{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,6]],"date-time":"2026-06-06T09:01:15Z","timestamp":1780736475527,"version":"3.54.1"},"reference-count":116,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["FOC"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:sec>\n                    <jats:title>Object<\/jats:title>\n                    <jats:p>Meningiomas are among the most common primary adult brain tumors. Although typically benign, roughly 2%\u20135% display malignant pathological features. The key molecular pathways involved in malignant transformation remain to be determined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Illumina expression microarrays were used to assess gene expression levels, and Illumina single-nucleotide polymorphism arrays were used to identify copy number variants in benign, atypical, and malignant meningiomas (19 tumors, including 4 malignant ones). The authors also reanalyzed 2 expression data sets generated on Affymetrix microarrays (n = 68, including 6 malignant ones; n = 56, including 3 malignant ones). A weighted gene coexpression network approach was used to identify coexpression modules associated with malignancy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At the genomic level, malignant meningiomas had more chromosomal losses than atypical and benign meningiomas, with average length of 528, 203, and 34 megabases, respectively. Monosomic loss of chromosome 22 was confirmed to be one of the primary chromosomal level abnormalities in all subtypes of meningiomas. At the transcriptome level, the authors identified 23 coexpression modules from the weighted gene coexpression network. Gene functional enrichment analysis highlighted a module with 356 genes that was highly related to tumorigenesis. Four intramodular hubs within the module (\n                      <jats:italic>GAB2, KLF2, ID1,<\/jats:italic>\n                      and\n                      <jats:italic>CTF1<\/jats:italic>\n                      ) were oncogenic in other cancers such as leukemia. A putative meningioma tumor suppressor\n                      <jats:italic>MN1<\/jats:italic>\n                      was also identified in this module with differential expression between malignant and benign meningiomas.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The authors' genomic and transcriptome analysis of meningiomas provides novel insights into the molecular pathways involved in malignant transformation of meningiomas, with implications for molecular heterogeneity of the disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3171\/2013.10.focus13326","type":"journal-article","created":{"date-parts":[[2013,12,1]],"date-time":"2013-12-01T03:33:23Z","timestamp":1385868803000},"page":"E3","source":"Crossref","is-referenced-by-count":19,"title":["Genomic and transcriptome analysis revealing an oncogenic functional module in meningiomas"],"prefix":"10.3171","volume":"35","author":[{"given":"Xiao","family":"Chang","sequence":"first","affiliation":[{"name":"Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingling","family":"Shi","sequence":"additional","affiliation":[{"name":"GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Gao","sequence":"additional","affiliation":[{"name":"Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Russin","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liyun","family":"Zeng","sequence":"additional","affiliation":[{"name":"Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuhan","family":"He","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas C.","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven L.","family":"Giannotta","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Weisenberger","sequence":"additional","affiliation":[{"name":"USC Epigenome Center, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel","family":"Zada","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Wang","sequence":"additional","affiliation":[{"name":"Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California;"},{"name":"Department of Psychiatry, Keck School of Medicine, University of Southern California, Los Angeles, California; and"},{"name":"Division of Bioinformatics, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William J.","family":"Mack","sequence":"additional","affiliation":[{"name":"Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California;"},{"name":"Department of Neurosurgery, Keck School of Medicine, University of Southern California, Los Angeles, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1-0350003","series-title":"BMC Bioinformatics","first-page":"2","article-title":"An automated method for finding molecular complexes in large protein interaction networks","volume":"4","author":"Bader","year":"2003"},{"key":"b2-0350003","series-title":"Nat Rev Genet","first-page":"101","article-title":"Network biology: understanding the cell's functional 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