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Article ; Online: Targeting network circuitry in glioma.

Robbins, Stephen M / Senger, Donna L

Nature cancer

2023 Volume 4, Issue 10, Page(s) 1406–1407

MeSH term(s)	Humans ; Glioma/therapy ; Brain Neoplasms/therapy
Language	English
Publishing date	2023-10-25
Publishing country	England
Document type	Journal Article
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-023-00640-w
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Article ; Online: To promote or inhibit glioma progression, that is the question for IL-33.

Robbins, Stephen M / Senger, Donna L

Cell stress

2020 Volume 5, Issue 1, Page(s) 19–22

Abstract: IL-33, a member of the IL-1 cytokine family has been shown to play a dual role within the body. First IL-33, similar to other IL-1 family members, is a secreted cytokine that binds to the cell surface receptor ST2 to induce a number of cell signaling ... ...

Abstract	IL-33, a member of the IL-1 cytokine family has been shown to play a dual role within the body. First IL-33, similar to other IL-1 family members, is a secreted cytokine that binds to the cell surface receptor ST2 to induce a number of cell signaling pathways. Second, IL-33 enters the nucleus where it binds chromatin and directs transcriptional control of an array of growth factors and cytokines. Consistent with its complex cellular regulation, IL-33 mediates an array of biological functions by acting on a wide range of innate and adaptive immune cells. Recently, we found that IL-33 is expressed in a large number of human glioma patient specimens where its expression within the tumor correlates with the increased presence of Iba+ cells that include both resident microglia and recruited monocyte and macrophages. Strikingly, glioma derived expression of IL-33 correlates with a dramatic decrease in overall survival of tumor-bearing animals and thus supports its role as an influential factor in gliomagenesis. Notably however, when the nuclear localization function of IL-33 is crippled, the tumor microenvironment is programmed to be anti-tumorigenic and results in prolonged overall survival suggesting that when educated appropriately this could represent a novel therapeutic strategy for glioma (De Boeck
Language	English
Publishing date	2020-12-03
Publishing country	Austria
Document type	Journal Article ; Comment
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2021.01.240
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Article ; Online: Eukaryotic initiation factor 5B (eIF5B) regulates temozolomide-mediated apoptosis in brain tumour stem cells (BTSCs).

Ross, Joseph A / Ahn, Bo Young / King, Jennifer / Bressler, Kamiko R / Senger, Donna L / Thakor, Nehal

Biochemistry and cell biology = Biochimie et biologie cellulaire

2019 Volume 98, Issue 6, Page(s) 647–652

Abstract: Glioblastoma multiforme (GBM) is among the deadliest cancers, owing in part to complex inter- and intra-tumor heterogeneity and the presence of a population of stem-like cells called brain tumour stem cells (BTSCs/BTICs). These cancer stem cells survive ... ...

Abstract	Glioblastoma multiforme (GBM) is among the deadliest cancers, owing in part to complex inter- and intra-tumor heterogeneity and the presence of a population of stem-like cells called brain tumour stem cells (BTSCs/BTICs). These cancer stem cells survive treatment and confer resistance to the current therapies - namely, radiation and the chemotherapeutic, temozolomide (TMZ). TMZ induces cell death by alkylating DNA, and BTSCs resist this mechanism via a robust DNA damage response. Hence, recent studies aimed to sensitize BTSCs to TMZ using combination therapy, such as inhibition of DNA repair machinery. We have previously demonstrated in established GBM cell lines that eukaryotic initiation factor 5B (eIF5B) promotes the translation of pro-survival and anti-apoptotic proteins. Consequently, silencing eIF5B sensitizes these cells to TRAIL-induced apoptosis. However, established cell lines do not always recapitulate the features of human glioma. Therefore, we investigated this mechanism in patient-derived BTSCs. We show that silencing eIF5B leads to increased TMZ sensitivity in two BTSC lines: BT25 and BT48. Depletion of eIF5B decreases the levels of anti-apoptotic proteins in BT48 and sensitizes these cells to TMZ-induced activation of caspase-3, cleavage of PARP, and apoptosis. We suggest that eIF5B represents a rational target to sensitize GBM tumors to the current standard-of-care.
MeSH term(s)	Apoptosis/drug effects ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Eukaryotic Initiation Factors/genetics ; Eukaryotic Initiation Factors/metabolism ; Humans ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Temozolomide/pharmacology
Chemical Substances	Eukaryotic Initiation Factors ; Neoplasm Proteins ; eukaryotic initiation factor-5B ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2019-10-31
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	54104-7
ISSN	1208-6002 ; 0829-8211
ISSN (online)	1208-6002
ISSN	0829-8211
DOI	10.1139/bcb-2019-0329
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Article ; Online: Multicentre, randomised, double-blind, placebo-controlled, proof of concept study of LSALT peptide as prevention of acute respiratory distress syndrome and acute kidney injury in patients infected with SARS-CoV-2 (COVID-19).

Somayaji, Ranjani / Luke, David R / Lau, Arthur / Guner, Rahmet / Tabak, Ŏ Fehmi / Hepokoski, Mark / Gardetto, Nancy / Conrad, Steven A / Kumar, Sunil D / Ghosh, Kalyan / Robbins, Stephen M / Senger, Donna L / Sun, Daisy / Lim, Rachel K S / Liu, Jonathan / Eser, Fatma / Karaali, Ridvan / Tremblay, Alain / Muruve, Daniel

BMJ open

2024 Volume 14, Issue 3, Page(s) e076142

Abstract: Objective: Dipeptidase-1 (DPEP-1) is a recently discovered leucocyte adhesion receptor for neutrophils and monocytes in the lungs and kidneys and serves as a potential therapeutic target to attenuate inflammation in moderate-to-severe COVID-19. We aimed ...

Abstract	Objective: Dipeptidase-1 (DPEP-1) is a recently discovered leucocyte adhesion receptor for neutrophils and monocytes in the lungs and kidneys and serves as a potential therapeutic target to attenuate inflammation in moderate-to-severe COVID-19. We aimed to evaluate the safety and efficacy of the DPEP-1 inhibitor, LSALT peptide, to prevent specific organ dysfunction in patients hospitalised with COVID-19. Design: Phase 2a randomised, placebo-controlled, double-blinded, trial. Setting: Hospitals in Canada, Turkey and the USA. Participants: A total of 61 subjects with moderate-to-severe COVID-19. Interventions: Randomisation to LSALT peptide 5 mg intravenously daily or placebo for up to 14 days. Primary and secondary outcome measures: The primary endpoint was the proportion of subjects alive and free of respiratory failure and/or the need for renal replacement therapy (RRT). Numerous secondary and exploratory endpoints were assessed including ventilation-free days, and changes in kidney function or serum biomarkers. Results: At 28 days, 27 (90.3%) and 28 (93.3%) of subjects in the placebo and LSALT groups were free of respiratory failure and the need for RRT (p=0.86). On days 14 and 28, the number of patients still requiring more intensive respiratory support (O Conclusion: In a Phase 2 study, LSALT peptide was demonstrated to be safe and tolerated in patients hospitalised with moderate-to-severe COVID-19. Trial registration number: NCT04402957.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Proof of Concept Study ; Double-Blind Method ; Respiratory Insufficiency ; Respiratory Distress Syndrome/prevention & control ; Acute Kidney Injury/prevention & control ; Treatment Outcome
Language	English
Publishing date	2024-03-15
Publishing country	England
Document type	Randomized Controlled Trial ; Multicenter Study ; Journal Article
ZDB-ID	2599832-8
ISSN	2044-6055 ; 2044-6055
ISSN (online)	2044-6055
ISSN	2044-6055
DOI	10.1136/bmjopen-2023-076142
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Article ; Online: Dipeptidase-1 governs renal inflammation during ischemia reperfusion injury.

Lau, Arthur / Rahn, Jennifer J / Chappellaz, Mona / Chung, Hyunjae / Benediktsson, Hallgrimur / Bihan, Dominique / von Mässenhausen, Anne / Linkermann, Andreas / Jenne, Craig N / Robbins, Stephen M / Senger, Donna L / Lewis, Ian A / Chun, Justin / Muruve, Daniel A

Science advances

2022 Volume 8, Issue 5, Page(s) eabm0142

Abstract: The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia ... ...

Abstract	The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia reperfusion injury (IRI) induces robust neutrophil and monocyte recruitment and causes acute kidney injury (AKI). Renal inflammation and the AKI phenotype were attenuated in
MeSH term(s)	Acute Kidney Injury/etiology ; Animals ; Dipeptidases/metabolism ; Female ; GPI-Linked Proteins/metabolism ; Humans ; Inflammation/complications ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury
Chemical Substances	GPI-Linked Proteins ; Dipeptidases (EC 3.4.13.-) ; dipeptidase (EC 3.4.13.18) ; dipeptidase 1 (EC 3.4.13.19)
Language	English
Publishing date	2022-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abm0142
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Article ; Online: Development of a peptide-based delivery platform for targeting malignant brain tumors.

Rahn, Jennifer J / Lun, Xueqing / Jorch, Selina K / Hao, Xiaoguang / Venugopal, Chitra / Vora, Parvez / Ahn, Bo Young / Babes, Liane / Alshehri, Mana M / Cairncross, J Gregory / Singh, Sheila K / Kubes, Paul / Senger, Donna L / Robbins, Stephen M

Biomaterials

2020 Volume 252, Page(s) 120105

Abstract: Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the ... ...

Abstract	Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the inability to detect and target glioblastoma disease reservoirs based on a diffuse invasive pattern and the presence of molecular and phenotypic heterogeneity. The goal of this study was to target the invasive and stem-like glioblastoma cells that evade first-line treatments using agents capable of delivering imaging enhancers or biotherapeutic cargo. To accomplish this, a combinatorial phage display library was biopanned against glioblastoma cell model systems that accurately recapitulate the intra- and inter-tumor heterogeneity and infiltrative nature of the disease. Candidate peptides were screened for specificity and ability to target glioblastoma cells in vivo. Cargo-conjugated peptides delivered contrast-enhancing agents to highly infiltrative tumor populations in intracranial xenograft models without the obvious need for blood brain barrier disruption. Simultaneous use of five independent targeting peptides provided greater coverage of this complex tumor and selected peptides have the capacity to deliver a therapeutic cargo (oncolytic virus VSVΔM51) to the tumor cells in vivo. Herein, we have identified a series of peptides with utility as an innovative platform to assist in targeting glioblastoma for the purpose of diagnostic or prognostic imaging, image-guided surgery, and/or improved delivery of therapeutic agents to glioblastoma cells implicated in disease relapse.
MeSH term(s)	Animals ; Brain Neoplasms ; Cell Line, Tumor ; Glioblastoma/drug therapy ; Humans ; Oncolytic Viruses ; Peptides
Chemical Substances	Peptides
Language	English
Publishing date	2020-05-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603079-8
ISSN	1878-5905 ; 0142-9612
ISSN (online)	1878-5905
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2020.120105
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Article: Development of a peptide-based delivery platform for targeting malignant brain tumors

Rahn, Jennifer J / Lun, Xueqing / Jorch, Selina K / Hao, Xiaoguang / Venugopal, Chitra / Vora, Parvez / Ahn, Bo Young / Babes, Liane / Alshehri, Mana M / Cairncross, J. Gregory / Singh, Sheila K / Kubes, Paul / Senger, Donna L / Robbins, Stephen M

Biomaterials. 2020 Sept., v. 252

2020

Abstract	Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the inability to detect and target glioblastoma disease reservoirs based on a diffuse invasive pattern and the presence of molecular and phenotypic heterogeneity. The goal of this study was to target the invasive and stem-like glioblastoma cells that evade first-line treatments using agents capable of delivering imaging enhancers or biotherapeutic cargo. To accomplish this, a combinatorial phage display library was biopanned against glioblastoma cell model systems that accurately recapitulate the intra- and inter-tumor heterogeneity and infiltrative nature of the disease. Candidate peptides were screened for specificity and ability to target glioblastoma cells in vivo. Cargo-conjugated peptides delivered contrast-enhancing agents to highly infiltrative tumor populations in intracranial xenograft models without the obvious need for blood brain barrier disruption. Simultaneous use of five independent targeting peptides provided greater coverage of this complex tumor and selected peptides have the capacity to deliver a therapeutic cargo (oncolytic virus VSVΔM51) to the tumor cells in vivo. Herein, we have identified a series of peptides with utility as an innovative platform to assist in targeting glioblastoma for the purpose of diagnostic or prognostic imaging, image-guided surgery, and/or improved delivery of therapeutic agents to glioblastoma cells implicated in disease relapse.
Keywords	bacteriophages ; biocompatible materials ; blood-brain barrier ; brain ; drug therapy ; glioblastoma ; humans ; peptides ; phenotypic variation ; radiotherapy ; relapse ; xenotransplantation
Language	English
Dates of publication	2020-09
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	603079-8
ISSN	0142-9612
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2020.120105
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Article ; Online: macroH2A2 antagonizes epigenetic programs of stemness in glioblastoma.

Nikolic, Ana / Maule, Francesca / Bobyn, Anna / Ellestad, Katrina / Paik, Seungil / Marhon, Sajid A / Mehdipour, Parinaz / Lun, Xueqing / Chen, Huey-Miin / Mallard, Claire / Hay, Alexander J / Johnston, Michael J / Gafuik, Christopher J / Zemp, Franz J / Shen, Yaoqing / Ninkovic, Nicoletta / Osz, Katalin / Labit, Elodie / Berger, N Daniel /

Brownsey, Duncan K / Kelly, John J / Biernaskie, Jeff / Dirks, Peter B / Derksen, Darren J / Jones, Steven J M / Senger, Donna L / Chan, Jennifer A / Mahoney, Douglas J / De Carvalho, Daniel D / Gallo, Marco

Nature communications

2023 Volume 14, Issue 1, Page(s) 3062

Abstract: Self-renewal is a crucial property of glioblastoma cells that is enabled by the choreographed functions of chromatin regulators and transcription factors. Identifying targetable epigenetic mechanisms of self-renewal could therefore represent an important ...

Abstract	Self-renewal is a crucial property of glioblastoma cells that is enabled by the choreographed functions of chromatin regulators and transcription factors. Identifying targetable epigenetic mechanisms of self-renewal could therefore represent an important step toward developing effective treatments for this universally lethal cancer. Here we uncover an epigenetic axis of self-renewal mediated by the histone variant macroH2A2. With omics and functional assays deploying patient-derived in vitro and in vivo models, we show that macroH2A2 shapes chromatin accessibility at enhancer elements to antagonize transcriptional programs of self-renewal. macroH2A2 also sensitizes cells to small molecule-mediated cell death via activation of a viral mimicry response. Consistent with these results, our analyses of clinical cohorts indicate that high transcriptional levels of this histone variant are associated with better prognosis of high-grade glioma patients. Our results reveal a targetable epigenetic mechanism of self-renewal controlled by macroH2A2 and suggest additional treatment approaches for glioblastoma patients.
MeSH term(s)	Humans ; Histones/genetics ; Histones/metabolism ; Glioblastoma/metabolism ; Gene Expression Regulation, Neoplastic ; Chromatin/metabolism ; Epigenesis, Genetic ; Cell Line, Tumor ; Neoplastic Stem Cells/metabolism ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism
Chemical Substances	Histones ; Chromatin
Language	English
Publishing date	2023-05-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38919-2
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Article ; Online: Single-cell spatial immune landscapes of primary and metastatic brain tumours.

Karimi, Elham / Yu, Miranda W / Maritan, Sarah M / Perus, Lucas J M / Rezanejad, Morteza / Sorin, Mark / Dankner, Matthew / Fallah, Parvaneh / Doré, Samuel / Zuo, Dongmei / Fiset, Benoit / Kloosterman, Daan J / Ramsay, LeeAnn / Wei, Yuhong / Lam, Stephanie / Alsajjan, Roa / Watson, Ian R / Roldan Urgoiti, Gloria / Park, Morag /

Brandsma, Dieta / Senger, Donna L / Chan, Jennifer A / Akkari, Leila / Petrecca, Kevin / Guiot, Marie-Christine / Siegel, Peter M / Quail, Daniela F / Walsh, Logan A

Nature

2023 Volume 614, Issue 7948, Page(s) 555–563

Abstract: Single-cell technologies have enabled the characterization of the tumour microenvironment at unprecedented depth and have revealed vast cellular diversity among tumour cells and their niche. Anti-tumour immunity relies on cell-cell relationships within ... ...

Abstract	Single-cell technologies have enabled the characterization of the tumour microenvironment at unprecedented depth and have revealed vast cellular diversity among tumour cells and their niche. Anti-tumour immunity relies on cell-cell relationships within the tumour microenvironment
MeSH term(s)	Humans ; Brain/immunology ; Brain/pathology ; Brain Neoplasms/immunology ; Brain Neoplasms/pathology ; Brain Neoplasms/secondary ; Glioblastoma/immunology ; Glioblastoma/pathology ; Glioma/immunology ; Glioma/pathology ; Macrophages/enzymology ; Tumor Microenvironment/immunology ; Single-Cell Analysis ; Neoplasm Metastasis ; Datasets as Topic
Chemical Substances	MPO protein, human (EC 1.11.1.7)
Language	English
Publishing date	2023-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-05680-3
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Article ; Online: Activation of NOTCH Signaling by Tenascin-C Promotes Growth of Human Brain Tumor-Initiating Cells.

Sarkar, Susobhan / Mirzaei, Reza / Zemp, Franz J / Wei, Wu / Senger, Donna L / Robbins, Stephen M / Yong, V Wee

Cancer research

2017 Volume 77, Issue 12, Page(s) 3231–3243

Abstract: Oncogenic signaling by NOTCH is elevated in brain tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is unknown. Here we provide evidence that tenascin-C (TNC), an extracellular matrix protein prominent in malignant ... ...

Abstract	Oncogenic signaling by NOTCH is elevated in brain tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is unknown. Here we provide evidence that tenascin-C (TNC), an extracellular matrix protein prominent in malignant glioma, increases NOTCH activity in BTIC to promote their growth. We demonstrate the proximal localization of TNC and BTIC in human glioblastoma specimens and in orthotopic murine xenografts of human BTIC implanted intracranially. In tissue culture, TNC was superior amongst several extracellular matrix proteins in enhancing the sphere-forming capacity of glioma patient-derived BTIC. Exogenously applied or autocrine TNC increased BTIC growth through an α2β1 integrin-mediated mechanism that elevated NOTCH ligand Jagged1 (JAG1). Microarray analyses and confirmatory PCR and Western analyses in BTIC determined that NOTCH signaling components including JAG1, ADAMTS15, and NICD1/2 were elevated in BITC after TNC exposure. Inhibition of γ-secretase and metalloproteinase proteolysis in the NOTCH pathway, or silencing of α2β1 integrin or JAG1, reduced the proliferative effect of TNC on BTIC. Collectively, our findings identified TNC as a pivotal initiator of elevated NOTCH signaling in BTIC and define the establishment of a TN-α2β1-JAG1-NOTCH signaling axis as a candidate therapeutic target in glioma patients.
MeSH term(s)	Animals ; Blotting, Western ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/physiology ; Gene Knockdown Techniques ; Glioma/metabolism ; Glioma/pathology ; Heterografts ; Humans ; Immunoprecipitation ; Mice ; Mice, SCID ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Oligonucleotide Array Sequence Analysis ; Real-Time Polymerase Chain Reaction ; Receptors, Notch/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Tenascin/metabolism ; Tenascin/pharmacology
Chemical Substances	Receptors, Notch ; Tenascin
Language	English
Publishing date	2017-06-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-16-2171
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