ReviewCancer research2008
Conspirators in a capital crime: co-deletion of p18INK4c and p16INK4a/p14ARF/p15INK4b in glioblastoma multiforme.
Review in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Long non-coding PANDAR as a novel biomarker in human cancer: A systematic review.Cell proliferation · 2018Pooled it
- Genomic, epigenomic and transcriptomic landscape of glioblastoma.Metabolic brain disease · 2024Review
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Cyclin-dependent kinase inhibitors exert distinct effects on patient-derived 2D and 3D glioblastoma cell culture models.Cell death discovery · 2021Article
- Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.Cellular and molecular life sciences : CMLS · 2021Review
- Investigation of the Effect of 5-Aza-2'-Deoxycytidine in Comparison to and in Combination with Trichostatin A onInternational journal of preventive medicine · 2021Article
- Article
- Replication stress triggers microsatellite destabilization and hypermutation leading to clonal expansion in vitro.Nature communications · 2019Article
- Bayesian variable selection with graphical structure learning: Applications in integrative genomics.PloS one · 2018Article
- Review
- RNA processing as an alternative route to attack glioblastoma.Human genetics · 2017Review
- Bi-allelic inactivation is more prevalent at relapse in multiple myeloma, identifying RB1 as an independent prognostic marker.Blood cancer journal · 2017Article
- An essential role for Ink4 and Cip/Kip cell-cycle inhibitors in preventing replicative stress.Cell death and differentiation · 2016Article
- Discovery of novel INK4C small-molecule inhibitors to promote human and murine hematopoietic stem cell ex vivo expansion.Scientific reports · 2015Article
- Impact of meriolins, a new class of cyclin-dependent kinase inhibitors, on malignant glioma proliferation and neo-angiogenesis.Neuro-oncology · 2014Article
- Inactivation ofToxicology reports · 2014Article
- Prognostic and predictive biomarkers in adult and pediatric gliomas: toward personalized treatment.Frontiers in oncology · 2014Review
- Deregulated signaling pathways in glioblastoma multiforme: molecular mechanisms and therapeutic targets.Cancer investigation · 2012Review
- Contrasting behavior of the p18INK4c and p16INK4a tumor suppressors in both replicative and oncogene-induced senescence.Cancer research · 2012Article
- The prognostic value of Ki-67, p53, epidermal growth factor receptor, 1p36, 9p21, 10q23, and 17p13 in skull base chordomas.Archives of pathology & laboratory medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) is one of the most dreaded cancer diagnoses due to its poor prognosis and the limited treatment options. Homozygous deletion of the p16(INK4a)/p14(ARF)/p15(INK4b) locus is among the most common genetic alterations in GBM. Two recent studies have shown that deletion and mutation of another INK4 family member, p18(INK4c), also drives the pathogenesis of GBM. This minireview will discuss the known roles for p18(INK4c) in the initiation and progression of cancer and suggest opportunities for future studies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.