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n2:pmcid: PMC0
bibo:doi: 10.1016%2Fj.gendis.2015.02.001
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Subject Item: _:vb42265856
rdf:type: n4:Section
dc:title: introduction
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Subject Item: _:vb42265857
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rdf:value: Glioblastoma multiforme (GBM) comprises the largest group of brain tumors which respond very poorly to current therapies.>>1<< In the United States, approximately 13,000 people die annually from GBM, and it is disappointing that only about 10% of patients survive 5 years.
n2:mentions: n3:15661684

Subject Item: _:vb42265858
rdf:type: n2:Context
rdf:value: comprises the largest group of brain tumors which respond very poorly to current therapies.1 In the United States, approximately 13,000 people die annually from GBM, and it is disappointing that only about 10% of patients survive 5 years.>>2<<, 3, 4 The combination of radiotherapy and adjunct temozolomide (TMZ) has increased the survival of patients with GBM, but the median survival of GBM patients is only about 14.6 months.
n2:mentions: n3:19269895

Subject Item: _:vb42265859
rdf:type: n2:Context
rdf:value: the largest group of brain tumors which respond very poorly to current therapies.1 In the United States, approximately 13,000 people die annually from GBM, and it is disappointing that only about 10% of patients survive 5 years.2, >>3<<, 4 The combination of radiotherapy and adjunct temozolomide (TMZ) has increased the survival of patients with GBM, but the median survival of GBM patients is only about 14.6 months.
n2:mentions: n3:15041700

Subject Item: _:vb42265860
rdf:type: n2:Context
rdf:value: the largest group of brain tumors which respond very poorly to current therapies.1 In the United States, approximately 13,000 people die annually from GBM, and it is disappointing that only about 10% of patients survive 5 years.2, 3, >>4<< The combination of radiotherapy and adjunct temozolomide (TMZ) has increased the survival of patients with GBM, but the median survival of GBM patients is only about 14.6 months.
n2:mentions: n3:15758010

Subject Item: _:vb42265861
rdf:type: n2:Context
rdf:value: that only about 10% of patients survive 5 years.2, 3, 4 The combination of radiotherapy and adjunct temozolomide (TMZ) has increased the survival of patients with GBM, but the median survival of GBM patients is only about 14.6 months.>>5<< The highly aggressive nature of GBM is due to multiple genetic alterations which result in augmented cytoprotective and survival pathways as well as numerous defects in the apoptotic signaling machinery and epigenetic alterations (Fig.
n2:mentions: n3:15758009

Subject Item: _:vb42265862
rdf:type: n2:Context
rdf:value: Modified from Masui et al.>>15<<B. Epigenetic changes in GBM. Numerous molecular alterations shown in this figure and described in the text occur in primary GBM.
n2:mentions: n3:22098029

Subject Item: _:vb42265863
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rdf:value: Mutation of IDH1 leads to aberrant DNA methylation and mutations in the important chromatin modifier ATRX, affecting chromatin structure. Figure was modified from Kondo et al.>>16<<
n2:mentions: n3:24843883

Subject Item: _:vb42265864
rdf:type: n2:Context
rdf:value: A growing body of evidence indicates that rare populations of cancer cells, termed cancer stem cells (CSCs) or cancer initiating cells (CICs), play a significant role in several cancers, including GBM.>>6<<, 7, 8 GBM tumors display high degree of phenotypic, cellular, genetic, and epigenetic heterogeneity, and it is believed that a major problem in the unresponsiveness of GBM tumors to therapy is the existence of GBM stem cells (GSCs) within
n2:mentions: n3:15549107

Subject Item: _:vb42265865
rdf:type: n2:Context
rdf:value: A growing body of evidence indicates that rare populations of cancer cells, termed cancer stem cells (CSCs) or cancer initiating cells (CICs), play a significant role in several cancers, including GBM.6, >>7<<, 8 GBM tumors display high degree of phenotypic, cellular, genetic, and epigenetic heterogeneity, and it is believed that a major problem in the unresponsiveness of GBM tumors to therapy is the existence of GBM stem cells (GSCs) within
n2:mentions: n3:24615680

Subject Item: _:vb42265866
rdf:type: n2:Context
rdf:value: A growing body of evidence indicates that rare populations of cancer cells, termed cancer stem cells (CSCs) or cancer initiating cells (CICs), play a significant role in several cancers, including GBM.6, 7, >>8<< GBM tumors display high degree of phenotypic, cellular, genetic, and epigenetic heterogeneity, and it is believed that a major problem in the unresponsiveness of GBM tumors to therapy is the existence of GBM stem cells (GSCs) within the
n2:mentions: n3:24152818

Subject Item: _:vb42265867
rdf:type: n2:Context
rdf:value: heterogeneity, and it is believed that a major problem in the unresponsiveness of GBM tumors to therapy is the existence of GBM stem cells (GSCs) within the tumor which are most crucial for driving invasive tumor growth and relapse.>>6<<, 9 Emerging results have revealed that in GBM and other malignancies, CSC enrichment may occur either from an increased symmetric self-renewal division rate of CSCs or a reprogramming of non-CSC to CSCs and conferring phenotypic
n2:mentions: n3:15549107

Subject Item: _:vb42265868
rdf:type: n2:Context
rdf:value: heterogeneity, and it is believed that a major problem in the unresponsiveness of GBM tumors to therapy is the existence of GBM stem cells (GSCs) within the tumor which are most crucial for driving invasive tumor growth and relapse.6, >>9<< Emerging results have revealed that in GBM and other malignancies, CSC enrichment may occur either from an increased symmetric self-renewal division rate of CSCs or a reprogramming of non-CSC to CSCs and conferring phenotypic plasticity
n2:mentions: n3:25504149

Subject Item: _:vb42265869
rdf:type: n4:Section
dc:title: epigenetic therapy
n4:contains: _:vb42265872 _:vb42265873 _:vb42265874 _:vb42265875 _:vb42265876 _:vb42265877 _:vb42265878 _:vb42265879 _:vb42265870 _:vb42265871

Subject Item: _:vb42265870
rdf:type: n2:Context
rdf:value: (EGFR) gene are frequently found in GBM. The most common variant is EGFR variant III (EGFRvIII) and this variant could be a marker for GSCs showing that epigenetic mechanisms have a role in maintaining heterogeneous EGFRvIII expression.>>116<< Demethylation induced a 20%–60% increase in the percentage of EGFRvIII-positive cells, indicating that some cells could re-express EGFRvIII.
n2:mentions: n3:22797070

Subject Item: _:vb42265871
rdf:type: n2:Context
rdf:value: Interestingly, inhibition of histone deacetylation resulted in a 50%–80% reduction in EGFRvIII expression.>>116<<
n2:mentions: n3:22797070

Subject Item: _:vb42265872
rdf:type: n2:Context
rdf:value: Two main features of cancer are aberrant gene function and altered patterns of gene expression, and evidence shows that epigenetic changes in collaboration with genetic alterations cause dysregulation in cancer.>>117<<, 118 However, the epigenetic changes in cancer are potentially reversible, and treating CSCs with demethylating agents or HDAC inhibitors may potentially reactivate silenced tumor suppressor and TF genes.
n2:mentions: n3:17320506

Subject Item: _:vb42265873
rdf:type: n2:Context
rdf:value: Two main features of cancer are aberrant gene function and altered patterns of gene expression, and evidence shows that epigenetic changes in collaboration with genetic alterations cause dysregulation in cancer.117, >>118<< However, the epigenetic changes in cancer are potentially reversible, and treating CSCs with demethylating agents or HDAC inhibitors may potentially reactivate silenced tumor suppressor and TF genes.
n2:mentions: n3:11257100

Subject Item: _:vb42265874
rdf:type: n2:Context
rdf:value: dysregulation in cancer.117, 118 However, the epigenetic changes in cancer are potentially reversible, and treating CSCs with demethylating agents or HDAC inhibitors may potentially reactivate silenced tumor suppressor and TF genes.>>118<< The DNA methyltransferase (DNMT) inhibitor 5-azacytidine is an effective anticancer agent and inhibitor of GSCs.
n2:mentions: n3:11257100

Subject Item: _:vb42265875
rdf:type: n2:Context
rdf:value: CSCs with demethylating agents or HDAC inhibitors may potentially reactivate silenced tumor suppressor and TF genes.118 The DNA methyltransferase (DNMT) inhibitor 5-azacytidine is an effective anticancer agent and inhibitor of GSCs.>>119<<, 120, 121 Another class of epigenetic inhibitors are HDAC inhibitors. HDACs are a family of 18 deacetylating enzymes that remove acetyl groups from lysine residues of histone proteins and other proteins including TFs.
n2:mentions: n3:12154409

Subject Item: _:vb42265876
rdf:type: n2:Context
rdf:value: with demethylating agents or HDAC inhibitors may potentially reactivate silenced tumor suppressor and TF genes.118 The DNA methyltransferase (DNMT) inhibitor 5-azacytidine is an effective anticancer agent and inhibitor of GSCs.119, >>120<<, 121 Another class of epigenetic inhibitors are HDAC inhibitors. HDACs are a family of 18 deacetylating enzymes that remove acetyl groups from lysine residues of histone proteins and other proteins including TFs.
n2:mentions: n3:21572997

Subject Item: _:vb42265877
rdf:type: n2:Context
rdf:value: 119, 120, >>121<< Another class of epigenetic inhibitors are HDAC inhibitors. HDACs are a family of 18 deacetylating enzymes that remove acetyl groups from lysine residues of histone proteins and other proteins including TFs.
n2:mentions: n3:24633350

Subject Item: _:vb42265878
rdf:type: n2:Context
rdf:value: of GSCs.119, 120, 121 Another class of epigenetic inhibitors are HDAC inhibitors. HDACs are a family of 18 deacetylating enzymes that remove acetyl groups from lysine residues of histone proteins and other proteins including TFs.>>122<< HDACs regulate the conformation and activity of chromatin and mostly function as transcriptional co-repressors as part of large multi-protein complexes.
n2:mentions: n3:18824292

Subject Item: _:vb42265879
rdf:type: n2:Context
rdf:value: 122 HDACs regulate the conformation and activity of chromatin and mostly function as transcriptional co-repressors as part of large multi-protein complexes.>>122<< HDAC inhibitors and DNA damaging agents synergistically inhibit the growth and induce apoptosis in GSC cells possibly because they promote an open chromatin conformation and allow more effective access of DNA damaging agents to the
n2:mentions: n3:18824292

Subject Item: _:vb42265880
rdf:type: n4:Section
dc:title: glioblastoma multiforme (gbm)
n4:contains: _:vb42265884 _:vb42265885 _:vb42265886 _:vb42265887 _:vb42265881 _:vb42265882 _:vb42265883 _:vb42265892 _:vb42265893 _:vb42265894 _:vb42265895 _:vb42265888 _:vb42265889 _:vb42265890 _:vb42265891 _:vb42265900 _:vb42265901 _:vb42265902 _:vb42265903 _:vb42265896 _:vb42265897 _:vb42265898 _:vb42265899 _:vb42265904

Subject Item: _:vb42265881
rdf:type: n2:Context
rdf:value: GBM comprises the most common and very aggressive form of primary brain tumors which respond very poorly to the current therapies.>>1<<, 2 This most malignant brain tumor is designated as World Health Organization (WHO) grade IV astrocytoma which expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).
n2:mentions: n3:15661684

Subject Item: _:vb42265882
rdf:type: n2:Context
rdf:value: GBM comprises the most common and very aggressive form of primary brain tumors which respond very poorly to the current therapies.1, >>2<< This most malignant brain tumor is designated as World Health Organization (WHO) grade IV astrocytoma which expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).
n2:mentions: n3:19269895

Subject Item: _:vb42265883
rdf:type: n2:Context
rdf:value: which respond very poorly to the current therapies.1, 2 This most malignant brain tumor is designated as World Health Organization (WHO) grade IV astrocytoma which expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).>>11<<, 12, 13, 14 Initiation and recurrence of primary GBM may be caused by a subpopulation of GSCs which may derive from mutated neural stem and precursor cells.
n2:mentions: n3:17618441

Subject Item: _:vb42265884
rdf:type: n2:Context
rdf:value: respond very poorly to the current therapies.1, 2 This most malignant brain tumor is designated as World Health Organization (WHO) grade IV astrocytoma which expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).11, 12, >>13<<, 14 Initiation and recurrence of primary GBM may be caused by a subpopulation of GSCs which may derive from mutated neural stem and precursor cells.
n2:mentions: n3:4091041

Subject Item: _:vb42265885
rdf:type: n2:Context
rdf:value: which expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).11, 12, 13, 14 Initiation and recurrence of primary GBM may be caused by a subpopulation of GSCs which may derive from mutated neural stem and precursor cells.>>8<<, 9, 10, 11, 12, 13, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig.
n2:mentions: n3:24152818

Subject Item: _:vb42265886
rdf:type: n2:Context
rdf:value: expresses the astrocyte marker, glial fibrillary acidic protein (GFAP).11, 12, 13, 14 Initiation and recurrence of primary GBM may be caused by a subpopulation of GSCs which may derive from mutated neural stem and precursor cells.8, >>9<<, 10, 11, 12, 13, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig.
n2:mentions: n3:25504149

Subject Item: _:vb42265887
rdf:type: n2:Context
rdf:value: 8, 9, 10, >>11<<, 12, 13, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig.
n2:mentions: n3:17618441

Subject Item: _:vb42265888
rdf:type: n2:Context
rdf:value: 8, 9, 10, 11, 12, >>13<<, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig.
n2:mentions: n3:4091041

Subject Item: _:vb42265889
rdf:type: n2:Context
rdf:value: cells.8, 9, 10, 11, 12, 13, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig. 1). While primary and secondary GBM's are histologically similar, they are genetically different.>>15<<, 16 Primary GBM frequently displays molecular alterations in EGFR, PDGFRA, PTEN, p53 tumor suppressor protein, NF1, CDKN2A/B, and telomerase reverse transcriptase (TERT) promoter mutations (see Fig.
n2:mentions: n3:22098029

Subject Item: _:vb42265890
rdf:type: n2:Context
rdf:value: cells.8, 9, 10, 11, 12, 13, 14 GBM tumors developed from lower-grade astrocytomas or oligodendrogliomas are termed secondary GBMs (Fig. 1). While primary and secondary GBM's are histologically similar, they are genetically different.15, >>16<< Primary GBM frequently displays molecular alterations in EGFR, PDGFRA, PTEN, p53 tumor suppressor protein, NF1, CDKN2A/B, and telomerase reverse transcriptase (TERT) promoter mutations (see Fig.
n2:mentions: n3:24843883

Subject Item: _:vb42265891
rdf:type: n2:Context
rdf:value: they are genetically different.15, 16 Primary GBM frequently displays molecular alterations in EGFR, PDGFRA, PTEN, p53 tumor suppressor protein, NF1, CDKN2A/B, and telomerase reverse transcriptase (TERT) promoter mutations (see Fig. 1).>>16<<, 17 Furthermore, as reported by Cadieux et al, global hypomethylation is frequently observed in primary human GBM.
n2:mentions: n3:24843883

Subject Item: _:vb42265892
rdf:type: n2:Context
rdf:value: are genetically different.15, 16 Primary GBM frequently displays molecular alterations in EGFR, PDGFRA, PTEN, p53 tumor suppressor protein, NF1, CDKN2A/B, and telomerase reverse transcriptase (TERT) promoter mutations (see Fig. 1).16, >>17<< Furthermore, as reported by Cadieux et al, global hypomethylation is frequently observed in primary human GBM.
n2:mentions: n3:24445767

Subject Item: _:vb42265893
rdf:type: n2:Context
rdf:value: 16, 17 Furthermore, as reported by Cadieux et al, global hypomethylation is frequently observed in primary human GBM.>>18<<
n2:mentions: n3:16951158

Subject Item: _:vb42265894
rdf:type: n2:Context
rdf:value: Primary GBM is heterogeneous in nature, and based on its patterns of gene expression and genetic changes, four different subtypes including proneural, neural, classical and mesenchymal have been identified.>>19<<, 20 While the biological significance and origin of these GBM subtypes are unclear, patients with specific GBM subtypes exhibit distinct survival times and different responses to therapy.
n2:mentions: n3:16530701

Subject Item: _:vb42265895
rdf:type: n2:Context
rdf:value: Primary GBM is heterogeneous in nature, and based on its patterns of gene expression and genetic changes, four different subtypes including proneural, neural, classical and mesenchymal have been identified.19, >>20<< While the biological significance and origin of these GBM subtypes are unclear, patients with specific GBM subtypes exhibit distinct survival times and different responses to therapy.
n2:mentions: n3:20129251

Subject Item: _:vb42265896
rdf:type: n2:Context
rdf:value: 19, 20 While the biological significance and origin of these GBM subtypes are unclear, patients with specific GBM subtypes exhibit distinct survival times and different responses to therapy.12, >>19<<, 20 A high frequency of isocitrate dehydrogenase 1 (IDH1) mutations and O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation among young adult patients with primary GBM compared to other subtypes correlates with increased
n2:mentions: n3:16530701

Subject Item: _:vb42265897
rdf:type: n2:Context
rdf:value: 19, 20 While the biological significance and origin of these GBM subtypes are unclear, patients with specific GBM subtypes exhibit distinct survival times and different responses to therapy.12, 19, >>20<< A high frequency of isocitrate dehydrogenase 1 (IDH1) mutations and O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation among young adult patients with primary GBM compared to other subtypes correlates with increased
n2:mentions: n3:20129251

Subject Item: _:vb42265898
rdf:type: n2:Context
rdf:value: frequency of isocitrate dehydrogenase 1 (IDH1) mutations and O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation among young adult patients with primary GBM compared to other subtypes correlates with increased survival.>>21<< The classical subtype is associated with a high frequency of EGFR aberrations and low expression of p53 tumor suppressor protein mutations.
n2:mentions: n3:23223340

Subject Item: _:vb42265899
rdf:type: n2:Context
rdf:value: adult patients with primary GBM compared to other subtypes correlates with increased survival.21 The classical subtype is associated with a high frequency of EGFR aberrations and low expression of p53 tumor suppressor protein mutations.>>22<< The mesenchymal subtype displays loss of the tumor suppressor gene NF1 with high CD44 and MERTK expression, and the neural subtype does not express any particular alterations of specific genes or pathways.
n2:mentions: n3:24410805

Subject Item: _:vb42265900
rdf:type: n2:Context
rdf:value: 22 The mesenchymal subtype displays loss of the tumor suppressor gene NF1 with high CD44 and MERTK expression, and the neural subtype does not express any particular alterations of specific genes or pathways.12, >>22<<
n2:mentions: n3:24410805

Subject Item: _:vb42265901
rdf:type: n2:Context
rdf:value: most complete information has been provided by The Cancer Genome Atlas (TCGA) Research Network which published a report by analysis of copy number, methylation patterns, expression profiling, and whole-genome sequencing of GBM samples.>>20<< Many genes including EGFR, PDGFRA, CDK4, MDM2, MDM4, MET, CDK6, N-Myc, Cyclin D2, PIK3CA, and AKT3 have been found amplified in GBM, further contributing to the complexity in developing therapies to treat GBM.
n2:mentions: n3:20129251

Subject Item: _:vb42265902
rdf:type: n2:Context
rdf:value: of GBM samples.20 Many genes including EGFR, PDGFRA, CDK4, MDM2, MDM4, MET, CDK6, N-Myc, Cyclin D2, PIK3CA, and AKT3 have been found amplified in GBM, further contributing to the complexity in developing therapies to treat GBM.>>20<< Moreover, significant abnormalities in several signaling pathways including the receptor tyrosine kinase pathway, the p53 pathway, and the RB pathway were found.
n2:mentions: n3:20129251

Subject Item: _:vb42265903
rdf:type: n2:Context
rdf:value: 20 Moreover, significant abnormalities in several signaling pathways including the receptor tyrosine kinase pathway, the p53 pathway, and the RB pathway were found.12, >>16<<,
n2:mentions: n3:24843883

Subject Item: _:vb42265904
rdf:type: n2:Context
rdf:value: 20 Moreover, significant abnormalities in several signaling pathways including the receptor tyrosine kinase pathway, the p53 pathway, and the RB pathway were found.12, 16, >>20<<
n2:mentions: n3:20129251

Subject Item: _:vb42265905
rdf:type: n4:Section
dc:title: cancer stem cell model
n4:contains: _:vb42265906 _:vb42265907 _:vb42265908 _:vb42265909 _:vb42265910 _:vb42265911 _:vb42265912 _:vb42265913 _:vb42265914 _:vb42265915 _:vb42265916 _:vb42265917 _:vb42265918 _:vb42265919 _:vb42265952 _:vb42265920 _:vb42265921 _:vb42265922 _:vb42265923 _:vb42265924 _:vb42265925 _:vb42265926 _:vb42265927 _:vb42265928 _:vb42265929 _:vb42265930 _:vb42265931 _:vb42265932 _:vb42265933 _:vb42265934 _:vb42265935 _:vb42265936 _:vb42265937 _:vb42265938 _:vb42265939 _:vb42265940 _:vb42265941 _:vb42265942 _:vb42265943 _:vb42265944 _:vb42265945 _:vb42265946 _:vb42265947 _:vb42265948 _:vb42265949 _:vb42265950 _:vb42265951

Subject Item: _:vb42265906
rdf:type: n2:Context
rdf:value: GBM tumors display a great degree of phenotypic and functional heterogeneity.>>7<<, 8, 12, 13 Heterogeneity among tumor cells arises within a single tumor as a result of genetic and epigenetic changes (Fig.
n2:mentions: n3:24615680

Subject Item: _:vb42265907
rdf:type: n2:Context
rdf:value: GBM tumors display a great degree of phenotypic and functional heterogeneity.7, >>8<<, 12, 13 Heterogeneity among tumor cells arises within a single tumor as a result of genetic and epigenetic changes (Fig.
n2:mentions: n3:24152818

Subject Item: _:vb42265908
rdf:type: n2:Context
rdf:value: 7, 8, 12, >>13<< Heterogeneity among tumor cells arises within a single tumor as a result of genetic and epigenetic changes (Fig.
n2:mentions: n3:4091041

Subject Item: _:vb42265909
rdf:type: n2:Context
rdf:value: 7, 8, 12, 13 Heterogeneity among tumor cells arises within a single tumor as a result of genetic and epigenetic changes (Fig. 2) as well as different microenvironments within different regions of tumor.>>23<<, 24 The genetic alterations and epigenetic changes of the cells within the same tumor is not well characterized, and for future personalized medicine strategies, it is necessary to explore intratumoral heterogeneity with respect to the
n2:mentions: n3:24642524

Subject Item: _:vb42265910
rdf:type: n2:Context
rdf:value: 2) as well as different microenvironments within different regions of tumor.23, >>24<< The genetic alterations and epigenetic changes of the cells within the same tumor is not well characterized, and for future personalized medicine strategies, it is necessary to explore intratumoral heterogeneity with respect to the
n2:mentions: n3:25114226

Subject Item: _:vb42265911
rdf:type: n2:Context
rdf:value: personalized medicine strategies, it is necessary to explore intratumoral heterogeneity with respect to the phenotype and genotype of the tumor as well as evaluating its epigenetic alterations to achieve effective treatment for GBM.>>25<<, 26 To better understand intratumoral heterogeneity in a given GBM tumor, Sottoriva et al demonstrated that investigating genome-wide GBM intratumoral genomic heterogeneity can be used to reveal tumor evolution.
n2:mentions: n3:23412337

Subject Item: _:vb42265912
rdf:type: n2:Context
rdf:value: personalized medicine strategies, it is necessary to explore intratumoral heterogeneity with respect to the phenotype and genotype of the tumor as well as evaluating its epigenetic alterations to achieve effective treatment for GBM.25, >>26<< To better understand intratumoral heterogeneity in a given GBM tumor, Sottoriva et al demonstrated that investigating genome-wide GBM intratumoral genomic heterogeneity can be used to reveal tumor evolution.
n2:mentions: n3:24154962

Subject Item: _:vb42265913
rdf:type: n2:Context
rdf:value: treatment for GBM.25, 26 To better understand intratumoral heterogeneity in a given GBM tumor, Sottoriva et al demonstrated that investigating genome-wide GBM intratumoral genomic heterogeneity can be used to reveal tumor evolution.>>25<< Furthermore, the authors showed that based on gene expression levels, tumor fragments from different anatomical regions of the same patient tumor may be classified into different GBM subtypes.
n2:mentions: n3:23412337

Subject Item: _:vb42265914
rdf:type: n2:Context
rdf:value: can be used to reveal tumor evolution.25 Furthermore, the authors showed that based on gene expression levels, tumor fragments from different anatomical regions of the same patient tumor may be classified into different GBM subtypes.>>25<< Significantly, by using single-molecule techniques, the authors described the clonal composition of single tumor fragments and showed that a hierarchy of mitotic clones coexists within the same fragment of tumor.
n2:mentions: n3:23412337

Subject Item: _:vb42265915
rdf:type: n2:Context
rdf:value: clones coexists within the same fragment of tumor. These impressive results unraveled the complexity of GBM tumors with respect to their heterogeneity which represents the signature of GBM clonal evolution at the single patient level.>>25<< These results demonstrate the urgent need for personalized medicine and the difficulty in developing effective therapies for each GBM patient.
n2:mentions: n3:23412337

Subject Item: _:vb42265916
rdf:type: n2:Context
rdf:value: Astrocytes, neurons, oligodendrocytes, and ependymal cells also have the potential to initiate tumorigenesis.>>33<<
n2:mentions: n3:24202333

Subject Item: _:vb42265917
rdf:type: n2:Context
rdf:value: The origin of tumor cell heterogeneity may occur from clonal evolution and from differentiation of CSCs.>>7<<, 27, 28, 29, 30, 31, 32 The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:24615680

Subject Item: _:vb42265918
rdf:type: n2:Context
rdf:value: The origin of tumor cell heterogeneity may occur from clonal evolution and from differentiation of CSCs.7, >>27<<, 28, 29, 30, 31, 32 The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:24048065

Subject Item: _:vb42265919
rdf:type: n2:Context
rdf:value: The origin of tumor cell heterogeneity may occur from clonal evolution and from differentiation of CSCs.7, 27, >>28<<, 29, 30, 31, 32 The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:20598659

Subject Item: _:vb42265920
rdf:type: n2:Context
rdf:value: 7, 27, 28, >>29<<, 30, 31, 32 The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:23766371

Subject Item: _:vb42265921
rdf:type: n2:Context
rdf:value: 7, 27, 28, 29, >>30<<, 31, 32 The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:24177718

Subject Item: _:vb42265922
rdf:type: n2:Context
rdf:value: 7, 27, 28, 29, 30, 31, >>32<< The CSC model well explains the versatility and plasticity of heterogeneous tumor populations.
n2:mentions: n3:19737509

Subject Item: _:vb42265923
rdf:type: n2:Context
rdf:value: of heterogeneous tumor populations. This model discusses how very small subpopulations of CSCs drive cancer progression and how small subpopulations of cancer cell types with specific features are produced within a given tumor.>>26<< CSCs are characterized by their ability to generate xenografts representing the initial tumor in immunodeficient animals and to divide asymmetrically to allow self-renewal as well as differentiation into a non-CSC population (Fig.
n2:mentions: n3:24154962

Subject Item: _:vb42265924
rdf:type: n2:Context
rdf:value: (Fig. 3). However, recent experimental evidence showing CSC plasticity suggests that the tumor cell populations are dynamic, and both CSCs and non-CSCs are capable of interconversion (Figure 3, Figure 4) due to environmental factors.>>7<<, 8, 33, 34, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:24615680

Subject Item: _:vb42265925
rdf:type: n2:Context
rdf:value: (Fig. 3). However, recent experimental evidence showing CSC plasticity suggests that the tumor cell populations are dynamic, and both CSCs and non-CSCs are capable of interconversion (Figure 3, Figure 4) due to environmental factors.7, >>8<<, 33, 34, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:24152818

Subject Item: _:vb42265926
rdf:type: n2:Context
rdf:value: 3). However, recent experimental evidence showing CSC plasticity suggests that the tumor cell populations are dynamic, and both CSCs and non-CSCs are capable of interconversion (Figure 3, Figure 4) due to environmental factors.7, 8, >>33<<, 34, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:24202333

Subject Item: _:vb42265927
rdf:type: n2:Context
rdf:value: 7, 8, 33, >>34<<, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:22357481

Subject Item: _:vb42265928
rdf:type: n2:Context
rdf:value: 7, 8, 33, 34, >>35<<, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:24708237

Subject Item: _:vb42265929
rdf:type: n2:Context
rdf:value: 7, 8, 33, 34, 35, >>36<<, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:21549324

Subject Item: _:vb42265930
rdf:type: n2:Context
rdf:value: 7, 8, 33, 34, 35, 36, >>37<<, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:24608791

Subject Item: _:vb42265931
rdf:type: n2:Context
rdf:value: 7, 8, 33, 34, 35, 36, 37, >>38<<, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:25018639

Subject Item: _:vb42265932
rdf:type: n2:Context
rdf:value: 7, 8, 33, 34, 35, 36, 37, 38, >>39<< The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.
n2:mentions: n3:25429620

Subject Item: _:vb42265933
rdf:type: n2:Context
rdf:value: capable of interconversion (Figure 3, Figure 4) due to environmental factors.7, 8, 33, 34, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.>>39<<, 40 As stated by Vries et al, any tumor cell can revert to a CSC after gaining a clonal advantage over the original CSC during its development.
n2:mentions: n3:25429620

Subject Item: _:vb42265934
rdf:type: n2:Context
rdf:value: of interconversion (Figure 3, Figure 4) due to environmental factors.7, 8, 33, 34, 35, 36, 37, 38, 39 The dedifferentiation of non-CSCs to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.39, >>40<< As stated by Vries et al, any tumor cell can revert to a CSC after gaining a clonal advantage over the original CSC during its development.
n2:mentions: n3:25404148

Subject Item: _:vb42265935
rdf:type: n2:Context
rdf:value: to CSCs further complicates the generation of tumor heterogeneity and CSC-targeted therapy.39, 40 As stated by Vries et al, any tumor cell can revert to a CSC after gaining a clonal advantage over the original CSC during its development.>>28<< While much evidence supports the CSC model in several cancers, reliability on cell surface markers for identifying authentic CSCs is limited.
n2:mentions: n3:20598659

Subject Item: _:vb42265936
rdf:type: n2:Context
rdf:value: on cell surface markers for identifying authentic CSCs is limited. However, clonal analysis and lineage tracing demonstrating the hierarchical organization of tumors in vivo provide strong evidence in support of the CSC concept.>>41<<, 42 In support of this CSC concept, Cheng et al by in vivo cell lineage tracing also showed that GSCs contribute to vascular pericytes that may remodel perivascular niches.
n2:mentions: n3:22855427

Subject Item: _:vb42265937
rdf:type: n2:Context
rdf:value: on cell surface markers for identifying authentic CSCs is limited. However, clonal analysis and lineage tracing demonstrating the hierarchical organization of tumors in vivo provide strong evidence in support of the CSC concept.41, >>42<< In support of this CSC concept, Cheng et al by in vivo cell lineage tracing also showed that GSCs contribute to vascular pericytes that may remodel perivascular niches.
n2:mentions: n3:25404147

Subject Item: _:vb42265938
rdf:type: n2:Context
rdf:value: 41, 42 In support of this CSC concept, Cheng et al by in vivo cell lineage tracing also showed that GSCs contribute to vascular pericytes that may remodel perivascular niches.>>43<<Figure
n2:mentions: n3:23540695

Subject Item: _:vb42265939
rdf:type: n2:Context
rdf:value: This is summary of the previously reported publications cited in the reference list.>>16<<, 64, 96, 97,
n2:mentions: n3:24843883

Subject Item: _:vb42265940
rdf:type: n2:Context
rdf:value: This is summary of the previously reported publications cited in the reference list.16, >>64<<, 96, 97,
n2:mentions: n3:25042866

Subject Item: _:vb42265941
rdf:type: n2:Context
rdf:value: This is summary of the previously reported publications cited in the reference list.16, 64, 96, >>97<<,
n2:mentions: n3:23714687

Subject Item: _:vb42265942
rdf:type: n2:Context
rdf:value: This is summary of the previously reported publications cited in the reference list.16, 64, 96, 97, >>130<<
n2:mentions: n3:24550934

Subject Item: _:vb42265943
rdf:type: n2:Context
rdf:value: of the initial tumor including tumor cell heterogeneity, invasiveness, migration and metastasis, tumor hypoxic response; resistance to drugs and radiation; resistance of tumors to apoptosis stimuli, and vascular characteristics.>>2<<, 6, 7, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:19269895

Subject Item: _:vb42265944
rdf:type: n2:Context
rdf:value: of the initial tumor including tumor cell heterogeneity, invasiveness, migration and metastasis, tumor hypoxic response; resistance to drugs and radiation; resistance of tumors to apoptosis stimuli, and vascular characteristics.2, >>6<<, 7, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:15549107

Subject Item: _:vb42265945
rdf:type: n2:Context
rdf:value: of the initial tumor including tumor cell heterogeneity, invasiveness, migration and metastasis, tumor hypoxic response; resistance to drugs and radiation; resistance of tumors to apoptosis stimuli, and vascular characteristics.2, 6, >>7<<, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:24615680

Subject Item: _:vb42265946
rdf:type: n2:Context
rdf:value: of the initial tumor including tumor cell heterogeneity, invasiveness, migration and metastasis, tumor hypoxic response; resistance to drugs and radiation; resistance of tumors to apoptosis stimuli, and vascular characteristics.2, 6, 7, >>8<<, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:24152818

Subject Item: _:vb42265947
rdf:type: n2:Context
rdf:value: 2, 6, 7, 8, >>44<<, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:22067563

Subject Item: _:vb42265948
rdf:type: n2:Context
rdf:value: 2, 6, 7, 8, 44, >>45<< Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.
n2:mentions: n3:24772249

Subject Item: _:vb42265949
rdf:type: n2:Context
rdf:value: characteristics.2, 6, 7, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.>>36<<, 46, 47, 48 The intimate network of various cell types and niche paracrine factors are responsible for controlling the necessary signaling pathways that regulate the properties of GSCs.
n2:mentions: n3:21549324

Subject Item: _:vb42265950
rdf:type: n2:Context
rdf:value: characteristics.2, 6, 7, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.36, >>46<<, 47, 48 The intimate network of various cell types and niche paracrine factors are responsible for controlling the necessary signaling pathways that regulate the properties of GSCs.
n2:mentions: n3:21483406

Subject Item: _:vb42265951
rdf:type: n2:Context
rdf:value: 6, 7, 8, 44, 45 Mounting evidence shows that the stem cell niche, i.e., the environment in which GSCs reside, is responsible for the maintenance of these cells with respect to “stemness” and therapeutic response.36, 46, >>47<<, 48 The intimate network of various cell types and niche paracrine factors are responsible for controlling the necessary signaling pathways that regulate the properties of GSCs.
n2:mentions: n3:24673436

Subject Item: _:vb42265952
rdf:type: n2:Context
rdf:value: 36, 46, 47, >>48<< The intimate network of various cell types and niche paracrine factors are responsible for controlling the necessary signaling pathways that regulate the properties of GSCs.
n2:mentions: n3:20535838

Subject Item: _:vb42265953
rdf:type: n4:Section
dc:title: gsc specific markers
n4:contains: _:vb42265954 _:vb42265955 _:vb42265956 _:vb42265957 _:vb42265958 _:vb42265959 _:vb42265960 _:vb42265961 _:vb42265962 _:vb42265963 _:vb42265964 _:vb42265965 _:vb42265966 _:vb42265967 _:vb42265968

Subject Item: _:vb42265954
rdf:type: n2:Context
rdf:value: While the CD133 identifies GSCs that form neurospheres and generate heterogeneous tumors when transplanted in immune-compromised mice, CD133-negative cells displaying similar properties have also been reported.>>49<<, 50, 51, 52, 53, 54 Interestingly, Brescia et al through clonal analysis reported that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular
n2:mentions: n3:23307586

Subject Item: _:vb42265955
rdf:type: n2:Context
rdf:value: While the CD133 identifies GSCs that form neurospheres and generate heterogeneous tumors when transplanted in immune-compromised mice, CD133-negative cells displaying similar properties have also been reported.49, >>50<<, 51, 52, 53, 54 Interestingly, Brescia et al through clonal analysis reported that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular
n2:mentions: n3:22431923

Subject Item: _:vb42265956
rdf:type: n2:Context
rdf:value: While the CD133 identifies GSCs that form neurospheres and generate heterogeneous tumors when transplanted in immune-compromised mice, CD133-negative cells displaying similar properties have also been reported.49, 50, >>51<<, 52, 53, 54 Interestingly, Brescia et al through clonal analysis reported that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular
n2:mentions: n3:19904829

Subject Item: _:vb42265957
rdf:type: n2:Context
rdf:value: 49, 50, 51, 52, >>53<<, 54 Interestingly, Brescia et al through clonal analysis reported that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular localization
n2:mentions: n3:19718438

Subject Item: _:vb42265958
rdf:type: n2:Context
rdf:value: 49, 50, 51, 52, 53, >>54<< Interestingly, Brescia et al through clonal analysis reported that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular localization
n2:mentions: n3:19718438

Subject Item: _:vb42265959
rdf:type: n2:Context
rdf:value: that actually there is not a hierarchical relation between CD133-positive and CD133-negative cells, and in fact CD133 is capable of changing its subcellular localization between the cytoplasm and the plasma membrane of GSC neurospheres.>>49<< Significantly, these authors demonstrated that silencing CD133 in human GBM neurospheres using lentivirus-mediated short hairpin RNA impaired the self-renewal and tumorigenic capacity of neurosphere cells.
n2:mentions: n3:23307586

Subject Item: _:vb42265960
rdf:type: n2:Context
rdf:value: GBM neurospheres using lentivirus-mediated short hairpin RNA impaired the self-renewal and tumorigenic capacity of neurosphere cells. Interestingly, hypoxia significantly increased the percentage of CD133-positive cells from 69% to 92%.>>55<< These data collectively suggest that CD133 is indispensible for GSC function and essential for maintaining the self-renewal and tumorigenic potential of GBM stem cells.
n2:mentions: n3:23340741

Subject Item: _:vb42265961
rdf:type: n2:Context
rdf:value: 55 These data collectively suggest that CD133 is indispensible for GSC function and essential for maintaining the self-renewal and tumorigenic potential of GBM stem cells.>>55<< Moreover, Denysenko et al demonstrated that CD133-positive cell lines showed increased proliferation rates in neurospheres and increased differentiation potential towards neuronal lineages, while cell lines with low CD133 expression
n2:mentions: n3:23340741

Subject Item: _:vb42265962
rdf:type: n2:Context
rdf:value: that CD133-positive cell lines showed increased proliferation rates in neurospheres and increased differentiation potential towards neuronal lineages, while cell lines with low CD133 expression showed mesenchymal properties in vitro.>>56<< Moreover, other factors may collaborate with CD133 and increase the stemness of GSCs.
n2:mentions: n3:23836332

Subject Item: _:vb42265963
rdf:type: n2:Context
rdf:value: For instance, EGFRvIII contributes to stemness through coexpression with CD133.>>57<< Moreover, while other biomarkers have been investigated in GBM including L1CAM, SOX2, CXCR4, Integrin α-6, and CD36, their roles in GSCs are not well defined.
n2:mentions: n3:23575351

Subject Item: _:vb42265964
rdf:type: n2:Context
rdf:value: instance, EGFRvIII contributes to stemness through coexpression with CD133.57 Moreover, while other biomarkers have been investigated in GBM including L1CAM, SOX2, CXCR4, Integrin α-6, and CD36, their roles in GSCs are not well defined.>>57<<
n2:mentions: n3:23575351

Subject Item: _:vb42265965
rdf:type: n2:Context
rdf:value: While tumor heterogeneity is evident in all four clinically relevant subtypes of GBM as described above, molecular signaling in GSCs in individual subtypes is poorly characterized.>>58<< In light of this, Mao et al recently identified and characterized two mutually exclusive GSC subtypes, proneural (PN) and mesenchymal (Mes) GSCs.
n2:mentions: n3:23650391

Subject Item: _:vb42265966
rdf:type: n2:Context
rdf:value: above, molecular signaling in GSCs in individual subtypes is poorly characterized.58 In light of this, Mao et al recently identified and characterized two mutually exclusive GSC subtypes, proneural (PN) and mesenchymal (Mes) GSCs.>>58<< Mes GSCs showed more aggressive phenotypes both in vitro and in intracranial xenografts of GBM in mice, and were very resistant to radiation compared with PN GSCs.
n2:mentions: n3:23650391

Subject Item: _:vb42265967
rdf:type: n2:Context
rdf:value: tumorigenic ability. By combining ploidy-based flow sorting with array-comparative genomic hybridization, Stieber et al found that primary GBMs are either mono- or polygenomic tumors (64% versus 36%, respectively) within primary GBMs.>>26<< The authors showed that monogenomic tumors are composed of a pseudodiploid tumor clone and normal stromal cells, whereas polygenomic tumors consisted of multiple tumor clones and always contain a pseudodiploid subpopulation.
n2:mentions: n3:24154962

Subject Item: _:vb42265968
rdf:type: n2:Context
rdf:value: Therefore, the clonal heterogeneity at the genetic level, tumorigenic potential, and GSC marker expression may influence GBM progression and govern its response to treatment.>>26<<
n2:mentions: n3:24154962

Subject Item: _:vb42265969
rdf:type: n4:Section
dc:title: gbm heterogeneity and gsc plasticity
n4:contains: _:vb42265970 _:vb42265971 _:vb42265972 _:vb42265973 _:vb42265974 _:vb42265975 _:vb42265976 _:vb42265977 _:vb42265978 _:vb42265979 _:vb42265980 _:vb42265981 _:vb42265982 _:vb42265983 _:vb42265984 _:vb42265985 _:vb42265986 _:vb42265987 _:vb42265988 _:vb42265989 _:vb42265990 _:vb42265991 _:vb42265992 _:vb42265993 _:vb42265994 _:vb42265995 _:vb42265996 _:vb42265997 _:vb42265998 _:vb42265999 _:vb42266000 _:vb42266001 _:vb42266002 _:vb42266003 _:vb42266004 _:vb42266005 _:vb42266006 _:vb42266007 _:vb42266008 _:vb42266009 _:vb42266010 _:vb42266011 _:vb42266012 _:vb42266013 _:vb42266014

Subject Item: _:vb42265970
rdf:type: n2:Context
rdf:value: Recent research efforts have been directed toward selectively targeting CSCs for therapy.>>29<< However, therapeutic response is influenced by the stemness of a tumor which is defined by cancer genetics, epigenetics, microenvironment, and dedifferentiation or conversion of non-CSCs to CSCs (Fig.
n2:mentions: n3:23766371

Subject Item: _:vb42265971
rdf:type: n2:Context
rdf:value: targeting CSCs for therapy.29 However, therapeutic response is influenced by the stemness of a tumor which is defined by cancer genetics, epigenetics, microenvironment, and dedifferentiation or conversion of non-CSCs to CSCs (Fig. 2).>>7<<, 8, 59, 60, 61, 62, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24615680

Subject Item: _:vb42265972
rdf:type: n2:Context
rdf:value: targeting CSCs for therapy.29 However, therapeutic response is influenced by the stemness of a tumor which is defined by cancer genetics, epigenetics, microenvironment, and dedifferentiation or conversion of non-CSCs to CSCs (Fig. 2).7, >>8<<, 59, 60, 61, 62, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24152818

Subject Item: _:vb42265973
rdf:type: n2:Context
rdf:value: CSCs for therapy.29 However, therapeutic response is influenced by the stemness of a tumor which is defined by cancer genetics, epigenetics, microenvironment, and dedifferentiation or conversion of non-CSCs to CSCs (Fig. 2).7, 8, >>59<<, 60, 61, 62, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:21463158

Subject Item: _:vb42265974
rdf:type: n2:Context
rdf:value: 7, 8, 59, >>60<<, 61, 62, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24607403

Subject Item: _:vb42265975
rdf:type: n2:Context
rdf:value: 7, 8, 59, 60, >>61<<, 62, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24998755

Subject Item: _:vb42265976
rdf:type: n2:Context
rdf:value: 7, 8, 59, 60, 61, >>62<<, 63 These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24726753

Subject Item: _:vb42265977
rdf:type: n2:Context
rdf:value: 7, 8, 59, 60, 61, 62, >>63<< These processes determine stemness and resistance to drugs and ionizing radiation in GBM tumors.
n2:mentions: n3:24115218

Subject Item: _:vb42265978
rdf:type: n2:Context
rdf:value: Moreover, growing evidence reveals a high degree of plasticity of cancer cells with the ability to effectively and reversibly transit between differentiated and CSC phenotypes in response to microenvironmental factors like hypoxia.>>62<<, 63, 64, 65, 66, 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to
n2:mentions: n3:24726753

Subject Item: _:vb42265979
rdf:type: n2:Context
rdf:value: Moreover, growing evidence reveals a high degree of plasticity of cancer cells with the ability to effectively and reversibly transit between differentiated and CSC phenotypes in response to microenvironmental factors like hypoxia.62, >>63<<, 64, 65, 66, 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to
n2:mentions: n3:24115218

Subject Item: _:vb42265980
rdf:type: n2:Context
rdf:value: growing evidence reveals a high degree of plasticity of cancer cells with the ability to effectively and reversibly transit between differentiated and CSC phenotypes in response to microenvironmental factors like hypoxia.62, 63, >>64<<, 65, 66, 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor
n2:mentions: n3:25042866

Subject Item: _:vb42265981
rdf:type: n2:Context
rdf:value: 62, 63, 64, >>65<<, 66, 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor
n2:mentions: n3:22298594

Subject Item: _:vb42265982
rdf:type: n2:Context
rdf:value: 62, 63, 64, 65, >>66<<, 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor growth.
n2:mentions: n3:19718046

Subject Item: _:vb42265983
rdf:type: n2:Context
rdf:value: 62, 63, 64, 65, 66, >>67<< Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor growth.
n2:mentions: n3:20309962

Subject Item: _:vb42265984
rdf:type: n2:Context
rdf:value: 67 Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor growth.>>62<<, 63, 64, 65, 66, 67 A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness”
n2:mentions: n3:24726753

Subject Item: _:vb42265985
rdf:type: n2:Context
rdf:value: Therefore, the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor growth.62, >>63<<, 64, 65, 66, 67 A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness”
n2:mentions: n3:24115218

Subject Item: _:vb42265986
rdf:type: n2:Context
rdf:value: the capacity of tumor cells to mutually interconvert is directed by genetic, epigenetic, and microenvironmental regulation by which tumor cells alter their phenotypic and functional role which contributes to tumor growth.62, 63, >>64<<, 65, 66, 67 A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated
n2:mentions: n3:25042866

Subject Item: _:vb42265987
rdf:type: n2:Context
rdf:value: 62, 63, 64, >>65<<, 66, 67 A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated by
n2:mentions: n3:22298594

Subject Item: _:vb42265988
rdf:type: n2:Context
rdf:value: 62, 63, 64, 65, >>66<<, 67 A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated by
n2:mentions: n3:19718046

Subject Item: _:vb42265989
rdf:type: n2:Context
rdf:value: 62, 63, 64, 65, 66, >>67<< A new model explaining the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated by
n2:mentions: n3:20309962

Subject Item: _:vb42265990
rdf:type: n2:Context
rdf:value: the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated by microenvironmental factors.>>68<<, 69 Indeed, Chaffer et al demonstrated that CSC cells can arise de novo from more differentiated cell types and that hierarchical models of stem cell biology achieve bidirectional interconversion between stem and non-stem compartments
n2:mentions: n3:21498687

Subject Item: _:vb42265991
rdf:type: n2:Context
rdf:value: the differential ability of tumor cells to interconvert explains the concept of “CSC plasticity” in which many cells within the tumor can serve as stem cells with various degrees of “stemness” regulated by microenvironmental factors.68, >>69<< Indeed, Chaffer et al demonstrated that CSC cells can arise de novo from more differentiated cell types and that hierarchical models of stem cell biology achieve bidirectional interconversion between stem and non-stem compartments (Fig.
n2:mentions: n3:23220226

Subject Item: _:vb42265992
rdf:type: n2:Context
rdf:value: Chaffer et al demonstrated that CSC cells can arise de novo from more differentiated cell types and that hierarchical models of stem cell biology achieve bidirectional interconversion between stem and non-stem compartments (Fig. 2).>>68<<
n2:mentions: n3:21498687

Subject Item: _:vb42265993
rdf:type: n2:Context
rdf:value: It has been demonstrated that GSCs can be more resistant to conventional anticancer agents like TMZ than their differentiated GBM cells.>>70<<, 71 Conversely, other reports have shown that primary GSCs are sensitive to TMZ therapy, and significant expansion of different GSC subpopulations after treatment of GBM patients with TMZ has been detected.
n2:mentions: n3:17051156

Subject Item: _:vb42265994
rdf:type: n2:Context
rdf:value: It has been demonstrated that GSCs can be more resistant to conventional anticancer agents like TMZ than their differentiated GBM cells.70, >>71<< Conversely, other reports have shown that primary GSCs are sensitive to TMZ therapy, and significant expansion of different GSC subpopulations after treatment of GBM patients with TMZ has been detected.
n2:mentions: n3:24643683

Subject Item: _:vb42265995
rdf:type: n2:Context
rdf:value: 70, 71 Conversely, other reports have shown that primary GSCs are sensitive to TMZ therapy, and significant expansion of different GSC subpopulations after treatment of GBM patients with TMZ has been detected.>>37<<, 72, 73 It has been reported that the chemoresistance of GSCs correlated with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs
n2:mentions: n3:24608791

Subject Item: _:vb42265996
rdf:type: n2:Context
rdf:value: 70, 71 Conversely, other reports have shown that primary GSCs are sensitive to TMZ therapy, and significant expansion of different GSC subpopulations after treatment of GBM patients with TMZ has been detected.37, >>72<<, 73 It has been reported that the chemoresistance of GSCs correlated with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs to
n2:mentions: n3:23897632

Subject Item: _:vb42265997
rdf:type: n2:Context
rdf:value: 70, 71 Conversely, other reports have shown that primary GSCs are sensitive to TMZ therapy, and significant expansion of different GSC subpopulations after treatment of GBM patients with TMZ has been detected.37, 72, >>73<< It has been reported that the chemoresistance of GSCs correlated with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs to new
n2:mentions: n3:18632623

Subject Item: _:vb42265998
rdf:type: n2:Context
rdf:value: correlated with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs to new CSCs contributes to the resistance of CSC to TMZ.>>74<<, 75, 76 To understand GBM post-therapy, Auffinger et al recently investigated the properties of GSCs after primary chemotherapy with TMZ.
n2:mentions: n3:24311636

Subject Item: _:vb42265999
rdf:type: n2:Context
rdf:value: correlated with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs to new CSCs contributes to the resistance of CSC to TMZ.74, >>75<<, 76 To understand GBM post-therapy, Auffinger et al recently investigated the properties of GSCs after primary chemotherapy with TMZ.
n2:mentions: n3:24657832

Subject Item: _:vb42266000
rdf:type: n2:Context
rdf:value: with elevated levels of the detoxifying protein MGMT, which confers strong intrinsic resistance to these cells, and that extrinsic factors and conversion of non-CSCs to new CSCs contributes to the resistance of CSC to TMZ.74, 75, >>76<< To understand GBM post-therapy, Auffinger et al recently investigated the properties of GSCs after primary chemotherapy with TMZ.
n2:mentions: n3:21988793

Subject Item: _:vb42266001
rdf:type: n2:Context
rdf:value: factors and conversion of non-CSCs to new CSCs contributes to the resistance of CSC to TMZ.74, 75, 76 To understand GBM post-therapy, Auffinger et al recently investigated the properties of GSCs after primary chemotherapy with TMZ.>>37<< These authors first showed that exposure of patient-derived as well as established GBM cell lines to therapeutic doses of TMZ increases the GSC pool over time both in vitro and in vivo.
n2:mentions: n3:24608791

Subject Item: _:vb42266002
rdf:type: n2:Context
rdf:value: phenotypic shift in the non-GSC population to a GSC-like state which expressed pluripotency and stemness markers such as CD133, SOX2, Oct4, and Nestin. Moreover, these new GSCs served as a reservoir for initiating relapse of the tumors.>>37<< The phenomenon of spontaneous conversion of a non-CSC population into a CSC-like population has also been reported in breast cancer.
n2:mentions: n3:24608791

Subject Item: _:vb42266003
rdf:type: n2:Context
rdf:value: 37 The phenomenon of spontaneous conversion of a non-CSC population into a CSC-like population has also been reported in breast cancer.>>61<< Therefore, collectively, these results plus published data on other tumors indicate that the tight cellular hierarchy within a tumor (i.e., the initial CSC hypothesis) does not control CSCs, and the cellular heterogeneity of the tumor
n2:mentions: n3:24998755

Subject Item: _:vb42266004
rdf:type: n2:Context
rdf:value: tumors indicate that the tight cellular hierarchy within a tumor (i.e., the initial CSC hypothesis) does not control CSCs, and the cellular heterogeneity of the tumor plus cellular plasticity control the stemness of CSCs including GSCs.>>37<<, 61, 77,
n2:mentions: n3:24608791

Subject Item: _:vb42266005
rdf:type: n2:Context
rdf:value: indicate that the tight cellular hierarchy within a tumor (i.e., the initial CSC hypothesis) does not control CSCs, and the cellular heterogeneity of the tumor plus cellular plasticity control the stemness of CSCs including GSCs.37, >>61<<, 77,
n2:mentions: n3:24998755

Subject Item: _:vb42266006
rdf:type: n2:Context
rdf:value: indicate that the tight cellular hierarchy within a tumor (i.e., the initial CSC hypothesis) does not control CSCs, and the cellular heterogeneity of the tumor plus cellular plasticity control the stemness of CSCs including GSCs.37, 61, >>77<<,
n2:mentions: n3:22472879

Subject Item: _:vb42266007
rdf:type: n2:Context
rdf:value: 37, 61, 77, >>78<<
n2:mentions: n3:24305593

Subject Item: _:vb42266008
rdf:type: n2:Context
rdf:value: of the molecular mechanisms involved in regulating GBM development. However, the specific intrinsic factors that govern GSCs self-renewal, stemness, differentiation, and dedifferentiation of GBM tumor cells to GSCs are not understood.>>7<<, 8, 37, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.
n2:mentions: n3:24615680

Subject Item: _:vb42266009
rdf:type: n2:Context
rdf:value: of the molecular mechanisms involved in regulating GBM development. However, the specific intrinsic factors that govern GSCs self-renewal, stemness, differentiation, and dedifferentiation of GBM tumor cells to GSCs are not understood.7, >>8<<, 37, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.
n2:mentions: n3:24152818

Subject Item: _:vb42266010
rdf:type: n2:Context
rdf:value: the molecular mechanisms involved in regulating GBM development. However, the specific intrinsic factors that govern GSCs self-renewal, stemness, differentiation, and dedifferentiation of GBM tumor cells to GSCs are not understood.7, 8, >>37<<, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.
n2:mentions: n3:24608791

Subject Item: _:vb42266011
rdf:type: n2:Context
rdf:value: 7, 8, 37, >>79<< Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.
n2:mentions: n3:24772249

Subject Item: _:vb42266012
rdf:type: n2:Context
rdf:value: 8, 37, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.>>47<<, 80, 81 Delineating the molecular mechanisms by which cellular plasticity is influenced by niche factors can govern the interconversion of non-CSCs to CSCs and enhance the “stemness” of the tumor.
n2:mentions: n3:24673436

Subject Item: _:vb42266013
rdf:type: n2:Context
rdf:value: 8, 37, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.47, >>80<<, 81 Delineating the molecular mechanisms by which cellular plasticity is influenced by niche factors can govern the interconversion of non-CSCs to CSCs and enhance the “stemness” of the tumor.
n2:mentions: n3:19618855

Subject Item: _:vb42266014
rdf:type: n2:Context
rdf:value: 8, 37, 79 Moreover, emerging evidence has revealed that specific GBM microenvironments (niches) also play a crucial role in maintaining the stemness of GSCs, and that changes in the niches may lead to these processes in GSCs.47, 80, >>81<< Delineating the molecular mechanisms by which cellular plasticity is influenced by niche factors can govern the interconversion of non-CSCs to CSCs and enhance the “stemness” of the tumor.
n2:mentions: n3:24834433

Subject Item: _:vb42266015
rdf:type: n4:Section
dc:title: transcription factors and gcss
n4:contains: _:vb42266024 _:vb42266025 _:vb42266026 _:vb42266027 _:vb42266028 _:vb42266029 _:vb42266030 _:vb42266016 _:vb42266017 _:vb42266018 _:vb42266019 _:vb42266020 _:vb42266021 _:vb42266022 _:vb42266023

Subject Item: _:vb42266016
rdf:type: n2:Context
rdf:value: events that create dynamic plasticity in response to environmental cues, and enables cells to function under different conditions with phenotypic and functional versatility within cell populations having identical genetic backgrounds.>>82<<, 83, 84 This morphological and functional flexibility or plasticity is particularly important for CSCs which generate tumor cells that transiently expand and then undergo differentiation to form the bulk of the tumor.
n2:mentions: n3:20839222

Subject Item: _:vb42266017
rdf:type: n2:Context
rdf:value: that create dynamic plasticity in response to environmental cues, and enables cells to function under different conditions with phenotypic and functional versatility within cell populations having identical genetic backgrounds.82, >>83<<, 84 This morphological and functional flexibility or plasticity is particularly important for CSCs which generate tumor cells that transiently expand and then undergo differentiation to form the bulk of the tumor.
n2:mentions: n3:24905005

Subject Item: _:vb42266018
rdf:type: n2:Context
rdf:value: that create dynamic plasticity in response to environmental cues, and enables cells to function under different conditions with phenotypic and functional versatility within cell populations having identical genetic backgrounds.82, 83, >>84<< This morphological and functional flexibility or plasticity is particularly important for CSCs which generate tumor cells that transiently expand and then undergo differentiation to form the bulk of the tumor.
n2:mentions: n3:17158741

Subject Item: _:vb42266019
rdf:type: n2:Context
rdf:value: backgrounds.82, 83, 84 This morphological and functional flexibility or plasticity is particularly important for CSCs which generate tumor cells that transiently expand and then undergo differentiation to form the bulk of the tumor.>>60<<, 85 However, the underlying molecular mechanisms operating this tumor cell plasticity is not clear.
n2:mentions: n3:24607403

Subject Item: _:vb42266020
rdf:type: n2:Context
rdf:value: backgrounds.82, 83, 84 This morphological and functional flexibility or plasticity is particularly important for CSCs which generate tumor cells that transiently expand and then undergo differentiation to form the bulk of the tumor.60, >>85<< However, the underlying molecular mechanisms operating this tumor cell plasticity is not clear.
n2:mentions: n3:24766799

Subject Item: _:vb42266021
rdf:type: n2:Context
rdf:value: of various epigenetic markers and gene expression results from GSCs, Suvà et al recently identified a core set of four neurodevelopmental transcription factors (TFs) including POU3F2, SOX2, SALL2, and OLIG2 essential for GBM propagation.>>86<< Significantly, more than 50% of the cells with all four TF (4 TF) also expressed the CSC marker CD133 compared to 4 TF-negative cells, which lack CD133.
n2:mentions: n3:24726434

Subject Item: _:vb42266022
rdf:type: n2:Context
rdf:value: TFs coordinately bind and activate stem-like tumor propagating cell (TPC)-specific regulatory elements. Interestingly, they are sufficient and essential to totally reprogram differentiated GBM cells and interconvert these cells to TPCs.>>86<< These exciting results revealed that these 4TFs are able to reproduce the epigenetic characteristic and phenotype of native or initial TPCs.
n2:mentions: n3:24726434

Subject Item: _:vb42266023
rdf:type: n2:Context
rdf:value: Moreover, by reconstructing the transcriptional network controlled by these factors, Suvà et al highlighted critical interactions and a regulatory role for a chromatin-modifying complex involving RCOR2 and LSD1.>>86<< These significant findings identified the RCOR2/LSD1 histone demethylase complex as a candidate therapeutic target in human GBM stem-like TPCs.
n2:mentions: n3:24726434

Subject Item: _:vb42266024
rdf:type: n2:Context
rdf:value: and a regulatory role for a chromatin-modifying complex involving RCOR2 and LSD1.86 These significant findings identified the RCOR2/LSD1 histone demethylase complex as a candidate therapeutic target in human GBM stem-like TPCs.>>86<< These data establish the epigenetic basis of plasticity and evolutionary and developmental hierarchies within GBM.
n2:mentions: n3:24726434

Subject Item: _:vb42266025
rdf:type: n2:Context
rdf:value: 86 These data establish the epigenetic basis of plasticity and evolutionary and developmental hierarchies within GBM.>>86<<
n2:mentions: n3:24726434

Subject Item: _:vb42266026
rdf:type: n2:Context
rdf:value: FOXM1 forms a protein complex with the mitotic kinase maternal embryonic leucine zipper kinase (MELK) in GSCs, leading to phosphorylation and activation of FOXM1.>>87<< Activated FOXM1 results in increased mitotic regulatory genes in GSCs.
n2:mentions: n3:23404835

Subject Item: _:vb42266027
rdf:type: n2:Context
rdf:value: mitotic regulatory genes in GSCs. TMZ treatment enriches both FOXM1- and MELK- positive GSCs, and adding Siomycin A, a CSC-targeted agent, to TMZ treatment in mice harboring GSC-derived intracranial tumors enhanced the effects of TMZ.>>87<< Identifying and developing therapeutic agents to inhibit TFs has been very complex.
n2:mentions: n3:23404835

Subject Item: _:vb42266028
rdf:type: n2:Context
rdf:value: kinase MELK in GSCs plays a critical role in GSC maintenance, a specific MELK inhibitor, OTSSP167, has been shown to have in vitro and in vivo effects on various human cancer xenograft models and is a promising agent for GBM therapy.>>88<< Moreover, Minata et al used the multi-kinase inhibitor C1 and showed that it induces mitotic catastrophe in GBMs, primarily through MELK kinase inhibition.
n2:mentions: n3:24657156

Subject Item: _:vb42266029
rdf:type: n2:Context
rdf:value: 88 Moreover, Minata et al used the multi-kinase inhibitor C1 and showed that it induces mitotic catastrophe in GBMs, primarily through MELK kinase inhibition.>>89<<
n2:mentions: n3:24739874

Subject Item: _:vb42266030
rdf:type: n2:Context
rdf:value: understand the regulation of GSC subpopulations, Chudnovsky et al recently identified a 397-kDa transcription factor, ZFHX4, which regulates differentiation, and its suppression increased GBM-free survival in intracranial xenografts.>>90<< The authors showed that ZFHX4 interacts with CHD4, a core member of the NuRD (nucleosome remodeling and deacetylase) complex.
n2:mentions: n3:24440720

Subject Item: _:vb42266031
rdf:type: n4:Section
dc:title: epigenetic regulation of gscs
n4:contains: _:vb42266032 _:vb42266033 _:vb42266034 _:vb42266035

Subject Item: _:vb42266032
rdf:type: n2:Context
rdf:value: acetylation and phosphorylation, ubiquitination, sumoylation, and ADP-ribosylation. DNA methylation results in covalent modification of cytosine nucleotides at the C5 position of particular areas of unmethylated CpG dinucleotides.>>91<< PcGs play crucial roles in regulating many cellular processes including development, pluripotency, senescence, and cancer.
n2:mentions: n3:19443100

Subject Item: _:vb42266033
rdf:type: n2:Context
rdf:value: modification of cytosine nucleotides at the C5 position of particular areas of unmethylated CpG dinucleotides.91 PcGs play crucial roles in regulating many cellular processes including development, pluripotency, senescence, and cancer.>>92<< PcGs are essential epigenetic factors and some members have histone methyltransferase activity.
n2:mentions: n3:25065329

Subject Item: _:vb42266034
rdf:type: n2:Context
rdf:value: 92 PcGs are essential epigenetic factors and some members have histone methyltransferase activity.>>91<<,
n2:mentions: n3:19443100

Subject Item: _:vb42266035
rdf:type: n2:Context
rdf:value: 92 PcGs are essential epigenetic factors and some members have histone methyltransferase activity.91, >>93<<
n2:mentions: n3:23684459

Subject Item: _:vb42266036
rdf:type: n4:Section
dc:title: micrornas and other epigenetic factors in gbcs
n4:contains: _:vb42266037 _:vb42266038 _:vb42266039 _:vb42266044 _:vb42266045 _:vb42266046 _:vb42266047 _:vb42266040 _:vb42266041 _:vb42266042 _:vb42266043 _:vb42266052 _:vb42266053 _:vb42266054 _:vb42266055 _:vb42266048 _:vb42266049 _:vb42266050 _:vb42266051 _:vb42266060 _:vb42266061 _:vb42266062 _:vb42266063 _:vb42266056 _:vb42266057 _:vb42266058 _:vb42266059

Subject Item: _:vb42266037
rdf:type: n2:Context
rdf:value: miRNAs are non-coding regulatory RNAs that are dysregulated in GSCs, suggesting they play an important role in posttranscriptional gene regulation and function in a variety of cellular processes.>>94<< Recent results have revealed that miRNAs play important regulatory roles in the GSC apoptotic pathway, differentiation, proliferation, migration and invasion, drug resistance, and radiation resistance.
n2:mentions: n3:23183822

Subject Item: _:vb42266038
rdf:type: n2:Context
rdf:value: a variety of cellular processes.94 Recent results have revealed that miRNAs play important regulatory roles in the GSC apoptotic pathway, differentiation, proliferation, migration and invasion, drug resistance, and radiation resistance.>>94<<, 95 Like CSCs from other types of cancer, GSCs are controlled by specific receptor signaling and the regulation of stem cell genes by transcription factors and miRNAs.
n2:mentions: n3:23183822

Subject Item: _:vb42266039
rdf:type: n2:Context
rdf:value: of cellular processes.94 Recent results have revealed that miRNAs play important regulatory roles in the GSC apoptotic pathway, differentiation, proliferation, migration and invasion, drug resistance, and radiation resistance.94, >>95<< Like CSCs from other types of cancer, GSCs are controlled by specific receptor signaling and the regulation of stem cell genes by transcription factors and miRNAs.
n2:mentions: n3:25042866

Subject Item: _:vb42266040
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.>>94<<, 95, 96, 97, 98, 99, 100 Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of
n2:mentions: n3:23183822

Subject Item: _:vb42266041
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.94, >>95<<, 96, 97, 98, 99, 100 Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of miRNAs
n2:mentions: n3:25042866

Subject Item: _:vb42266042
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.94, 95, 96, >>97<<, 98, 99, 100 Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of miRNAs for
n2:mentions: n3:23714687

Subject Item: _:vb42266043
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.94, 95, 96, 97, >>98<<, 99, 100 Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of miRNAs for
n2:mentions: n3:23390502

Subject Item: _:vb42266044
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.94, 95, 96, 97, 98, >>99<<, 100 Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of miRNAs for eliminating
n2:mentions: n3:25487955

Subject Item: _:vb42266045
rdf:type: n2:Context
rdf:value: 4) and demonstrated that miRNA expression patterns are correlated with the developmental lineage and differentiation state of tumor cells, as well as innovative biomarkers.94, 95, 96, 97, 98, 99, >>100<< Several published articles have summarized a wide range of miRNAs in GSCs and the molecular mechanisms of miRNAs involved in the signaling pathways regulating these processes, as well as potential usefulness of miRNAs for eliminating GSCs
n2:mentions: n3:25070777

Subject Item: _:vb42266046
rdf:type: n2:Context
rdf:value: 4).96, >>101<<, 102, 103 From the viewpoint of the CSC hypothesis, several deregulated miRNAs have been strongly implicated in regulating the GSCs self-renewal capacity, maintenance of stemness and plasticity, and resistance to drugs and radiation
n2:mentions: n3:25218589

Subject Item: _:vb42266047
rdf:type: n2:Context
rdf:value: 4).96, 101, >>102<<, 103 From the viewpoint of the CSC hypothesis, several deregulated miRNAs have been strongly implicated in regulating the GSCs self-renewal capacity, maintenance of stemness and plasticity, and resistance to drugs and radiation therapy,
n2:mentions: n3:25394756

Subject Item: _:vb42266048
rdf:type: n2:Context
rdf:value: miRNAs have been strongly implicated in regulating the GSCs self-renewal capacity, maintenance of stemness and plasticity, and resistance to drugs and radiation therapy, as well as unresponsiveness to apoptotic stimuli (Fig. 4).>>8<<, 103, 104, 105, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.
n2:mentions: n3:24152818

Subject Item: _:vb42266049
rdf:type: n2:Context
rdf:value: 8, 103, >>104<<, 105, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.
n2:mentions: n3:21728042

Subject Item: _:vb42266050
rdf:type: n2:Context
rdf:value: 8, 103, 104, >>105<<, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.
n2:mentions: n3:23331007

Subject Item: _:vb42266051
rdf:type: n2:Context
rdf:value: 8, 103, 104, 105, >>106<<, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.
n2:mentions: n3:19468690

Subject Item: _:vb42266052
rdf:type: n2:Context
rdf:value: 8, 103, 104, 105, 106, >>107<< Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.
n2:mentions: n3:25494473

Subject Item: _:vb42266053
rdf:type: n2:Context
rdf:value: 8, 103, 104, 105, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.103, >>108<<, 109,
n2:mentions: n3:24691539

Subject Item: _:vb42266054
rdf:type: n2:Context
rdf:value: 8, 103, 104, 105, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.103, 108, >>109<<,
n2:mentions: n3:25232498

Subject Item: _:vb42266055
rdf:type: n2:Context
rdf:value: 8, 103, 104, 105, 106, 107 Therefore, miRNAs can serve as potential targets for anti-GSC therapeutics.103, 108, 109, >>110<<
n2:mentions: n3:19010882

Subject Item: _:vb42266056
rdf:type: n2:Context
rdf:value: between miR-128, which is significantly downregulated in GBM, and the loss of GSC self-renewal, which occurs by direct regulation of the neural stem cell (NSC) self-renewal factor B lymphoma Mo-MLV insertion region 1 homolog (BMI1).>>110<< The polycomb repressor complex (PRC) is an epigenetic regulator of transcription and its action is mediated by two protein complexes, PRC1 and PRC2.
n2:mentions: n3:19010882

Subject Item: _:vb42266057
rdf:type: n2:Context
rdf:value: PRC functions as an oncogene in GBM where it is involved in GSC maintenance and radioresistance.>>111<< miR-128 directly targets the mRNA of SUZ12, an important component of PRC2, in addition to BMI1, a component of PRC1.111 This reduction of SUZ12 expression blocks the partially redundant functions of PRC1/PRC2, thereby significantly
n2:mentions: n3:23733246

Subject Item: _:vb42266058
rdf:type: n2:Context
rdf:value: 111 miR-128 directly targets the mRNA of SUZ12, an important component of PRC2, in addition to BMI1, a component of PRC1.>>111<< This reduction of SUZ12 expression blocks the partially redundant functions of PRC1/PRC2, thereby significantly reducing PRC activity and its associated histone modifications.
n2:mentions: n3:23733246

Subject Item: _:vb42266059
rdf:type: n2:Context
rdf:value: GSC niches, particularly, perivascular and hypoxic region microenvironments.112 Moreover, GSC survival, proliferation, and maintenance is regulated by oncogenic cytoprotective signaling pathways and epigenetic modifications (Fig. 3).>>113<< Recently, Nabilsi et al investigated the extent to which epigenetic differences contribute to intratumoral cellular heterogeneity by developing a high-throughput method, termed MAPit-patch.
n2:mentions: n3:24105770

Subject Item: _:vb42266060
rdf:type: n2:Context
rdf:value: and epigenetic modifications (Fig. 3).113 Recently, Nabilsi et al investigated the extent to which epigenetic differences contribute to intratumoral cellular heterogeneity by developing a high-throughput method, termed MAPit-patch.>>113<< The authors found several differentially expressed and methylated promoters that are associated with altered gene expression between NSC and GBM cell populations.
n2:mentions: n3:24105770

Subject Item: _:vb42266061
rdf:type: n2:Context
rdf:value: In addition, considering each promoter individually, substantial epigenetic heterogeneity was observed across the sequenced molecules, indicating the presence of epigenetically distinct cellular subpopulations within a GBM tumor.>>113<< Their results showed the biological relevance of epigenetically distinct subpopulations to the phenotypic heterogeneity of tumor cell populations.
n2:mentions: n3:24105770

Subject Item: _:vb42266062
rdf:type: n2:Context
rdf:value: Mechanistically, Natsume et al have shown that this conversion is accompanied by the gain or loss of polycomb repressive complex 2 (PRC2), which modifies chromatin structure.>>114<< PRC2 mediates lysine-27 trimethylation on histone H3 and affects pluripotency or development-associated genes (e.g., Nanog, Wnt1, and BMP5) in GSCs as well as alterations in the subcellular localization of EZH2, a catalytic component of
n2:mentions: n3:23720055

Subject Item: _:vb42266063
rdf:type: n2:Context
rdf:value: Mechanistic studies revealed that epigenetic regulation by PRC2 is a key mediator of tumor cell plasticity, which is required for the adaptation of GBM cells to their microenvironment.>>114<<
n2:mentions: n3:23720055

Subject Item: _:vb42266064
rdf:type: n4:Section
dc:title: clinical significance of gsc plasticity
n4:contains: _:vb42266068 _:vb42266069 _:vb42266070 _:vb42266071 _:vb42266065 _:vb42266066 _:vb42266067 _:vb42266072 _:vb42266073

Subject Item: _:vb42266065
rdf:type: n2:Context
rdf:value: example, in GBM cells TMZ is cytotoxic to cells by triggering DNA damage, but it can be rapidly repaired by the protein MGMT. In a subset of GBM, the MGMT promoter methylation, impairs the repair mechanism and confers chemosensitivity.>>123<< While numerous GSC targeted therapies have been identified, the usefulness of these compounds from the viewpoint of pharmacokinetics and toxicity profiles and whether they cross the blood–brain barrier (BBB) remain to be found.
n2:mentions: n3:25096963

Subject Item: _:vb42266066
rdf:type: n2:Context
rdf:value: effective agents for GBM therapy. For example, several drugs that target epigenetic alterations, including HDAC inhibitors and DNA methyltransferase (DNMT), approved for hematological malignancies, are available for solid tumor therapy.>>124<< Recently, Jiang et al used GBM cells and GSCs to identify several FDA-approved compounds that potentially could be useful in GBM treatment.
n2:mentions: n3:22836913

Subject Item: _:vb42266067
rdf:type: n2:Context
rdf:value: (DNMT), approved for hematological malignancies, are available for solid tumor therapy.124 Recently, Jiang et al used GBM cells and GSCs to identify several FDA-approved compounds that potentially could be useful in GBM treatment.>>125<< Their findings provided the basis for the rational combination of statins and topoisomerase inhibitors for GBM therapy.
n2:mentions: n3:24433351

Subject Item: _:vb42266068
rdf:type: n2:Context
rdf:value: of statins and topoisomerase inhibitors for GBM therapy. Moreover, using high-throughput chemical screens, Hothi et al identified an FDA-approved agent for the treatment of alcoholism, disulfiram (DSF), as an inhibitor of human GSCs.>>126<< Interestingly, DSF is a relatively non-toxic drug that can cross the BBB, and it is a direct and potent inhibitor of human MGMT in brain tumor cells.
n2:mentions: n3:23165409

Subject Item: _:vb42266069
rdf:type: n2:Context
rdf:value: for the treatment of alcoholism, disulfiram (DSF), as an inhibitor of human GSCs.126 Interestingly, DSF is a relatively non-toxic drug that can cross the BBB, and it is a direct and potent inhibitor of human MGMT in brain tumor cells.>>126<<, 127 These results support the repurposing of DSF for GBM therapy.127 Another group of agents potentially useful for GBM therapy are epigenetic inhibitors.
n2:mentions: n3:23165409

Subject Item: _:vb42266070
rdf:type: n2:Context
rdf:value: the treatment of alcoholism, disulfiram (DSF), as an inhibitor of human GSCs.126 Interestingly, DSF is a relatively non-toxic drug that can cross the BBB, and it is a direct and potent inhibitor of human MGMT in brain tumor cells.126, >>127<< These results support the repurposing of DSF for GBM therapy.127 Another group of agents potentially useful for GBM therapy are epigenetic inhibitors.
n2:mentions: n3:24193513

Subject Item: _:vb42266071
rdf:type: n2:Context
rdf:value: human GSCs.126 Interestingly, DSF is a relatively non-toxic drug that can cross the BBB, and it is a direct and potent inhibitor of human MGMT in brain tumor cells.126, 127 These results support the repurposing of DSF for GBM therapy.>>127<< Another group of agents potentially useful for GBM therapy are epigenetic inhibitors.
n2:mentions: n3:24193513

Subject Item: _:vb42266072
rdf:type: n2:Context
rdf:value: treating GSCs with the histone deacetylase inhibitors trichostatin A (TSA) and valproic acid (VPA) significantly reduced proliferation rates, decreased the expression of stem cell markers, and induced differentiation of these cells.>>128<< Using these agents may increase the efficacy of conventional cancer treatments for eliminating GSCs.
n2:mentions: n3:24874578

Subject Item: _:vb42266073
rdf:type: n2:Context
rdf:value: Moreover, it has been shown that GBM patients have displayed stable disease and partial responses to the redox agent perylene-quinone hypericin (HYP), a compound targeting multiple epigenetic mechanisms.>>129<<
n2:mentions: n3:24066060

Subject Item: _:vb583491844
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n2:RelevantScore: 21
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