Evidence map›Paper›PMID 18394558›Full record

ArticleCancer cell2008

Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development.

Ruprecht Wiedemeyer, Cameron Brennan, Timothy P Heffernan, Yonghong Xiao, John Mahoney, Alexei Protopopov, Hongwu Zheng, Graham Bignell, Frank Furnari, Webster K Cavenee and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.1field-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

75 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Kidney inflammaging is promoted by CCR2Cellular and molecular life sciences : CMLS · 2021
    Article
  6. Article
  7. Article
  8. HeterogeneousCancers · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Forging a signature of in vivo senescence.Nature reviews. Cancer · 2015
    Review
  15. Article
  16. Article
  17. Article
  18. Epigenetic setting and reprogramming for neural cell fate determination and differentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  19. Article
  20. Article

15 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

18 authors at 7 institutions in 2 countries.

Ruprecht WiedemeyerDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.
Cameron Brennan
Timothy P Heffernan
Yonghong Xiao
John Mahoney
Alexei Protopopov
Hongwu Zheng
Graham Bignell
Frank Furnari
Webster K Cavenee
William C Hahn
Koichi Ichimura
V Peter Collins
Gerald C Chu
Michael R Stratton
Keith L Ligon
P Andrew Futreal
Lynda Chin
Harvard University · USDana-Farber Cancer Institute · USWellcome Sanger Institute · GBLudwig Cancer Research · USUniversity of Cambridge · GBBrigham and Women's Hospital · USCornell University · US

Funding

Transgenic Mouse and Biobank CoreP01CA095616 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2003 to 2012
$20.3M
DERMATOLOGY TRAINING GRANTT32AR007098 · NIAMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI THOMAS S. KUPPER · 1986 to 2026
$8.1M
Genomic &Genetic Characterization of Amplicons in GBMsR01CA099041 · NCI · DANA-FARBER CANCER INSTITUTE · PI CHIN, LYNDA · 2003 to 2007
$1.5M
NCI NIH HHS P01 CA095616NCI NIH HHS P01CA95616NCI NIH HHS R01 CA099041NCI NIH HHS R01CA99041NIAMS NIH HHS T32 AR007098Wellcome Trust
6 · The paper itself

Abstract

We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion. Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C). Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.

Indexed as

Feedback, PhysiologicalAnimalsAstrocytesCell Line, TumorCells, CulturedCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Gene DeletionGene DosageGene Expression Regulation, NeoplasticGenome, HumanGlioblastomaHumansMiceUp-RegulationCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18

Identifiers

PMID18394558
PMCPMC2292238
OpenAlexW2123845663

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.