563›Full record

ArticleNeuro-oncology2012

Maintenance of primary tumor phenotype and genotype in glioblastoma stem cells.

Hiroaki Wakimoto, Gayatry Mohapatra, Ryuichi Kanai, William T Curry, Stephen Yip, Mai Nitta, Anoop P Patel, Zachary R Barnard, Anat O Stemmer-Rachamimov, David N Louis and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

171 citing papers in PubMed, 237 citations in OpenAlex.

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  9. Wnt inhibition alleviates resistance to anti-PD1 therapy and improves antitumor immunity in glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2025
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111 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Hiroaki WakimotoDepartment of Neurosurgery, Massachusetts General Hospital, Boston, MA 02114, USA. hwakimoto@partners.org
Gayatry Mohapatra
Ryuichi Kanai
William T Curry
Stephen Yip
Mai Nitta
Anoop P Patel
Zachary R Barnard
Anat O Stemmer-Rachamimov
David N Louis
Robert L Martuza
Samuel D Rabkin
Harvard University · USBC Cancer Agency · CACenter for Cancer Research · USMassachusetts General Hospital · US

Funding

Vector Query and Therapy For TSC and NF2 LesionsP01NS024279 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KWIATKOWSKI, DAVID J. · 1987 to 2012
$14.7M
GENETICALLY ENGINEERED VIRUSES FOR BRAIN TUMOR THERAPYR01NS032677 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MARTUZA, ROBERT L · 1994 to 2022
$9.0M
TOWARD A MOLECULAR CLASSIFICATION OF HUMAN GLIOMASR01CA057683 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LOUIS, DAVID N · 1992 to 2013
$4.7M
Profiling and targeting micro-RNA expression during oncolytic virotherapyR21NS067541 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI FULCI, GIULIA, WAKIMOTO, HIROAKI · 2009 to 2010
$481k
NCI NIH HHS R01CA57683NINDS NIH HHS P01NS024279NINDS NIH HHS R01 NS032677NINDS NIH HHS R01NS032677NINDS NIH HHS R21NS067541
6 · The paper itself

Abstract

The clinicopathological heterogeneity of glioblastoma (GBM) and the various genetic and phenotypic subtypes in GBM stem cells (GSCs) are well described. However, the relationship between GSCs and the corresponding primary tumor from which they were isolated is poorly understood. We have established GSC-enriched neurosphere cultures from 15 newly diagnosed GBM specimens and examined the relationship between the histopathological and genomic features of GSC-derived orthotopic xenografts and those of the respective patient tumors. GSC-initiated xenografts recapitulate the distinctive cytological hallmarks and diverse histological variants associated with the corresponding patient GBM, including giant cell and gemistocytic GBM, and primitive neuroectodermal tumor (PNET)-like components. This indicates that GSCs generate tumors that preserve patient-specific disease phenotypes. The majority of GSC-derived intracerebral xenografts (11 of 15) demonstrated a highly invasive behavior crossing the midline, whereas the remainder formed discrete nodular and vascular masses. In some cases, GSC invasiveness correlated with preoperative MRI, but not with the status of PI3-kinase/Akt pathways or O(6)-methylguanine methyltransferase expression. Genome-wide screening by array comparative genomic hybridization and fluorescence in situ hybridization revealed that GSCs harbor unique genetic copy number aberrations. GSCs acquiring amplifications of the myc family genes represent only a minority of tumor cells within the original patient tumors. Thus, GSCs are a genetically distinct subpopulation of neoplastic cells within a GBM. These studies highlight the value of GSCs for preclinical modeling of clinically relevant, patient-specific GBM and, thus, pave the way for testing novel anti-GSC/GBM agents for personalized therapy.

Indexed as

AnimalsBrain NeoplasmsCell DifferentiationFemaleGenotypeGlioblastomaHumansImmunohistochemistryMiceMice, SCIDNeoplasm InvasivenessNeoplastic Stem CellsPhenotypeProto-Oncogene Proteins c-aktTransplantation, HeterologousTumor Cells, CulturedProto-Oncogene Proteins c-akt

Identifiers

PMID22067563
PMCPMC3266381
OpenAlexW2123369892

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.