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Article ; Online: It's all in the combination: decoding the epigenome for cancer research and diagnostics.

Furth, Noa / Shema, Efrat

Current opinion in genetics & development

2022 Volume 73, Page(s) 101899

Abstract: Genome regulation is governed by the dynamics of chromatin modifications. The extensive and diverse array of DNA and histone modifications allow multiple elements to act combinatorically and direct tissue-specific and cell-specific outcomes. Yet, our ... ...

Abstract	Genome regulation is governed by the dynamics of chromatin modifications. The extensive and diverse array of DNA and histone modifications allow multiple elements to act combinatorically and direct tissue-specific and cell-specific outcomes. Yet, our ability to elucidate these complex combinations and link them to normal genome regulation, as well as understand their deregulation in cancer, has been hindered by the lack of suitable technologies. Here, we describe recent findings indicating the importance of the combinatorial epigenome, and novel methodologies to measure and characterize these combinations. These complementary methods span multiple disciplines, providing a means to decode epigenetic combinations and link them to biological outcomes. Finally, we discuss the promise of harnessing the rich combinatorial epigenetic information to improve cancer diagnostics and monitoring.
MeSH term(s)	Chromatin/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic/genetics ; Epigenome/genetics ; Epigenomics ; Genome ; Histone Code/genetics ; Neoplasms/diagnosis ; Neoplasms/genetics
Chemical Substances	Chromatin
Language	English
Publishing date	2022-01-25
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1077312-5
ISSN	1879-0380 ; 0959-437X
ISSN (online)	1879-0380
ISSN	0959-437X
DOI	10.1016/j.gde.2022.101899
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Article ; Online: The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway.

Furth, Noa / Aylon, Yael

Cell death and differentiation

2017 Volume 24, Issue 9, Page(s) 1488–1501

Abstract: Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as ... ...

Abstract	Proper cellular functionality and homeostasis are maintained by the convergent integration of various signaling cascades, which enable cells to respond to internal and external changes. The Dbf2-related kinases LATS1 and LATS2 (LATS) have emerged as central regulators of cell fate, by modulating the functions of numerous oncogenic or tumor suppressive effectors, including the canonical Hippo effectors YAP/TAZ, the Aurora mitotic kinase family, estrogen signaling and the tumor suppressive transcription factor p53. While the basic functions of the LATS kinase module are strongly conserved over evolution, the genomic duplication event leading to the emergence of two closely related kinases in higher organisms has increased the complexity of this signaling network. Here, we review the LATS1 and LATS2 intrinsic features as well as their reported cellular activities, emphasizing unique characteristics of each kinase. While differential activities between the two paralogous kinases have been reported, many converge to similar pathways and outcomes. Interestingly, the regulatory networks controlling the mRNA expression pattern of LATS1 and LATS2 differ strongly, and may contribute to the differences in protein binding partners of each kinase and in the subcellular locations in which each kinase exerts its functions.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/physiology ; Gene Expression Regulation/genetics ; Gene Expression Regulation/physiology ; Humans ; Phosphorylation/genetics ; Phosphorylation/physiology ; Protein Processing, Post-Translational/genetics ; Protein Processing, Post-Translational/physiology ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Tumor Suppressor Proteins ; LATS1 protein, human (EC 2.7.1.-) ; LATS2 protein, human (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-06-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2017.99
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Article: Single-molecule systems for detection and monitoring of plasma circulating nucleosomes and oncoproteins in Diffuse Midline Glioma.

Erez, Nir / Furth, Noa / Fedyuk, Vadim / Wadden, Jack / Aittaleb, Rayan / Schwark, Kallen / Niculcea, Michael / Miclea, Madeline / Mody, Rajen / Franson, Andrea / Eze, Augistine / Nourmohammadi, Niku / Nazarian, Javad / Venneti, Sriram / Koschmann, Carl / Shema, Efrat

bioRxiv : the preprint server for biology

2023

Abstract: The analysis of cell-free tumor DNA (ctDNA) and proteins in the blood of cancer patients potentiates a new generation of non-invasive diagnostics and treatment monitoring approaches. However, confident detection of these tumor-originating markers is ... ...

Abstract	The analysis of cell-free tumor DNA (ctDNA) and proteins in the blood of cancer patients potentiates a new generation of non-invasive diagnostics and treatment monitoring approaches. However, confident detection of these tumor-originating markers is challenging, especially in the context of brain tumors, in which extremely low amounts of these analytes circulate in the patient's plasma. Here, we applied a sensitive single-molecule technology to profile multiple histone modifications on millions of individual nucleosomes from the plasma of Diffuse Midline Glioma (DMG) patients. The system reveals epigenetic patterns that are unique to DMG, significantly differentiating this group of patients from healthy subjects or individuals diagnosed with other cancer types. We further develop a method to directly capture and quantify the tumor-originating oncoproteins, H3-K27M and mutant p53, from the plasma of children diagnosed with DMG. This single-molecule system allows for accurate molecular classification of patients, utilizing less than 1ml of liquid-biopsy material. Furthermore, we show that our simple and rapid detection strategy correlates with MRI measurements and droplet-digital PCR (ddPCR) measurements of ctDNA, highlighting the utility of this approach for non-invasive treatment monitoring of DMG patients. This work underscores the clinical potential of single-molecule-based, multi-parametric assays for DMG diagnosis and treatment monitoring.
Language	English
Publishing date	2023-11-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.21.568019
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Article ; Online: p53 shades of Hippo.

Furth, Noa / Aylon, Yael / Oren, Moshe

Cell death and differentiation

2017 Volume 25, Issue 1, Page(s) 81–92

Abstract: The three p53 family members, p53, p63 and p73, are structurally similar and share many biochemical activities. Yet, along with their common fundamental role in protecting genomic fidelity, each has acquired distinct functions related to diverse cell ... ...

Abstract	The three p53 family members, p53, p63 and p73, are structurally similar and share many biochemical activities. Yet, along with their common fundamental role in protecting genomic fidelity, each has acquired distinct functions related to diverse cell autonomous and non-autonomous processes. Similar to the p53 family, the Hippo signaling pathway impacts a multitude of cellular processes, spanning from cell cycle and metabolism to development and tumor suppression. The core Hippo module consists of the tumor-suppressive MST-LATS kinases and oncogenic transcriptional co-effectors YAP and TAZ. A wealth of accumulated data suggests a complex and delicate regulatory network connecting the p53 and Hippo pathways, in a highly context-specific manner. This generates multiple layers of interaction, ranging from interdependent and collaborative signaling to apparent antagonistic activity. Furthermore, genetic and epigenetic alterations can disrupt this homeostatic network, paving the way to genomic instability and cancer. This strengthens the need to better understand the nuances that control the molecular function of each component and the cross-talk between the different components. Here, we review interactions between the p53 and Hippo pathways within a subset of physiological contexts, focusing on normal stem cells and development, as well as regulation of apoptosis, senescence and metabolism in transformed cells.
MeSH term(s)	Animals ; Apoptosis ; Carcinogenesis ; Cellular Senescence ; Humans ; Neoplastic Stem Cells/metabolism ; Ploidies ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Stem Cells/metabolism ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Transcription Factors ; Tumor Suppressor Protein p53 ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-10-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2017.163
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Article ; Online: miR‐4734 conditionally suppresses ER stress‐associated proinflammatory responses

Michael, Dan / Feldmesser, Ester / Gonen, Chagay / Furth, Noa / Maman, Alexander / Heyman, Ori / Argoetti, Amir / Tofield, Adin / Baichman‐Kass, Amichai / Ben‐Dov, Aviyah / Benbenisti, Dan / Hen, Nadav / Rotkopf, Ron / Ganci, Federica / Blandino, Giovanni / Ulitsky, Igor / Oren, Moshe

FEBS Letters. 2023 May, v. 597, no. 9 p.1233-1245

2023

Abstract: Prolonged metabolic stress can lead to severe pathologies. In metabolically challenged primary fibroblasts, we assigned a novel role for the poorly characterized miR‐4734 in restricting ATF4 and IRE1‐mediated upregulation of a set of proinflammatory ... ...

Abstract	Prolonged metabolic stress can lead to severe pathologies. In metabolically challenged primary fibroblasts, we assigned a novel role for the poorly characterized miR‐4734 in restricting ATF4 and IRE1‐mediated upregulation of a set of proinflammatory cytokines and endoplasmic reticulum stress‐associated genes. Conversely, inhibition of this miRNA augmented the expression of those genes. Mechanistically, miR‐4734 was found to restrict the expression of the transcriptional activator NF‐kappa‐B inhibitor zeta (NFKBIZ), which is required for optimal expression of the proinflammatory genes and whose mRNA is targeted directly by miR‐4734. Concordantly, overexpression of NFKBIZ compromised the effects of miR‐4734, underscoring the importance of this direct targeting. As the effects of miR‐4734 were evident under stress but not under basal conditions, it may possess therapeutic utility towards alleviating stress‐induced pathologies.
Keywords	cytokines ; endoplasmic reticulum ; fibroblasts ; microRNA ; therapeutics ; transactivators
Language	English
Dates of publication	2023-05
Size	p. 1233-1245.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.14548
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: H3-K27M-mutant nucleosomes interact with MLL1 to shape the glioma epigenetic landscape.

Furth, Noa / Algranati, Danielle / Dassa, Bareket / Beresh, Olga / Fedyuk, Vadim / Morris, Natasha / Kasper, Lawryn H / Jones, Dan / Monje, Michelle / Baker, Suzanne J / Shema, Efrat

Cell reports

2022 Volume 39, Issue 7, Page(s) 110836

Abstract: Cancer-associated mutations in genes encoding histones dramatically reshape chromatin and support tumorigenesis. Lysine to methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to abrogate ... ...

Abstract	Cancer-associated mutations in genes encoding histones dramatically reshape chromatin and support tumorigenesis. Lysine to methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to abrogate polycomb repressive complex 2 (PRC2) activity. We applied single-molecule systems to image individual nucleosomes and delineate the combinatorial epigenetic patterns associated with H3-K27M expression. We found that chromatin marks on H3-K27M-mutant nucleosomes are dictated both by their incorporation preferences and by intrinsic properties of the mutation. Mutant nucleosomes not only preferentially bind PRC2 but also directly interact with MLL1, leading to genome-wide redistribution of H3K4me3. H3-K27M-mediated deregulation of repressive and active chromatin marks leads to unbalanced "bivalent" chromatin, which may support a poorly differentiated cellular state. This study provides evidence for a direct effect of H3-K27M oncohistone on the MLL1-H3K4me3 pathway and highlights the capability of single-molecule tools to reveal mechanisms of chromatin deregulation in cancer.
MeSH term(s)	Brain Neoplasms/genetics ; Child ; Chromatin/genetics ; Chromatin/metabolism ; Epigenesis, Genetic ; Glioma/genetics ; Glioma/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/genetics ; Histones/metabolism ; Humans ; Mutation ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Nucleosomes/genetics ; Nucleosomes/metabolism ; Polycomb Repressive Complex 2/genetics ; Polycomb Repressive Complex 2/metabolism
Chemical Substances	Chromatin ; Histones ; KMT2A protein, human ; Nucleosomes ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2022-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110836
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Article ; Online: Single-cell epigenetic analysis reveals principles of chromatin states in H3.3-K27M gliomas.

Harpaz, Nofar / Mittelman, Tamir / Beresh, Olga / Griess, Ofir / Furth, Noa / Salame, Tomer-Meir / Oren, Roni / Fellus-Alyagor, Liat / Harmelin, Alon / Alexandrescu, Sanda / Marques, Joana Graca / Filbin, Mariella G / Ron, Guy / Shema, Efrat

Molecular cell

2022 Volume 82, Issue 14, Page(s) 2696–2713.e9

Abstract: Cancer cells are highly heterogeneous at the transcriptional level and epigenetic state. Methods to study epigenetic heterogeneity are limited in throughput and information obtained per cell. Here, we adapted cytometry by time-of-flight (CyTOF) to ... ...

Abstract	Cancer cells are highly heterogeneous at the transcriptional level and epigenetic state. Methods to study epigenetic heterogeneity are limited in throughput and information obtained per cell. Here, we adapted cytometry by time-of-flight (CyTOF) to analyze a wide panel of histone modifications in primary tumor-derived lines of diffused intrinsic pontine glioma (DIPG). DIPG is a lethal glioma, driven by a histone H3 lysine 27 mutation (H3-K27M). We identified two epigenetically distinct subpopulations in DIPG, reflecting inherent heterogeneity in expression of the mutant histone. These two subpopulations are robust across tumor lines derived from different patients and show differential proliferation capacity and expression of stem cell and differentiation markers. Moreover, we demonstrate the use of these high-dimensional data to elucidate potential interactions between histone modifications and epigenetic alterations during the cell cycle. Our work establishes new concepts for the analysis of epigenetic heterogeneity in cancer that could be applied to diverse biological systems.
MeSH term(s)	Brain Stem Neoplasms/genetics ; Brain Stem Neoplasms/metabolism ; Brain Stem Neoplasms/pathology ; Chromatin/genetics ; Epigenesis, Genetic ; Glioma/metabolism ; Histones/genetics ; Histones/metabolism ; Humans ; Mutation
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2022-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.05.023
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Article ; Online: An Aurora A-Lats-Aurora B axis ensures proper chromosome segregation.

Furth, Noa / Oren, Moshe

Cell cycle (Georgetown, Tex.)

2011 Volume 10, Issue 18, Page(s) 3055

MeSH term(s)	Animals ; Humans ; Mitosis ; Protein-Serine-Threonine Kinases/metabolism ; Spindle Apparatus/metabolism ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Tumor Suppressor Proteins ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2011-09-15
Publishing country	United States
Document type	News ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.10.18.17046
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Article ; Online: H3-K27M-mutant nucleosomes interact with MLL1 to shape the glioma epigenetic landscape

Noa Furth / Danielle Algranati / Bareket Dassa / Olga Beresh / Vadim Fedyuk / Natasha Morris / Lawryn H. Kasper / Dan Jones / Michelle Monje / Suzanne J. Baker / Efrat Shema

Cell Reports, Vol 39, Iss 7, Pp 110836- (2022)

2022

Abstract: Summary: Cancer-associated mutations in genes encoding histones dramatically reshape chromatin and support tumorigenesis. Lysine to methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to ... ...

Abstract	Summary: Cancer-associated mutations in genes encoding histones dramatically reshape chromatin and support tumorigenesis. Lysine to methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to abrogate polycomb repressive complex 2 (PRC2) activity. We applied single-molecule systems to image individual nucleosomes and delineate the combinatorial epigenetic patterns associated with H3-K27M expression. We found that chromatin marks on H3-K27M-mutant nucleosomes are dictated both by their incorporation preferences and by intrinsic properties of the mutation. Mutant nucleosomes not only preferentially bind PRC2 but also directly interact with MLL1, leading to genome-wide redistribution of H3K4me3. H3-K27M-mediated deregulation of repressive and active chromatin marks leads to unbalanced “bivalent” chromatin, which may support a poorly differentiated cellular state. This study provides evidence for a direct effect of H3-K27M oncohistone on the MLL1-H3K4me3 pathway and highlights the capability of single-molecule tools to reveal mechanisms of chromatin deregulation in cancer.
Keywords	CP: Cancer ; CP: Molecular biology ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Breast cancer plasticity is restricted by a LATS1-NCOR1 repressive axis

Yael Aylon / Noa Furth / Giuseppe Mallel / Gilgi Friedlander / Nishanth Belugali Nataraj / Meng Dong / Ori Hassin / Rawan Zoabi / Benjamin Cohen / Vanessa Drendel / Tomer Meir Salame / Saptaparna Mukherjee / Nofar Harpaz / Randy Johnson / Walter E. Aulitzky / Yosef Yarden / Efrat Shema / Moshe Oren

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 20

Abstract: LATS1 is reported to regulate the transition of luminal-basal-like cell plasticity in breast cancer. Here the authors report that LATS1 limits the progression of luminal breast cancer by associating with NCOR1 nuclear corepressor to repress ERα- ... ...

Abstract	LATS1 is reported to regulate the transition of luminal-basal-like cell plasticity in breast cancer. Here the authors report that LATS1 limits the progression of luminal breast cancer by associating with NCOR1 nuclear corepressor to repress ERα-downregulated genes in luminal cells.
Keywords	Science ; Q
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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