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Buch ; Dissertation / Habilitation: The influence of N-Myc downstream regulated gene 1 on the glioma microenvironment

Thomé, Carina

2017

Verfasserangabe	presented by M.Sc. Molecular Biosciences Carina Thomé
Sprache	Englisch
Umfang	VI, 74 Blätter, Illustrationen, Diagramme
Erscheinungsort	Heidelberg
Erscheinungsland	Deutschland
Dokumenttyp	Buch ; Dissertation / Habilitation
Dissertation / Habilitation	Dissertation, Ruperto-Carola University of Heidelberg, 2017
HBZ-ID	HT019382495
Datenquelle	Katalog ZB MED Medizin, Gesundheit

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Artikel ; Online: Perioperative imaging in patients treated with resection of brain metastases: a survey by the European Association of Neuro-Oncology (EANO) Youngsters committee.

Kiesel, Barbara / Thomé, Carina M / Weiss, Tobias / Jakola, Asgeir S / Darlix, Amélie / Pellerino, Alessia / Furtner, Julia / Kerschbaumer, Johannes / Freyschlag, Christian F / Wick, Wolfgang / Preusser, Matthias / Widhalm, Georg / Berghoff, Anna S

BMC cancer

2020 Band 20, Heft 1, Seite(n) 410

Abstract: Background: Neurosurgical resection represents an important treatment option in the modern, multimodal therapy approach of brain metastases (BM). Guidelines for perioperative imaging exist for primary brain tumors to guide postsurgical treatment. ... ...

Abstract	Background: Neurosurgical resection represents an important treatment option in the modern, multimodal therapy approach of brain metastases (BM). Guidelines for perioperative imaging exist for primary brain tumors to guide postsurgical treatment. Optimal perioperative imaging of BM patients is so far a matter of debate as no structured guidelines exist. Methods: A comprehensive questionnaire about perioperative imaging was designed by the European Association of Neuro-Oncology (EANO) Youngsters Committee. The survey was distributed to physicians via the EANO network to perform a descriptive overview on the current habits and their variability on perioperative imaging. Chi square test was used for dichotomous variables. Results: One hundred twenty physicians worldwide responded to the survey. MRI was the preferred preoperative imaging method (93.3%). Overall 106/120 (88.3%) physicians performed postsurgical imaging routinely including MRI alone (62/120 [51.7%]), postoperative CT (29/120 [24.2%]) and MRI + CT (15/120 [12.5%]). No correlation of postsurgical MRI utilization in academic vs. non-academic hospitals (58/89 [65.2%] vs. 19/31 [61.3%], p = 0.698) was found. Early postoperative MRI within ≤72 h after resection is obtained by 60.8% of the participants. The most frequent reason for postsurgical imaging was to evaluate the extent of tumor resection (73/120 [60.8%]). In case of residual tumor, 32/120 (26.7%) participants indicated to adjust radiotherapy, 34/120 (28.3%) to consider re-surgery to achieve complete resection and 8/120 (6.7%) to evaluate both. Conclusions: MRI was the preferred imaging method in the preoperative setting. In the postoperative course, imaging modalities and timing showed high variability. International guidelines for perioperative imaging with special focus on postoperative MRI to assess residual tumor are warranted to optimize standardized management and adjuvant treatment decisions for BM patients.
Mesh-Begriff(e)	Brain Neoplasms/pathology ; Brain Neoplasms/surgery ; Europe ; Humans ; Neoplasm, Residual/pathology ; Neoplasm, Residual/surgery ; Neuroimaging/methods ; Neurosurgical Procedures/methods ; Perioperative Care ; Prognosis ; Surveys and Questionnaires
Sprache	Englisch
Erscheinungsdatum	2020-05-12
Erscheinungsland	England
Dokumenttyp	Journal Article
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-020-06897-z
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: FOCAD loss impacts microtubule assembly, G2/M progression and patient survival in astrocytic gliomas.

Brand, Frank / Förster, Alisa / Christians, Anne / Bucher, Martin / Thomé, Carina M / Raab, Marc S / Westphal, Manfred / Pietsch, Torsten / von Deimling, Andreas / Reifenberger, Guido / Claus, Peter / Hentschel, Bettina / Weller, Michael / Weber, Ruthild G

Acta neuropathologica

2019 Band 139, Heft 1, Seite(n) 175–192

Abstract: In search of novel genes associated with glioma pathogenesis, we have previously shown frequent deletions of the KIAA1797/FOCAD gene in malignant gliomas, and a tumor suppressor function of the encoded focadhesin impacting proliferation and migration of ... ...

Abstract	In search of novel genes associated with glioma pathogenesis, we have previously shown frequent deletions of the KIAA1797/FOCAD gene in malignant gliomas, and a tumor suppressor function of the encoded focadhesin impacting proliferation and migration of glioma cells in vitro and in vivo. Here, we examined an association of reduced FOCAD gene copy number with overall survival of patients with astrocytic gliomas, and addressed the molecular mechanisms that govern the suppressive effect of focadhesin on glioma growth. FOCAD loss was associated with inferior outcome in patients with isocitrate dehydrogenase 1 or 2 (IDH)-mutant astrocytic gliomas of WHO grades II-IV. Multivariate analysis considering age at diagnosis as well as IDH mutation, MGMT promoter methylation, and CDKN2A/B homozygous deletion status confirmed reduced FOCAD gene copy number as a prognostic factor for overall survival. Using a yeast two-hybrid screen and pull-down assays, tubulin beta-6 and other tubulin family members were identified as novel focadhesin-interacting partners. Tubulins and focadhesin co-localized to centrosomes where focadhesin was enriched in proximity to centrioles. Focadhesin was recruited to microtubules via its interaction partner SLAIN motif family member 2 and reduced microtubule assembly rates, possibly explaining the focadhesin-dependent decrease in cell migration. During the cell cycle, focadhesin levels peaked in G2/M phase and influenced time-dependent G2/M progression potentially via polo like kinase 1 phosphorylation, providing a possible explanation for focadhesin-dependent cell growth reduction. We conclude that FOCAD loss may promote biological aggressiveness and worsen clinical outcome of diffuse astrocytic gliomas by enhancing microtubule assembly and accelerating G2/M phase progression.
Mesh-Begriff(e)	Adult ; Aged ; Aged, 80 and over ; Astrocytoma/genetics ; Astrocytoma/mortality ; Astrocytoma/pathology ; Brain Neoplasms/genetics ; Brain Neoplasms/mortality ; Brain Neoplasms/pathology ; Cell Division/genetics ; Female ; G2 Phase/genetics ; Humans ; Male ; Microtubules/genetics ; Middle Aged ; Sequence Deletion ; Tumor Suppressor Proteins/genetics ; Young Adult
Chemische Substanzen	FOCAD protein, human ; Tumor Suppressor Proteins
Sprache	Englisch
Erscheinungsdatum	2019-08-31
Erscheinungsland	Germany
Dokumenttyp	Journal Article ; 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/s00401-019-02067-z
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Targeting Resistance against the MDM2 Inhibitor RG7388 in Glioblastoma Cells by the MEK Inhibitor Trametinib.

Berberich, Anne / Kessler, Tobias / Thomé, Carina M / Pusch, Stefan / Hielscher, Thomas / Sahm, Felix / Oezen, Iris / Schmitt, Lara-Marie / Ciprut, Sara / Hucke, Nanina / Ruebmann, Petra / Fischer, Manuel / Lemke, Dieter / Breckwoldt, Michael O / von Deimling, Andreas / Bendszus, Martin / Platten, Michael / Wick, Wolfgang

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Band 25, Heft 1, Seite(n) 253–265

Abstract: Purpose: Resistance is an obstacle of glioma therapy. Despite targeted interventions, tumors harbor primary resistance or become resistant over short course of treatment. This study examined the mouse double minute 2 (MDM2) inhibitor RG7388 together ... ...

Abstract	Purpose: Resistance is an obstacle of glioma therapy. Despite targeted interventions, tumors harbor primary resistance or become resistant over short course of treatment. This study examined the mouse double minute 2 (MDM2) inhibitor RG7388 together with radiotherapy and analyzed strategies to overcome acquired MDM2 inhibitor resistance in glioblastoma. Experimental design: Effects of RG7388 and radiotherapy were analyzed in p53 wild-type glioblastoma cell lines and glioma-initiating cells. RG7388 resistant cells were generated by increasing RG7388 doses over 3 months. Regulated pathways were investigated by microarray, qRT-PCR, and immunoblot analysis and specifically inhibited to evaluate rational salvage therapies at RG7388 resistance. Effects of RG7388 and trametinib treatment were challenged in an orthotopical mouse model with RG7388 resistant U87MG glioblastoma cells. Results: MDM2 inhibition required functional p53 and showed synergistic activity with radiotherapy in first-line treatment. Long-term exposure to RG7388 induced resistance by activation of the extracellular signal-regulated kinases 1/2 (ERK1/2)-insulin growth factor binding protein 1 (IGFBP1) signaling cascade, which was specifically overcome by ERK1/2 pathway inhibition with trametinib and knockdown of IGFBP1. Combining trametinib with continued RG7388 treatment enhanced antitumor effects at RG7388 resistance Conclusions: These data provide a rationale for combining RG7388 and radiotherapy as first-line therapy with a specific relevance for tumors insensitive to alkylating standard chemotherapy and for the addition of trametinib to continued RG7388 treatment as salvage therapy after acquired resistance against RG7388 for clinical practice.
Mesh-Begriff(e)	Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Cell Line, Tumor ; Drug Resistance, Neoplasm/drug effects ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/pathology ; Glioblastoma/radiotherapy ; Heterografts ; Humans ; Insulin-Like Growth Factor Binding Protein 1/genetics ; Mice ; Proto-Oncogene Proteins c-mdm2/genetics ; Pyridones/pharmacology ; Pyrimidinones/pharmacology ; Pyrrolidines/pharmacology ; Signal Transduction/drug effects ; Tumor Suppressor Protein p53/genetics ; para-Aminobenzoates/pharmacology
Chemische Substanzen	IGFBP1 protein, human ; Insulin-Like Growth Factor Binding Protein 1 ; Pyridones ; Pyrimidinones ; Pyrrolidines ; RG7388 ; TP53 protein, human ; Tumor Suppressor Protein p53 ; para-Aminobenzoates ; trametinib (33E86K87QN) ; MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
Sprache	Englisch
Erscheinungsdatum	2018-10-01
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-18-1580
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Identification and Characterization of Cancer Cells That Initiate Metastases to the Brain and Other Organs.

Berghoff, Anna S / Liao, Yunxiang / Karreman, Matthia A / Ilhan-Mutlu, Ayseguel / Gunkel, Katharina / Sprick, Martin R / Eisen, Christian / Kessler, Tobias / Osswald, Matthias / Wünsche, Susanne / Feinauer, Manuel / Gril, Brunhilde / Marmé, Frederic / Michel, Laura L / Bago-Horvath, Zuszanna / Sahm, Felix / Becker, Natalia / Breckwoldt, Michael O / Solecki, Gergely /

Gömmel, Miriam / Huang, Lulu / Rübmann, Petra / Thome, Carina M / Ratliff, Miriam / Trumpp, Andreas / Steeg, Patricia S / Preusser, Matthias / Wick, Wolfgang / Winkler, Frank

Molecular cancer research : MCR

2020 Band 19, Heft 4, Seite(n) 688–701

Abstract: Specific biological properties of those circulating cancer cells that are the origin of brain metastases (BM) are not well understood. Here, single circulating breast cancer cells were fate-tracked during all steps of the brain metastatic cascade in mice ...

Abstract	Specific biological properties of those circulating cancer cells that are the origin of brain metastases (BM) are not well understood. Here, single circulating breast cancer cells were fate-tracked during all steps of the brain metastatic cascade in mice after intracardial injection over weeks. A novel
Mesh-Begriff(e)	Animals ; Brain/physiopathology ; Brain Neoplasms/secondary ; Cell Line, Tumor ; Female ; Humans ; Mice ; Neoplasm Metastasis ; Neoplastic Cells, Circulating/metabolism
Sprache	Englisch
Erscheinungsdatum	2020-12-22
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0863
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Inhibition of CD95/CD95L (FAS/FASLG) Signaling with APG101 Prevents Invasion and Enhances Radiation Therapy for Glioblastoma.

Blaes, Jonas / Thomé, Carina M / Pfenning, Philipp-Niclas / Rübmann, Petra / Sahm, Felix / Wick, Antje / Bunse, Theresa / Schmenger, Torsten / Sykora, Jaromir / von Deimling, Andreas / Wiestler, Benedikt / Merz, Christian / Jugold, Manfred / Haberkorn, Uwe / Abdollahi, Amir / Debus, Jürgen / Gieffers, Christian / Kunz, Claudia / Bendszus, Martin /

Kluge, Michael / Platten, Michael / Fricke, Harald / Wick, Wolfgang / Lemke, Dieter

Molecular cancer research : MCR

2018 Band 16, Heft 5, Seite(n) 767–776

Abstract: CD95 (Fas/APO-1), a death receptor family member, activity has been linked to tumorigenicity in multiple cancers, including glioblastoma multiforme (GBM). A phase II clinical trial on relapsed glioblastoma patients demonstrated that targeted inhibition ... ...

Abstract	CD95 (Fas/APO-1), a death receptor family member, activity has been linked to tumorigenicity in multiple cancers, including glioblastoma multiforme (GBM). A phase II clinical trial on relapsed glioblastoma patients demonstrated that targeted inhibition of CD95 signaling via the CD95 ligand (CD95L) binding and neutralizing Fc-fusion protein APG101 (asunercept) prolonged patient survival. Although CD95 signaling may be relevant for multiple aspects of tumor growth, the mechanism of action of APG101 in glioblastoma is not clear. APG101 action was examined by
Mesh-Begriff(e)	Animals ; Fas Ligand Protein/antagonists & inhibitors ; Glioblastoma/genetics ; Glioblastoma/pathology ; Glioblastoma/radiotherapy ; Humans ; Immunoglobulin G/pharmacology ; Immunoglobulin G/therapeutic use ; Mice ; Recombinant Fusion Proteins/pharmacology ; Recombinant Fusion Proteins/therapeutic use ; Signal Transduction ; fas Receptor/therapeutic use
Chemische Substanzen	FASLG protein, human ; Fas Ligand Protein ; Immunoglobulin G ; Recombinant Fusion Proteins ; fas Receptor ; APG101 (F333OQQ9UV)
Sprache	Englisch
Erscheinungsdatum	2018-02-16
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-17-0563
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: The stress kinase GCN2 does not mediate suppression of antitumor T cell responses by tryptophan catabolism in experimental melanomas.

Sonner, Jana K / Deumelandt, Katrin / Ott, Martina / Thomé, Carina M / Rauschenbach, Katharina J / Schulz, Sandra / Munteanu, Bogdan / Mohapatra, Soumya / Adam, Isabell / Hofer, Ann-Cathrin / Feuerer, Markus / Opitz, Christiane A / Hopf, Carsten / Wick, Wolfgang / Platten, Michael

Oncoimmunology

2016 Band 5, Heft 12, Seite(n) e1240858

Abstract: Tryptophan metabolism is a key process that shapes the immunosuppressive tumor microenvironment. The two rate-limiting enzymes that mediate tryptophan depletion, indoleamine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO), have moved into the ... ...

Abstract	Tryptophan metabolism is a key process that shapes the immunosuppressive tumor microenvironment. The two rate-limiting enzymes that mediate tryptophan depletion, indoleamine-2,3-dioxygenase (IDO) and tryptophan-2,3-dioxygenase (TDO), have moved into the focus of research and inhibitors targeting IDO and TDO have entered clinical trials. Local tryptophan depletion is generally viewed as the crucial immunosuppressive mechanism. In T cells, the kinase general control non-derepressible 2 (GCN2) has been identified as a molecular sensor of tryptophan deprivation. GCN2 activation by tryptophan depletion induces apoptosis and mitigates T cell proliferation. Here, we investigated whether GCN2 attenuates tumor rejection in experimental B16 melanoma using T cell-specific
Sprache	Englisch
Erscheinungsdatum	2016-11-15
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2016.1240858
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Age-dependent neuroplasticity mechanisms in Alzheimer Tg2576 mice following modulation of brain amyloid-β levels.

Lilja, Anna M / Röjdner, Jennie / Mustafiz, Tamanna / Thomé, Carina M / Storelli, Elisa / Gonzalez, Daniel / Unger-Lithner, Christina / Greig, Nigel H / Nordberg, Agneta / Marutle, Amelia

PloS one

2013 Band 8, Heft 3, Seite(n) e58752

Abstract: The objective of this study was to investigate the effects of modulating brain amyloid-β (Aβ) levels at different stages of amyloid pathology on synaptic function, inflammatory cell changes and hippocampal neurogenesis, i.e. processes perturbed in ... ...

Abstract	The objective of this study was to investigate the effects of modulating brain amyloid-β (Aβ) levels at different stages of amyloid pathology on synaptic function, inflammatory cell changes and hippocampal neurogenesis, i.e. processes perturbed in Alzheimer's disease (AD). Young (4- to 6-month-old) and older (15- to 18-month-old) APP(SWE) transgenic (Tg2576) mice were treated with the AD candidate drug (+)-phenserine for 16 consecutive days. We found significant reductions in insoluble Aβ1-42 levels in the cortices of both young and older transgenic mice, while significant reductions in soluble Aβ1-42 levels and insoluble Aβ1-40 levels were only found in animals aged 15-18 months. Autoradiography binding with the amyloid ligand Pittsburgh Compound B ((3)H-PIB) revealed a trend for reduced fibrillar Aβ deposition in the brains of older phenserine-treated Tg2576 mice. Phenserine treatment increased cortical synaptophysin levels in younger mice, while decreased interleukin-1β and increased monocyte chemoattractant protein-1 and tumor necrosis factor-alpha levels were detected in the cortices of older mice. The reduction in Aβ1-42 levels was associated with an increased number of bromodeoxyuridine-positive proliferating cells in the hippocampi of both young and older Tg2576 mice. To determine whether the increased cell proliferation was accompanied by increased neuronal production, the endogenous early neuronal marker doublecortin (DCX) was examined in the dentate gyrus (DG) using immunohistochemical detection. Although no changes in the total number of DCX(+)-expressing neurons were detected in the DG in Tg2576 mice at either age following (+)-phenserine treatment, dendritic arborization was increased in differentiating neurons in young Tg2576 mice. Collectively, these findings indicate that reducing Aβ1-42 levels in Tg2576 mice at an early pathological stage affects synaptic function by modulating the maturation and plasticity of newborn neurons in the brain. In contrast, lowering Aβ levels in Tg2576 mice when Aβ plaque pathology is prominent mainly alters the levels of proinflammatory cytokines and chemokines.
Mesh-Begriff(e)	Age Factors ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Brain/drug effects ; Brain/metabolism ; Brain/pathology ; Cell Proliferation/drug effects ; Disease Models, Animal ; Female ; Hippocampus/drug effects ; Hippocampus/metabolism ; Interleukin-1beta/metabolism ; Male ; Mice ; Mice, Transgenic ; Neuronal Plasticity ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Physostigmine/administration & dosage ; Physostigmine/analogs & derivatives ; Plaque, Amyloid ; Synapses/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemische Substanzen	Amyloid beta-Peptides ; Interleukin-1beta ; Tumor Necrosis Factor-alpha ; Physostigmine (9U1VM840SP) ; phenserine (SUE285UG3S)
Sprache	Englisch
Erscheinungsdatum	2013-03-15
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0058752
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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