LIVIVO - Search results -

Search results

Result 1 - 10 of total 119

Search options

Article ; Online: MGMT testing always worth an emotion.

Hegi, Monika E / Ichimura, Koichi

2021 Volume 23, Issue 9, Page(s) 1417–1418

MeSH term(s)	DNA Modification Methylases/genetics ; DNA Repair Enzymes/genetics ; Emotions ; Humans ; Tumor Suppressor Proteins
Chemical Substances	Tumor Suppressor Proteins ; DNA Modification Methylases (EC 2.1.1.-) ; MGMT protein, human (EC 2.1.1.63) ; DNA Repair Enzymes (EC 6.5.1.-)
Language	English
Publishing date	2021-07-07
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	2028601-6
ISSN	1523-5866 ; 1522-8517
ISSN (online)	1523-5866
ISSN	1522-8517
DOI	10.1093/neuonc/noab163
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5307: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Molecular insights into brain tumors: ready for translation into novel treatment strategies?

Hegi, Monika E

Current opinion in neurology

2013 Volume 26, Issue 6, Page(s) 678–680

MeSH term(s)	Brain Neoplasms/genetics ; Brain Neoplasms/therapy ; Genetic Testing ; Humans ; Translational Medical Research
Language	English
Publishing date	2013-12
Publishing country	England
Document type	Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1182686-1
ISSN	1473-6551 ; 1350-7540
ISSN (online)	1473-6551
ISSN	1350-7540
DOI	10.1097/WCO.0000000000000038
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2524: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Epigenetic silencing of HTATIP2 in glioblastoma contributes to treatment resistance by enhancing nuclear translocation of the DNA repair protein MPG.

Nguyen, Thi Tham / Rajakannu, Premnath / Pham, Minh Diêu Thanh / Weman, Leo / Jucht, Alexander / Buri, Michelle C / Van Dommelen, Kristof / Hegi, Monika E

Molecular oncology

2023 Volume 17, Issue 9, Page(s) 1744–1762

Abstract: Glioblastoma, the most malignant brain tumor in adults, exhibits characteristic patterns of epigenetic alterations that await elucidation. The DNA methylome of glioblastoma revealed recurrent epigenetic silencing of HTATIP2, which encodes a negative ... ...

Abstract	Glioblastoma, the most malignant brain tumor in adults, exhibits characteristic patterns of epigenetic alterations that await elucidation. The DNA methylome of glioblastoma revealed recurrent epigenetic silencing of HTATIP2, which encodes a negative regulator of importin β-mediated cytoplasmic-nuclear protein translocation. Its deregulation may thus alter the functionality of cancer-relevant nuclear proteins, such as the base excision repair (BER) enzyme N-methylpurine DNA glycosylase (MPG), which has been associated with treatment resistance in GBM. We found that induction of HTATIP2 expression in GBM cells leads to a significant shift of predominantly nuclear to cytoplasmic MPG, whereas depletion of endogenous HTATIP2 results in enhanced nuclear MPG localization. Reduced nuclear MPG localization, prompted by HTATIP2 expression or by depletion of MPG, yielded less phosphorylated-H2AX-positive cells upon treatment with an alkylating agent. This suggested reduced MPG-mediated formation of apurinic/apyrimidinic sites, leaving behind unrepaired DNA lesions, reflecting a reduced capacity of BER in response to the alkylating agent. Epigenetic silencing of HTATIP2 may thus increase nuclear localization of MPG, thereby enhancing the capacity of the glioblastoma cells to repair treatment-related lesions and contributing to treatment resistance.
MeSH term(s)	Humans ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/pathology ; DNA Repair/genetics ; DNA Glycosylases/genetics ; Alkylating Agents ; Nuclear Proteins/genetics ; Epigenesis, Genetic ; Acetyltransferases/genetics ; Acetyltransferases/metabolism ; Transcription Factors/metabolism
Chemical Substances	DNA Glycosylases (EC 3.2.2.-) ; Alkylating Agents ; Nuclear Proteins ; HTATIP2 protein, human (EC 2.3.1.48) ; Acetyltransferases (EC 2.3.1.-) ; Transcription Factors
Language	English
Publishing date	2023-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13494
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6637: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Improving survival in molecularly selected glioblastoma.

Stupp, Roger / Lukas, Rimas V / Hegi, Monika E

Lancet (London, England)

2019 Volume 393, Issue 10172, Page(s) 615–617

MeSH term(s)	Adult ; Brain Neoplasms ; Combined Modality Therapy ; DNA Modification Methylases ; DNA Repair Enzymes ; Glioblastoma ; Humans ; Lomustine ; Temozolomide ; Tumor Suppressor Proteins
Chemical Substances	Tumor Suppressor Proteins ; Lomustine (7BRF0Z81KG) ; DNA Modification Methylases (EC 2.1.1.-) ; MGMT protein, human (EC 2.1.1.63) ; DNA Repair Enzymes (EC 6.5.1.-) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2019-02-14
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/S0140-6736(18)33211-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ua VI Zs.5: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 94: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Glioma epigenetics: From subclassification to novel treatment options.

Gusyatiner, Olga / Hegi, Monika E

Seminars in cancer biology

2017 Volume 51, Page(s) 50–58

Abstract: Gliomas are the most common malignant primary brain tumors, of which glioblastoma is the most malignant form (WHO grade IV), and notorious for treatment resistance. Over the last decade mutations in epigenetic regulator genes have been identified as key ... ...

Abstract	Gliomas are the most common malignant primary brain tumors, of which glioblastoma is the most malignant form (WHO grade IV), and notorious for treatment resistance. Over the last decade mutations in epigenetic regulator genes have been identified as key drivers of subtypes of gliomas with distinct clinical features. Most characteristic are mutations in IDH1 or IDH2 in lower grade gliomas, and histone 3 mutations in pediatric high grade gliomas that are also associated with characteristic DNA methylation patterns. Furthermore, in adult glioblastoma patients epigenetic silencing of the DNA repair gene MGMT by promoter methylation is predictive for benefit from alkylating agent therapy. These epigenetic alterations are used as biomarkers and play a central role for classification of gliomas (WHO 2016) and treatment decisions. Here we review the pivotal role of epigenetic alterations in the etiology and biology of gliomas. We summarize the complex interactions between "driver" mutations, DNA methylation, histone post-translational modifications, and overall chromatin organization, and how they inform current efforts of testing epigenetic compounds and combinations in preclinical and clinical studies.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Glioma/classification ; Glioma/genetics ; Glioma/therapy ; Humans
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2017-11-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2017.11.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2922: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Interrogation of endothelial and mural cells in brain metastasis reveals key immune-regulatory mechanisms.

Bejarano, Leire / Kauzlaric, Annamaria / Lamprou, Eleni / Lourenco, Joao / Fournier, Nadine / Ballabio, Michelle / Colotti, Roberto / Maas, Roeltje / Galland, Sabine / Massara, Matteo / Soukup, Klara / Lilja, Johanna / Brouland, Jean-Philippe / Hottinger, Andreas F / Daniel, Roy T / Hegi, Monika E / Joyce, Johanna A

Cancer cell

2024 Volume 42, Issue 3, Page(s) 378–395.e10

Abstract: Brain metastasis (BrM) is a common malignancy, predominantly originating from lung, melanoma, and breast cancers. The vasculature is a key component of the BrM tumor microenvironment with critical roles in regulating metastatic seeding and progression. ... ...

Abstract	Brain metastasis (BrM) is a common malignancy, predominantly originating from lung, melanoma, and breast cancers. The vasculature is a key component of the BrM tumor microenvironment with critical roles in regulating metastatic seeding and progression. However, the heterogeneity of the major BrM vascular components, namely endothelial and mural cells, is still poorly understood. We perform single-cell and bulk RNA-sequencing of sorted vascular cell types and detect multiple subtypes enriched specifically in BrM compared to non-tumor brain, including previously unrecognized immune regulatory subtypes. We integrate the human data with mouse models, creating a platform to interrogate vascular targets for the treatment of BrM. We find that the CD276 immune checkpoint molecule is significantly upregulated in the BrM vasculature, and anti-CD276 blocking antibodies prolonged survival in preclinical trials. This study provides important insights into the complex interactions between the vasculature, immune cells, and cancer cells, with translational relevance for designing therapeutic interventions.
MeSH term(s)	Mice ; Animals ; Humans ; Female ; Brain Neoplasms/pathology ; Brain/metabolism ; Melanoma ; Breast Neoplasms/pathology ; Transcription Factors/metabolism ; Tumor Microenvironment ; B7 Antigens
Chemical Substances	Transcription Factors ; CD276 protein, human ; B7 Antigens
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2023.12.018
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Senescence Is the Main Trait Induced by Temozolomide in Glioblastoma Cells.

Beltzig, Lea / Schwarzenbach, Christian / Leukel, Petra / Frauenknecht, Katrin B M / Sommer, Clemens / Tancredi, Alessandro / Hegi, Monika E / Christmann, Markus / Kaina, Bernd

Cancers

2022 Volume 14, Issue 9

Abstract: First-line drug in the treatment of glioblastoma, the most severe brain cancer, is temozolomide (TMZ), a DNA-methylating agent that induces the critical damage O6-methylguanine (O6MeG). This lesion is cytotoxic through the generation of mismatch repair- ... ...

Abstract	First-line drug in the treatment of glioblastoma, the most severe brain cancer, is temozolomide (TMZ), a DNA-methylating agent that induces the critical damage O6-methylguanine (O6MeG). This lesion is cytotoxic through the generation of mismatch repair-mediated DNA double-strand breaks (DSBs), which trigger apoptotic pathways. Previously, we showed that O6MeG also induces cellular senescence (CSEN). Here, we show that TMZ-induced CSEN is a late response which has similar kinetics to apoptosis, but at a fourfold higher level. CSEN cells show a high amount of DSBs, which are located outside of telomeres, a high level of ROS and oxidized DNA damage (8-oxo-guanine), and sustained activation of the DNA damage response and histone methylation. Despite the presence of DSBs, CSEN cells are capable of repairing radiation-induced DSBs. Glioblastoma cells that acquired resistance to TMZ became simultaneously resistant to TMZ-induced CSEN. Using a Tet-On glioblastoma cell system, we show that upregulation of MGMT immediately after TMZ completely abrogated apoptosis and CSEN, while induction of MGMT long-term (>72 h) after TMZ did not reduce apoptosis and CSEN. Furthermore, upregulation of MGMT in the senescent cell population had no impact on the survival of senescent cells, indicating that O6MeG is required for induction, but not for maintenance of the senescent state. We further show that, in recurrent GBM specimens, a significantly higher level of DSBs and CSEN-associated histone H3K27me3 was observed than in the corresponding primary tumors. Overall, the data indicate that CSEN is a key node induced in GBM following chemotherapy.
Language	English
Publishing date	2022-04-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14092233
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression.

Tancredi, Alessandro / Gusyatiner, Olga / Bady, Pierre / Buri, Michelle C / Lomazzi, Rémy / Chiesi, Davide / Messerer, Mahmoud / Hegi, Monika E

Cell death & disease

2022 Volume 13, Issue 12, Page(s) 1037

Abstract: Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule ... ...

Abstract	Bromodomain and extra-terminal tail (BET) proteins have been identified as potential epigenetic targets in cancer, including glioblastoma. These epigenetic modifiers link the histone code to gene transcription that can be disrupted with small molecule BET inhibitors (BETi). With the aim of developing rational combination treatments for glioblastoma, we analyzed BETi-induced differential gene expression in glioblastoma derived-spheres, and identified 6 distinct response patterns. To uncover emerging actionable vulnerabilities that can be targeted with a second drug, we extracted the 169 significantly disturbed DNA Damage Response genes and inspected their response pattern. The most prominent candidate with consistent downregulation, was the O-6-methylguanine-DNA methyltransferase (MGMT) gene, a known resistance factor for alkylating agent therapy in glioblastoma. BETi not only reduced MGMT expression in GBM cells, but also inhibited its induction, typically observed upon temozolomide treatment. To determine the potential clinical relevance, we evaluated the specificity of the effect on MGMT expression and MGMT mediated treatment resistance to temozolomide. BETi-mediated attenuation of MGMT expression was associated with reduction of BRD4- and Pol II-binding at the MGMT promoter. On the functional level, we demonstrated that ectopic expression of MGMT under an unrelated promoter was not affected by BETi, while under the same conditions, pharmacologic inhibition of MGMT restored the sensitivity to temozolomide, reflected in an increased level of γ-H2AX, a proxy for DNA double-strand breaks. Importantly, expression of MSH6 and MSH2, which are required for sensitivity to unrepaired O6-methylguanine-lesions, was only briefly affected by BETi. Taken together, the addition of BET-inhibitors to the current standard of care, comprising temozolomide treatment, may sensitize the 50% of patients whose glioblastoma exert an unmethylated MGMT promoter.
MeSH term(s)	Humans ; Temozolomide/pharmacology ; Temozolomide/therapeutic use ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/pathology ; Dacarbazine/pharmacology ; Dacarbazine/therapeutic use ; Nuclear Proteins/metabolism ; Antineoplastic Agents, Alkylating/pharmacology ; DNA Methylation/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Transcription Factors/metabolism ; DNA Modification Methylases/genetics ; DNA Modification Methylases/metabolism ; O(6)-Methylguanine-DNA Methyltransferase/genetics ; O(6)-Methylguanine-DNA Methyltransferase/metabolism ; O(6)-Methylguanine-DNA Methyltransferase/therapeutic use ; DNA Repair Enzymes/genetics ; DNA Repair Enzymes/metabolism ; DNA/metabolism ; Cell Cycle Proteins/metabolism
Chemical Substances	Temozolomide (YF1K15M17Y) ; Dacarbazine (7GR28W0FJI) ; Nuclear Proteins ; Antineoplastic Agents, Alkylating ; Transcription Factors ; DNA Modification Methylases (EC 2.1.1.-) ; O(6)-Methylguanine-DNA Methyltransferase (EC 2.1.1.63) ; DNA Repair Enzymes (EC 6.5.1.-) ; DNA (9007-49-2) ; BRD4 protein, human ; Cell Cycle Proteins ; MGMT protein, human (EC 2.1.1.63)
Language	English
Publishing date	2022-12-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-022-05497-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Withholding temozolomide in glioblastoma patients with unmethylated MGMT promoter--still a dilemma?

Hegi, Monika E / Stupp, Roger

Neuro-oncology

2015 Volume 17, Issue 11, Page(s) 1425–1427

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; DNA Methylation/genetics ; DNA Modification Methylases/genetics ; DNA Repair Enzymes/genetics ; Dacarbazine/analogs & derivatives ; Dacarbazine/therapeutic use ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Humans ; Promoter Regions, Genetic/genetics ; Tumor Suppressor Proteins/genetics
Chemical Substances	Antineoplastic Agents ; Tumor Suppressor Proteins ; Dacarbazine (7GR28W0FJI) ; DNA Modification Methylases (EC 2.1.1.-) ; MGMT protein, human (EC 2.1.1.63) ; DNA Repair Enzymes (EC 6.5.1.-) ; temozolomide (YF1K15M17Y)
Language	English
Publishing date	2015-11
Publishing country	England
Document type	Editorial
ZDB-ID	2028601-6
ISSN	1523-5866 ; 1522-8517
ISSN (online)	1523-5866
ISSN	1522-8517
DOI	10.1093/neuonc/nov198
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5307: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Immunogenomic analysis of human brain metastases reveals diverse immune landscapes across genetically distinct tumors.

Álvarez-Prado, Ángel F / Maas, Roeltje R / Soukup, Klara / Klemm, Florian / Kornete, Mara / Krebs, Fanny S / Zoete, Vincent / Berezowska, Sabina / Brouland, Jean-Philippe / Hottinger, Andreas F / Daniel, Roy T / Hegi, Monika E / Joyce, Johanna A

Cell reports. Medicine

2023 Volume 4, Issue 1, Page(s) 100900

Abstract: Brain metastases (BrMs) are the most common form of brain tumors in adults and frequently originate from lung and breast primary cancers. BrMs are associated with high mortality, emphasizing the need for more effective therapies. Genetic profiling of ... ...

Abstract	Brain metastases (BrMs) are the most common form of brain tumors in adults and frequently originate from lung and breast primary cancers. BrMs are associated with high mortality, emphasizing the need for more effective therapies. Genetic profiling of primary tumors is increasingly used as part of the effort to guide targeted therapies against BrMs, and immune-based strategies for the treatment of metastatic cancer are gaining momentum. However, the tumor immune microenvironment (TIME) of BrM is extremely heterogeneous, and whether specific genetic profiles are associated with distinct immune states remains unknown. Here, we perform an extensive characterization of the immunogenomic landscape of human BrMs by combining whole-exome/whole-genome sequencing, RNA sequencing of immune cell populations, flow cytometry, immunofluorescence staining, and tissue imaging analyses. This revealed unique TIME phenotypes in genetically distinct lung- and breast-BrMs, thereby enabling the development of personalized immunotherapies tailored by the genetic makeup of the tumors.
MeSH term(s)	Adult ; Humans ; Female ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Melanoma ; Immunotherapy ; Skin Neoplasms ; Tumor Microenvironment/genetics
Language	English
Publishing date	2023-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2022.100900
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED