Genetic pathways to primary and secondary glioblastoma.

By H. Ohgaki, P. Kleihues. American Journal of Pathology, 2007

1,541 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/b4786941177335ef91077d5122b1a42a0311d92c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. H. Ohgaki
2. Gad Getz
3. P. Kleihues
4. Takuya Watanabe
5. S. Nobusawa
6. R. Jenkins
7. McKinsey L. Goodenberger
8. Eric S. Lander

In Genetics

1. H. Ohgaki
2. P. Kleihues
3. R. Jenkins
4. McKinsey L. Goodenberger
5. Peter W. Laird
6. S. Baylin
7. Takuya Watanabe
8. S. Nobusawa

In Pathology and Forensic Medicine

1. H. Ohgaki
2. P. Kleihues
3. John N. Weinstein
4. Peter W. Laird
5. David Haussler
6. S. Baylin

Citations in the corpus

• Mutual exclusivity analysis identifies oncogenic network modules. (2012, background): “These modules recapitulate findings from TCGA and earlier studies that glioblastomas nearly universally circumvent cell cycle inhibition through genetic alterations to the Rb pathway (Ohgaki and Kleihues 2007; The Cancer Genome Atlas Research Network 2008).”
• The Somatic Genomic Landscape of Glioblastoma (2013, background): “33 10 (4), respectively), tumors genotypically more consistent with secondary GBM (Ohgaki and Kleihues, 2007).”
• IDH1 Mutations as Molecular Signature and Predictive Factor of Secondary Glioblastomas (2009, background): “These glioblastoma subtypes constitute distinct disease entities that affect patients of different age, and develop through different genetic pathways (2, 3).”
• Genetics of adult glioma. (2012, background): “The majority of diffuse astrocytomas arise because of early concomitant mutations in IDH1, TP53, and ATRX (28,41,52).”
• The brain tumor microenvironment (2011, background): “It is well established that primary glioblastoma are diagnosed mainly in older patients and are virtually unknown in infants (Ohgaki and Kleihues, 2007).”
• Brain Tumor Epidemiology: Consensus from the Brain Tumor Epidemiology Consortium (BTEC) (2008, background): “There is a very strong and consistent, inverse correlation between age and survival for the various histologic subtypes of glioma (www.cbtrus.org accessed March 1, 2008), and younger patients benefit more from radiation therapy than older patients.164 In addition, combined loss of chromosomes 1p and”
• Automated Network Analysis Identifies Core Pathways in Glioblastoma (2010, background): “Prognosis for glioblastoma patients remains dismal, as most patients die within one year after diagnosis [3] and generally respond poorly to current therapeutic approaches [4,5].”
• Epidemiologic and Molecular Prognostic Review of Glioblastoma (2014, background): “Primary GBMs show EGFR overexpression, phosphatase and tensin homolog gene (PTEN) mutations, loss of heterozygosity (LOH) 10q, p16 deletions, less frequently mouse doubleminute 2 (MDM2) amplification, high frequency of telomerase reverse transcriptase (hTERT) promoter mutations and absence of IDH1 m”
• Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. (2010, background): “Overall, secondary GBMs have a higher frequency of promoter methylation than primary GBM (Ohgaki and Kleihues, 2007).”
• The Definition of Primary and Secondary Glioblastoma (2012, background): “Subsequently,many studies provided evidence that primary and secondary glioblastomas develop through distinct genetic pathways (6, 7).”