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  1. AU="Heathcock, Lindsey"
  2. AU="Liang, Raymond"
  3. AU="Smolenov, Igor"
  4. AU=Soh Mitsuhito
  5. AU="Ivanov, Sergej"
  6. AU="Pinheiro, Martha Valéria Tavares"
  7. AU="Barres, Ben"
  8. AU="García-Cenador, M B"
  9. AU="Youssef B. Fawaz"
  10. AU="Mohamed, Dina Mahmoud"
  11. AU="Asante-Addo, Collins"
  12. AU="Belluti, Federica"
  13. AU="Sebastian Fetscher"
  14. AU="Reshef, Yakir A"
  15. AU="Gerstenberger, John"
  16. AU="Bilbul, Melanie" AU="Bilbul, Melanie"
  17. AU="Martínez-Vernaza, Samuel"
  18. AU="Takenoya, Takashi"
  19. AU="Russell, Roslin"
  20. AU=Kim Ka Young
  21. AU="Mateja, Allyson"
  22. AU="Todorov, Alexander B."
  23. AU=Mosallanezhad Behzad
  24. AU=Rochman Yrina AU=Rochman Yrina
  25. AU="Wang, Hong-Bo"
  26. AU="Zhong, Boyu"
  27. AU=Gimeno-Costa Ricardo AU=Gimeno-Costa Ricardo
  28. AU="Wu, Jiangbo"
  29. AU="MacIntyre, Michael F"
  30. AU="Moon, H K"
  31. AU="Clark, Mindie"
  32. AU="Nichols, Aaron L"
  33. AU="Cash-Goldwasser, Shama"
  34. AU="Christopher B. Daniels"
  35. AU="Wakama, Hitoshi"
  36. AU="Crowe, K"
  37. AU="Merz, Sabine"
  38. AU=Rossolatos George
  39. AU="Nalla, Shahed"
  40. AU="Alvarado, Miriam"
  41. AU="Garduño-Sánchez, Marco"
  42. AU="Khan, Sherbano"
  43. AU="Kakava, Felicia"

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  1. Artikel ; Online: Advocating For a Culture of Support for Lactating Medical Residents in Hawai'i.

    Ramsey, Kara Wong / Beckwith, Nina / Heathcock, Lindsey / Myers, Theresa / Balaraman, Venkataraman

    Hawai'i journal of health & social welfare

    2021  Band 80, Heft 12, Seite(n) 304–306

    Abstract: Lactating medical residents face unique barriers due to intense clinical work schedules, limited support in the clinic and hospital workspaces, and competing pressures between career development and childcare. The objective of this project was to explore ...

    Abstract Lactating medical residents face unique barriers due to intense clinical work schedules, limited support in the clinic and hospital workspaces, and competing pressures between career development and childcare. The objective of this project was to explore the perceived culture of breastfeeding support among medical trainees and design an action plan to improve support for lactating residents in Hawai'i. Resident and faculty representatives from the Hawai'i Residency Programs and the University of Hawai'i John A Burns School of Medicine participated in an 8 month national learning collaborative to review the existing resident lactation policy and resident perception of lactation support. In a pre-survey, the majority of residents (88%) agreed that 20-30 minutes every 2-3 hours should be allowed to express milk but only 18% felt comfortable asking for a change in schedule to accommodate time to pump. An action plan was created with the following objectives: (1) revamping the existing policy to address protected pumping times, lactation spaces, and responsibilities of administration, faculty, and residents; (2) improving lactation space through uniform provision of educational material on available facilities and efficiency tips for new parents, and (3) improving awareness of the unique challenges lactating residents face and empowering faculty and trainees to advocate for lactating residents through department and educational presentations. Medical residents in Hawai'i recognize the importance of breastfeeding but perceive a lack of support in the workplace. A comprehensive action plan to revamp the resident lactation policy and improve faculty and resident education may foster an increased culture of lactation support and healthy development of the physician workforce.
    Mesh-Begriff(e) Breast Feeding ; Female ; Hawaii ; Humans ; Internship and Residency ; Lactation ; Physicians
    Sprache Englisch
    Erscheinungsdatum 2021-10-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2983566-5
    ISSN 2641-5224 ; 2641-5216
    ISSN (online) 2641-5224
    ISSN 2641-5216
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: DNA copy number analysis of Grade II-III and Grade IV gliomas reveals differences in molecular ontogeny including chromothripsis associated with IDH mutation status.

    Cohen, Adam / Sato, Mariko / Aldape, Kenneth / Mason, Clinton C / Alfaro-Munoz, Kristin / Heathcock, Lindsey / South, Sarah T / Abegglen, Lisa M / Schiffman, Joshua D / Colman, Howard

    Acta neuropathologica communications

    2015  Band 3, Seite(n) 34

    Abstract: Introduction: Isocitrate dehydrogenase (IDH) mutation status and grade define subgroups of diffuse gliomas differing based on age, tumor location, presentation, and prognosis. While some biologic differences between IDH mutated (IDH (mut)) and wild-type ...

    Abstract Introduction: Isocitrate dehydrogenase (IDH) mutation status and grade define subgroups of diffuse gliomas differing based on age, tumor location, presentation, and prognosis. While some biologic differences between IDH mutated (IDH (mut)) and wild-type (IDH (wt)) gliomas are clear, the distinct alterations associated with progression of the two subtypes to glioblastoma (GBM, Grade IV) have not been well described. We analyzed copy number alterations (CNAs) across grades (Grade II-III and GBM) in both IDH (mut) and IDH (wt) infiltrating gliomas using molecular inversion probe arrays.
    Results: Ninety four patient samples were divided into four groups: Grade II-III IDH (wt) (n = 17), Grade II-III IDH (mut) (n = 28), GBM IDH (wt) (n = 25), and GBM IDH (mut) (n = 24). We validated prior observations that IDH (wt) GBM have a high frequency of chromosome 7 gain (including EGFR) and chromosome 10 loss (including PTEN) compared with IDH (mut) GBM. Hierarchical clustering of IDH (mut) gliomas demonstrated distinct CNA patterns distinguishing lower grade gliomas versus GBM. However, similar hierarchical clustering of IDH (wt) gliomas demonstrated no CNA distinction between lower grade glioma and GBM. Functional analyses showed that IDH (wt) gliomas had more chromosome gains in regions containing receptor tyrosine kinase pathways. In contrast, IDH (mut) gliomas more commonly demonstrated amplification of cyclins and cyclin dependent kinase genes. One of the most common alterations associated with transformation of lower grade to GBM IDH (mut) gliomas was the loss of chromosomal regions surrounding PTEN. IDH (mut) GBM tumors demonstrated significantly higher levels of overall CNAs compared to lower grade IDH (mut) tumors and all grades of IDH (wt) tumors, and IDH (mut) GBMs also demonstrated significant increase in incidence of chromothripsis.
    Conclusions: Taken together, these analyses demonstrate distinct molecular ontogeny between IDH (wt) and IDH (mut) gliomas. Our data also support the novel findings that malignant progression of IDH (mut) gliomas to GBM involves increased genomic instability and genomic catastrophe, while IDH (wt) lower grade tumors are virtually identical to GBMs at the level of DNA copy number alterations.
    Mesh-Begriff(e) Brain Neoplasms/classification ; Brain Neoplasms/genetics ; Chromosomal Instability/genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 10/genetics ; Cohort Studies ; DNA Copy Number Variations/genetics ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Gene Ontology ; Glioma/classification ; Glioma/genetics ; Humans ; Isocitrate Dehydrogenase/genetics ; Male ; Survival Analysis
    Chemische Substanzen Isocitrate Dehydrogenase (EC 1.1.1.41)
    Sprache Englisch
    Erscheinungsdatum 2015-06-20
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-015-0213-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: IDH mutation status and role of WHO grade and mitotic index in overall survival in grade II-III diffuse gliomas.

    Olar, Adriana / Wani, Khalida M / Alfaro-Munoz, Kristin D / Heathcock, Lindsey E / van Thuijl, Hinke F / Gilbert, Mark R / Armstrong, Terri S / Sulman, Erik P / Cahill, Daniel P / Vera-Bolanos, Elizabeth / Yuan, Ying / Reijneveld, Jaap C / Ylstra, Bauke / Wesseling, Pieter / Aldape, Kenneth D

    Acta neuropathologica

    2015  Band 129, Heft 4, Seite(n) 585–596

    Abstract: Diffuse gliomas are up till now graded based upon morphology. Recent findings indicate that isocitrate dehydrogenase (IDH) mutation status defines biologically distinct groups of tumors. The role of tumor grade and mitotic index in patient outcome has ... ...

    Abstract Diffuse gliomas are up till now graded based upon morphology. Recent findings indicate that isocitrate dehydrogenase (IDH) mutation status defines biologically distinct groups of tumors. The role of tumor grade and mitotic index in patient outcome has not been evaluated following stratification by IDH mutation status. To address this, we interrogated 558 WHO grade II-III diffuse gliomas for IDH1/2 mutations and investigated the prognostic impact of WHO grade within IDH-mutant and IDH-wild type tumor subsets independently. The prognostic impact of grade was modest in IDH-mutant [hazard ratio (HR) = 1.21, 95 % confidence interval (CI) = 0.91-1.61] compared to IDH-wild type tumors (HR = 1.74, 95 % CI = 0.95-3.16). Using a dichotomized mitotic index cut-off of 4/1000 tumor cells, we found that while mitotic index was significantly associated with outcome in IDH-wild type tumors (log-rank p < 0.0001, HR = 4.41, 95 % CI = 2.55-7.63), it was not associated with outcome in IDH-mutant tumors (log-rank p = 0.5157, HR = 1.10, 95 % CI = 0.80-1.51), and could demonstrate a statistical interaction (p < 0.0001) between IDH mutation and mitotic index (i.e., suggesting that the effect of mitotic index on patient outcome is dependent on IDH mutation status). Patient age, an established prognostic factor in diffuse glioma, was significantly associated with outcome only in the IDH-wild type subset, and consistent with prior data, 1p/19q co-deletion conferred improved outcome in the IDH-mutant cohort. These findings suggest that stratification of grade II-III gliomas into subsets defined by the presence or absence of IDH mutation leads to subgroups with distinct prognostic characteristics. Further evaluation of grading criteria and prognostic markers is warranted within IDH-mutant versus IDH-wild type diffuse grade II-III gliomas as independent entities.
    Mesh-Begriff(e) Adolescent ; Adult ; Aged ; Brain Neoplasms/diagnosis ; Brain Neoplasms/genetics ; Chromosome Deletion ; Chromosomes, Human, Pair 1/genetics ; Female ; Glioma/diagnosis ; Glioma/genetics ; Humans ; Isocitrate Dehydrogenase/genetics ; Male ; Middle Aged ; Mitotic Index ; Mutation/genetics ; Retrospective Studies ; Survival Analysis ; Young Adult
    Chemische Substanzen Isocitrate Dehydrogenase (EC 1.1.1.41)
    Sprache Englisch
    Erscheinungsdatum 2015-02-21
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-015-1398-z
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Significance of complete 1p/19q co-deletion, IDH1 mutation and MGMT promoter methylation in gliomas: use with caution.

    Boots-Sprenger, Sandra H E / Sijben, Angelique / Rijntjes, Jos / Tops, Bastiaan B J / Idema, Albert J / Rivera, Andreana L / Bleeker, Fonnet E / Gijtenbeek, Anja M / Diefes, Kristin / Heathcock, Lindsey / Aldape, Kenneth D / Jeuken, Judith W M / Wesseling, Pieter

    Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

    2013  Band 26, Heft 7, Seite(n) 922–929

    Abstract: The histopathological diagnosis of diffuse gliomas often lacks the precision that is needed for tailored treatment of individual patients. Assessment of the molecular aberrations will probably allow more robust and prognostically relevant classification ... ...

    Abstract The histopathological diagnosis of diffuse gliomas often lacks the precision that is needed for tailored treatment of individual patients. Assessment of the molecular aberrations will probably allow more robust and prognostically relevant classification of these tumors. Markers that have gained a lot of interest in this respect are co-deletion of complete chromosome arms 1p and 19q, (hyper)methylation of the MGMT promoter and IDH1 mutations. The aim of this study was to assess the prognostic significance of complete 1p/19q co-deletion, MGMT promoter methylation and IDH1 mutations in patients suffering from diffuse gliomas. The presence of these molecular aberrations was investigated in a series of 561 diffuse astrocytic and oligodendroglial tumors (low grade n=110, anaplastic n=118 and glioblastoma n=333) and correlated with age at diagnosis and overall survival. Complete 1p/19q co-deletion, MGMT promoter methylation and/or IDH1 mutation generally signified a better prognosis for patients with a diffuse glioma including glioblastoma. However, in all 10 patients with a histopathological diagnosis of glioblastoma included in this study complete 1p/19q co-deletion was not associated with improved survival. Furthermore, in glioblastoma patients >50 years of age the favorable prognostic significance of IDH1 mutation and MGMT promoter methylation was absent. In conclusion, molecular diagnostics is a powerful tool to obtain prognostically relevant information for glioma patients. However, for individual patients the molecular information should be interpreted with caution and weighed in the context of parameters such as age and histopathological diagnosis.
    Mesh-Begriff(e) Adult ; Biomarkers, Tumor/genetics ; Brain Neoplasms/classification ; Brain Neoplasms/genetics ; Brain Neoplasms/mortality ; Chromosome Deletion ; Chromosomes, Human, Pair 1/genetics ; Chromosomes, Human, Pair 19/genetics ; DNA Methylation ; DNA Modification Methylases/genetics ; DNA Repair Enzymes/genetics ; Female ; Gene Deletion ; Glioma/classification ; Glioma/genetics ; Glioma/mortality ; Humans ; Isocitrate Dehydrogenase/genetics ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Mutation ; Pathology, Molecular ; Prognosis ; Promoter Regions, Genetic ; Tumor Suppressor Proteins/genetics
    Chemische Substanzen Biomarkers, Tumor ; Tumor Suppressor Proteins ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.) ; DNA Modification Methylases (EC 2.1.1.-) ; MGMT protein, human (EC 2.1.1.63) ; DNA Repair Enzymes (EC 6.5.1.-)
    Sprache Englisch
    Erscheinungsdatum 2013-02-22
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 645073-8
    ISSN 1530-0285 ; 0893-3952
    ISSN (online) 1530-0285
    ISSN 0893-3952
    DOI 10.1038/modpathol.2012.166
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: A survey of intragenic breakpoints in glioblastoma identifies a distinct subset associated with poor survival.

    Zheng, Siyuan / Fu, Jun / Vegesna, Rahulsimham / Mao, Yong / Heathcock, Lindsey E / Torres-Garcia, Wandaliz / Ezhilarasan, Ravesanker / Wang, Shuzhen / McKenna, Aaron / Chin, Lynda / Brennan, Cameron W / Yung, W K Alfred / Weinstein, John N / Aldape, Kenneth D / Sulman, Erik P / Chen, Ken / Koul, Dimpy / Verhaak, Roel G W

    Genes & development

    2013  Band 27, Heft 13, Seite(n) 1462–1472

    Abstract: With the advent of high-throughput sequencing technologies, much progress has been made in the identification of somatic structural rearrangements in cancer genomes. However, characterization of the complex alterations and their associated mechanisms ... ...

    Abstract With the advent of high-throughput sequencing technologies, much progress has been made in the identification of somatic structural rearrangements in cancer genomes. However, characterization of the complex alterations and their associated mechanisms remains inadequate. Here, we report a comprehensive analysis of whole-genome sequencing and DNA copy number data sets from The Cancer Genome Atlas to relate chromosomal alterations to imbalances in DNA dosage and describe the landscape of intragenic breakpoints in glioblastoma multiforme (GBM). Gene length, guanine-cytosine (GC) content, and local presence of a copy number alteration were closely associated with breakpoint susceptibility. A dense pattern of repeated focal amplifications involving the murine double minute 2 (MDM2)/cyclin-dependent kinase 4 (CDK4) oncogenes and associated with poor survival was identified in 5% of GBMs. Gene fusions and rearrangements were detected concomitant within the breakpoint-enriched region. At the gene level, we noted recurrent breakpoints in genes such as apoptosis regulator FAF1. Structural alterations of the FAF1 gene disrupted expression and led to protein depletion. Restoration of the FAF1 protein in glioma cell lines significantly increased the FAS-mediated apoptosis response. Our study uncovered a previously underappreciated genomic mechanism of gene deregulation that can confer growth advantages on tumor cells and may generate cancer-specific vulnerabilities in subsets of GBM.
    Mesh-Begriff(e) Adaptor Proteins, Signal Transducing ; Animals ; Apoptosis Regulatory Proteins ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Chromosome Breakage ; Cyclin-Dependent Kinase 4/genetics ; Cyclin-Dependent Kinase 4/metabolism ; DNA Copy Number Variations/genetics ; Gene Fusion/genetics ; Gene Rearrangement/genetics ; Genomic Instability/genetics ; Glioblastoma/genetics ; Glioblastoma/mortality ; Glioblastoma/pathology ; Intracellular Signaling Peptides and Proteins ; Mice ; Proto-Oncogene Proteins c-mdm2/genetics ; Proto-Oncogene Proteins c-mdm2/metabolism ; Survival Analysis
    Chemische Substanzen Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; Carrier Proteins ; Faf1 protein, mouse ; Intracellular Signaling Peptides and Proteins ; Mdm2 protein, mouse (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Cdk4 protein, mouse (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22)
    Sprache Englisch
    Erscheinungsdatum 2013-06-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.213686.113
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: The transcriptional coactivator TAZ regulates mesenchymal differentiation in malignant glioma.

    Bhat, Krishna P L / Salazar, Katrina L / Balasubramaniyan, Veerakumar / Wani, Khalida / Heathcock, Lindsey / Hollingsworth, Faith / James, Johanna D / Gumin, Joy / Diefes, Kristin L / Kim, Se Hoon / Turski, Alice / Azodi, Yasaman / Yang, Yuhui / Doucette, Tiffany / Colman, Howard / Sulman, Erik P / Lang, Frederick F / Rao, Ganesh / Copray, Sjef /
    Vaillant, Brian D / Aldape, Kenneth D

    Genes & development

    2011  Band 25, Heft 24, Seite(n) 2594–2609

    Abstract: Recent molecular classification of glioblastoma (GBM) has shown that patients with a mesenchymal (MES) gene expression signature exhibit poor overall survival and treatment resistance. Using regulatory network analysis of available expression microarray ... ...

    Abstract Recent molecular classification of glioblastoma (GBM) has shown that patients with a mesenchymal (MES) gene expression signature exhibit poor overall survival and treatment resistance. Using regulatory network analysis of available expression microarray data sets of GBM, including The Cancer Genome Atlas (TCGA), we identified the transcriptional coactivator with PDZ-binding motif (TAZ), to be highly associated with the MES network. TAZ expression was lower in proneural (PN) GBMs and lower-grade gliomas, which correlated with CpG island hypermethylation of the TAZ promoter compared with MES GBMs. Silencing of TAZ in MES glioma stem cells (GSCs) decreased expression of MES markers, invasion, self-renewal, and tumor formation. Conversely, overexpression of TAZ in PN GSCs as well as murine neural stem cells (NSCs) induced MES marker expression and aberrant osteoblastic and chondrocytic differentiation in a TEAD-dependent fashion. Using chromatin immunoprecipitation (ChIP), we show that TAZ is directly recruited to a majority of MES gene promoters in a complex with TEAD2. The coexpression of TAZ, but not a mutated form of TAZ that lacks TEAD binding, with platelet-derived growth factor-B (PDGF-B) resulted in high-grade tumors with MES features in a murine model of glioma. Our studies uncover a direct role for TAZ and TEAD in driving the MES differentiation of malignant glioma.
    Mesh-Begriff(e) Animals ; Brain Neoplasms/physiopathology ; Cell Line, Tumor ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Epigenomics ; Gene Expression Regulation, Neoplastic ; Glioma/physiopathology ; Humans ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Cells, Cultured
    Chemische Substanzen DNA-Binding Proteins ; TEAD2 protein, human ; Tead2 protein, mouse ; Transcription Factors ; tafazzin protein, mouse (EC 2.3.-) ; TAFAZZIN protein, human (EC 2.3.1.-)
    Sprache Englisch
    Erscheinungsdatum 2011-12-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.176800.111
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.

    Bhat, Krishna P L / Balasubramaniyan, Veerakumar / Vaillant, Brian / Ezhilarasan, Ravesanker / Hummelink, Karlijn / Hollingsworth, Faith / Wani, Khalida / Heathcock, Lindsey / James, Johanna D / Goodman, Lindsey D / Conroy, Siobhan / Long, Lihong / Lelic, Nina / Wang, Suzhen / Gumin, Joy / Raj, Divya / Kodama, Yoshinori / Raghunathan, Aditya / Olar, Adriana /
    Joshi, Kaushal / Pelloski, Christopher E / Heimberger, Amy / Kim, Se Hoon / Cahill, Daniel P / Rao, Ganesh / Den Dunnen, Wilfred F A / Boddeke, Hendrikus W G M / Phillips, Heidi S / Nakano, Ichiro / Lang, Frederick F / Colman, Howard / Sulman, Erik P / Aldape, Kenneth

    Cancer cell

    2013  Band 24, Heft 3, Seite(n) 331–346

    Abstract: Despite extensive study, few therapeutic targets have been identified for glioblastoma (GBM). Here we show that patient-derived glioma sphere cultures (GSCs) that resemble either the proneural (PN) or mesenchymal (MES) transcriptomal subtypes differ ... ...

    Abstract Despite extensive study, few therapeutic targets have been identified for glioblastoma (GBM). Here we show that patient-derived glioma sphere cultures (GSCs) that resemble either the proneural (PN) or mesenchymal (MES) transcriptomal subtypes differ significantly in their biological characteristics. Moreover, we found that a subset of the PN GSCs undergoes differentiation to a MES state in a TNF-α/NF-κB-dependent manner with an associated enrichment of CD44 subpopulations and radioresistant phenotypes. We present data to suggest that the tumor microenvironment cell types such as macrophages/microglia may play an integral role in this process. We further show that the MES signature, CD44 expression, and NF-κB activation correlate with poor radiation response and shorter survival in patients with GBM.
    Mesh-Begriff(e) Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation/genetics ; Cluster Analysis ; DNA Methylation ; Disease Models, Animal ; Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Glioblastoma/mortality ; Humans ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; Mice ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Oligodendrocyte Transcription Factor 2 ; Prognosis ; Radiation Tolerance/genetics ; Signal Transduction ; Transcriptome ; Tumor Necrosis Factor-alpha/pharmacology ; Xenograft Model Antitumor Assays
    Chemische Substanzen Basic Helix-Loop-Helix Transcription Factors ; Hyaluronan Receptors ; NF-kappa B ; Nerve Tissue Proteins ; OLIG2 protein, human ; Oligodendrocyte Transcription Factor 2 ; Tumor Necrosis Factor-alpha
    Sprache Englisch
    Erscheinungsdatum 2013-08-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccr.2013.08.001
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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