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Article: Hypermethylated Colorectal Cancer Tumours Present a Myc-Driven Hypermetabolism with a One-Carbon Signature Associated with Worsen Prognosis.

Desterke, Christophe / Jaulin, Fanny / Dornier, Emmanuel

2024 Volume 12, Issue 3

Abstract: Colorectal cancer (CRC) is the second cause of cancer-related death; the CpG-island methylation pathway (CIMP) is associated with KRAS/BRAF mutations, two oncogenes rewiring cell metabolism, worse prognosis, and resistance to classical chemotherapies. ... ...

Abstract	Colorectal cancer (CRC) is the second cause of cancer-related death; the CpG-island methylation pathway (CIMP) is associated with KRAS/BRAF mutations, two oncogenes rewiring cell metabolism, worse prognosis, and resistance to classical chemotherapies. Despite this, the question of a possible metabolic rewiring in CIMPs has never been investigated. Here, we analyse whether metabolic dysregulations are associated with tumour methylation by evaluating the transcriptome of CRC tumours. CIMP-high patients were found to present a hypermetabolism, activating mainly carbohydrates, folates, sphingolipids, and arachidonic acid metabolic pathways. A third of these genes had epigenetic targets of Myc in their proximal promoter, activating carboxylic acid, tetrahydrofolate interconversion, nucleobase, and oxoacid metabolisms. In the Myc signature, the expression of GAPDH, TYMS, DHFR, and TK1 was enough to predict methylation levels, microsatellite instability (MSI), and mutations in the mismatch repair (MMR) machinery, which are strong indicators of responsiveness to immunotherapies. Finally, we discovered that CIMP tumours harboured an increase in genes involved in the one-carbon metabolism, a pathway critical to providing nucleotides for cancer growth and methyl donors for DNA methylation, which is associated with worse prognosis and tumour hypermethylation. Transcriptomics could hence become a tool to help clinicians stratify their patients better.
Language	English
Publishing date	2024-03-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12030590
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Article ; Online: HLA-DQ Diversity Is Associated With Humoral Response to Vaccines in Patients Awaiting or After Liver Transplantation.

Féray, Cyrille / Allain, Vincent / Desterke, Christophe / Roche, Bruno / Coilly, Audrey / Caillat-Zucman, Sophie

Gastroenterology

2024 Volume 166, Issue 5, Page(s) 915–917.e3

MeSH term(s)	Humans ; Liver Transplantation ; HLA-DQ Antigens/immunology ; HLA-DQ Antigens/genetics ; Immunity, Humoral/drug effects ; Female ; Male ; Middle Aged ; Waiting Lists ; Adult ; Vaccination
Chemical Substances	HLA-DQ Antigens
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Research Support, Non-U.S. Gov't ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2024.01.009
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Article: Impact of HCV Infection on Hepatocyte Polarity and Plasticity.

Agnetti, Jean / Desterke, Christophe / Gassama-Diagne, Ama

Pathogens (Basel, Switzerland)

2022 Volume 11, Issue 3

Abstract: The hepatitis C virus (HCV) is an oncogenic virus that alters the cell polarization machinery in order to enter the hepatocyte and replicate. While these alterations are relatively well defined, their consequences in the evolution of the disease remain ... ...

Abstract	The hepatitis C virus (HCV) is an oncogenic virus that alters the cell polarization machinery in order to enter the hepatocyte and replicate. While these alterations are relatively well defined, their consequences in the evolution of the disease remain poorly documented. Since 2012, HCV infection can be effectively cured with the advent of direct acting antivirals (DAA). Nevertheless, patients cured of their HCV infection still have a high risk of developing hepatocellular carcinoma (HCC). Importantly, it has been shown that some of the deregulations induced by HCV are maintained despite a sustained virologic response (SVR), including the down-regulation of some hepatocyte functions such as bile acid metabolism, exemplifying cell dedifferentiation, and the up-regulation of the epithelial-mesenchymal transition (EMT). EMT is a process by which epithelial cells lose their differentiation and their specific polarity to acquire mesenchymal cell properties, including migration and extracellular matrix remodeling capabilities. Of note, epithelial cell polarity acts as a gatekeeper against EMT. Thus, it remains important to elucidate the mechanisms by which HCV alters polarity and promotes EMT that could participate in viral-induced hepatic carcinogenesis. In this review, we define the main steps involved in the polarization process of epithelial cells and recall the essential cellular actors involved. We also highlight the particularities of hepatocyte polarity, responsible for their unique morphology. We then focus on the alterations by HCV of epithelial cell polarity and the consequences of the transformation of hepatocytes involved in the carcinogenesis process.
Language	English
Publishing date	2022-03-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens11030337
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Article ; Online: BIRC-3 mutated monoclonal B lymphocytosis without evolution to chronic lymphocytic leukemia (CLL).

Nasr, Amen Allah / Fund, Xavier / Barreau, Sylvain / Desterke, Christophe / Borie, Claire / Oudrhiri, Noufissa / Faivre, Jamila / Bennaceur-Griscelli, A / Turhan, A G

Leukemia & lymphoma

2024 Volume 65, Issue 5, Page(s) 692–695

MeSH term(s)	Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Lymphocytosis/genetics ; Lymphocytosis/diagnosis ; Lymphocytosis/pathology ; Mutation ; Baculoviral IAP Repeat-Containing 3 Protein/genetics ; B-Lymphocytes/pathology ; B-Lymphocytes/metabolism ; B-Lymphocytes/immunology ; Male ; Aged ; Clonal Evolution/genetics ; Middle Aged ; Female
Chemical Substances	Baculoviral IAP Repeat-Containing 3 Protein (EC 2.3.2.27) ; BIRC3 protein, human (EC 2.3.2.27)
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Letter ; Case Reports ; Journal Article
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2024.2308665
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Article ; Online: Modeling RET-Rearranged Non-Small Cell Lung Cancer (NSCLC): Generation of Lung Progenitor Cells (LPCs) from Patient-Derived Induced Pluripotent Stem Cells (iPSCs).

Marcoux, Paul / Hwang, Jin Wook / Desterke, Christophe / Imeri, Jusuf / Bennaceur-Griscelli, Annelise / Turhan, Ali G

Cells

2023 Volume 12, Issue 24

Abstract: REarranged during Transfection (RET) oncogenic rearrangements can occur in 1-2% of lung adenocarcinomas. While RET-driven NSCLC models have been developed using various approaches, no model based on patient-derived induced pluripotent stem cells (iPSCs) ... ...

Abstract	REarranged during Transfection (RET) oncogenic rearrangements can occur in 1-2% of lung adenocarcinomas. While RET-driven NSCLC models have been developed using various approaches, no model based on patient-derived induced pluripotent stem cells (iPSCs) has yet been described. Patient-derived iPSCs hold great promise for disease modeling and drug screening. However, generating iPSCs with specific oncogenic drivers, like
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Cell Differentiation/genetics ; Induced Pluripotent Stem Cells ; Lung/pathology ; Lung Neoplasms/pathology ; Proto-Oncogene Proteins c-ret/genetics
Chemical Substances	Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-12-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12242847
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Article ; Online: Direct Reprogramming of Hepatocytes Into JAK/Stat-Dependent LGR5+ Liver Cells Able to Initiate Intrahepatic Cholangiocarcinoma.

Chaker, Diana / Desterke, Christophe / Moniaux, Nicolas / Bani, Mohamed-Amine / Oudrhiri, Noufissa / Faivre, Jamila / Turhan, Ali G / Bennaceur-Griscelli, Annelise / Griscelli, Frank

Stem cells (Dayton, Ohio)

2024 Volume 42, Issue 4, Page(s) 301–316

Abstract: Somatic cells that have been partially reprogrammed by the factors Oct4, Sox2, Klf4, and cMyc (OSKM) have been demonstrated to be potentially tumorigenic in vitro and in vivo due to the acquisition of cancer-associated genomic alterations and the absence ...

Abstract	Somatic cells that have been partially reprogrammed by the factors Oct4, Sox2, Klf4, and cMyc (OSKM) have been demonstrated to be potentially tumorigenic in vitro and in vivo due to the acquisition of cancer-associated genomic alterations and the absence of OSKM clearance over time. In the present study, we obtained partially reprogrammed, SSEA1-negative cells by transducing murine hepatocytes with Δ1Δ3-deleted adenoviruses that expressed the 4 OSKM factors. We observed that, under long-term 2D and 3D culture conditions, hepatocytes could be converted into LGR5-positive cells with self-renewal capacity that was dependent on 3 cross-signaling pathways: IL6/Jak/Stat3, LGR5/R-spondin, and Wnt/β-catenin. Following engraftment in syngeneic mice, LGR5-positive cells that expressed the cancer markers CD51, CD166, and CD73 were capable of forming invasive and metastatic tumors reminiscent of intrahepatic cholangiocarcinoma (ICC): they were positive for CK19 and CK7, featured associations of cord-like structures, and contained cuboidal and atypical cells with dissimilar degrees of pleomorphism and mitosis. The LGR5+-derived tumors exhibited a highly vascularized stroma with substantial fibrosis. In addition, we identified pro-angiogenic factors and signaling pathways involved in neo-angiogenesis and vascular development, which represent potential new targets for anti-angiogenic strategies to overcome tumor resistance to current ICC treatments.
MeSH term(s)	Animals ; Mice ; Hepatocytes/metabolism ; Cholangiocarcinoma/genetics ; Cholangiocarcinoma/metabolism ; Bile Duct Neoplasms/genetics ; Bile Duct Neoplasms/metabolism ; Bile Ducts, Intrahepatic/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Wnt Signaling Pathway/genetics
Chemical Substances	Receptors, G-Protein-Coupled
Language	English
Publishing date	2024-01-23
Publishing country	England
Document type	Journal Article
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1093/stmcls/sxae006
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Article: Ferroptosis Inducers Upregulate PD-L1 in Recurrent Triple-Negative Breast Cancer.

Desterke, Christophe / Xiang, Yao / Elhage, Rima / Duruel, Clémence / Chang, Yunhua / Hamaï, Ahmed

Cancers

2023 Volume 16, Issue 1

Abstract: 1) Background: Triple-negative breast cancer (TNBC) is a distinct subgroup of breast cancer presenting a high level of recurrence, and neo-adjuvant chemotherapy is beneficial in its therapy management. Anti-PD-L1 immunotherapy improves the effect of neo- ...

Abstract	(1) Background: Triple-negative breast cancer (TNBC) is a distinct subgroup of breast cancer presenting a high level of recurrence, and neo-adjuvant chemotherapy is beneficial in its therapy management. Anti-PD-L1 immunotherapy improves the effect of neo-adjuvant therapy in TNBC. (2) Methods: Immune-modulation and ferroptosis-related R-packages were developed for integrative omics analyses under ferroptosis-inducer treatments: TNBC cells stimulated with ferroptosis inducers (GSE173905, GSE154425), single cell data (GSE191246) and mass spectrometry on breast cancer stem cells. Clinical association analyses were carried out with breast tumors (TCGA and METABRIC cohorts). Protein-level validation was investigated through protein atlas proteome experiments. (3) Results: Erastin/RSL3 ferroptosis inducers upregulate CD274 in TNBC cells (MDA-MB-231 and HCC38). In breast cancer, CD274 expression is associated with overall survival. Breast tumors presenting high expression of CD274 upregulated some ferroptosis drivers associated with prognosis: IDO1, IFNG and TNFAIP3. At the protein level, the induction of Cd274 and Tnfaip3 was confirmed in breast cancer stem cells under salinomycin treatment. In a 4T1 tumor treated with cyclophosphamide, the single cell expression of Cd274 was found to increase both in myeloid- and lymphoid-infiltrated cells, independently of its receptor Pdcd1. The CD274 ferroptosis-driver score computed on a breast tumor transcriptome stratified patients on their prognosis: low score was observed in the basal subgroup, with a higher level of recurrent risk scores (oncotypeDx, ggi and gene70 scores). In the METABRIC cohort, CD274, IDO1, IFNG and TNFAIP3 were found to be overexpressed in the TNBC subgroup. The CD274 ferroptosis-driver score was found to be associated with overall survival, independently of TNM classification and age diagnosis. The tumor expression of CD274, TNFAIP3, IFNG and IDO1, in a biopsy of breast ductal carcinoma, was confirmed at the protein level (4) Conclusions: Ferroptosis inducers upregulate PD-L1 in TNBC cells, known to be an effective target of immunotherapy in high-risk early TNBC patients who received neo-adjuvant therapy. Basal and TNBC tumors highly expressed CD274 and ferroptosis drivers: IFNG, TNFAIP3 and IDO1. The CD274 ferroptosis-driver score is associated with prognosis and to the risk of recurrence in breast cancer. A potential synergy of ferroptosis inducers with anti-PD-L1 immunotherapy is suggested for recurrent TNBC.
Language	English
Publishing date	2023-12-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers16010155
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Article ; Online: Adverse Crosstalk between Extracellular Matrix Remodeling and Ferroptosis in Basal Breast Cancer.

Desterke, Christophe / Cosialls, Emma / Xiang, Yao / Elhage, Rima / Duruel, Clémence / Chang, Yunhua / Hamaï, Ahmed

Cells

2023 Volume 12, Issue 17

Abstract: 1) Background: Breast cancer is a frequent heterogeneous disorder diagnosed in women and causes a high number of mortality among this population due to rapid metastasis and disease recurrence. Ferroptosis can inhibit breast cancer cell growth, improve ... ...

Abstract	(1) Background: Breast cancer is a frequent heterogeneous disorder diagnosed in women and causes a high number of mortality among this population due to rapid metastasis and disease recurrence. Ferroptosis can inhibit breast cancer cell growth, improve the sensitivity of chemotherapy and radiotherapy, and inhibit distant metastases, potentially impacting the tumor microenvironment. (2) Methods: Through data mining, the ferroptosis/extracellular matrix remodeling literature text-mining results were integrated into the breast cancer transcriptome cohort, taking into account patients with distant relapse-free survival (DRFS) under adjuvant therapy (anthracyclin + taxanes) with validation in an independent METABRIC cohort, along with the MDA-MB-231 and HCC338 transcriptome functional experiments with ferroptosis activations (GSE173905). (3) Results: Ferroptosis/extracellular matrix remodeling text-mining identified 910 associated genes. Univariate Cox analyses focused on breast cancer (GSE25066) selected 252 individual significant genes, of which 170 were found to have an adverse expression. Functional enrichment of these 170 adverse genes predicted basal breast cancer signatures. Through text-mining, some ferroptosis-significant adverse-selected genes shared citations in the domain of ECM remodeling, such as TNF, IL6, SET, CDKN2A, EGFR, HMGB1, KRAS, MET, LCN2, HIF1A, and TLR4. A molecular score based on the expression of the eleven genes was found predictive of the worst prognosis breast cancer at the univariate level: basal subtype, short DRFS, high-grade values 3 and 4, and estrogen and progesterone receptor negative and nodal stages 2 and 3. This eleven-gene signature was validated as regulated by ferroptosis inductors (erastin and RSL3) in the triple-negative breast cancer cellular model MDA-MB-231. (4) Conclusions: The crosstalk between ECM remodeling-ferroptosis functionalities allowed for defining a molecular score, which has been characterized as an independent adverse parameter in the prognosis of breast cancer patients. The gene signature of this molecular score has been validated to be regulated by erastin/RSL3 ferroptosis activators. This molecular score could be promising to evaluate the ECM-related impact of ferroptosis target therapies in breast cancer.
MeSH term(s)	Humans ; Female ; Ferroptosis/genetics ; Neoplasm Recurrence, Local ; Cell Physiological Phenomena ; Triple Negative Breast Neoplasms/genetics ; Estrogens ; Tumor Microenvironment/genetics
Chemical Substances	Estrogens
Language	English
Publishing date	2023-08-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12172176
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Article ; Online: Impact of HCV Infection on Hepatocyte Polarity and Plasticity

Jean Agnetti / Christophe Desterke / Ama Gassama-Diagne

Pathogens, Vol 11, Iss 337, p

2022 Volume 337

Abstract	The hepatitis C virus (HCV) is an oncogenic virus that alters the cell polarization machinery in order to enter the hepatocyte and replicate. While these alterations are relatively well defined, their consequences in the evolution of the disease remain poorly documented. Since 2012, HCV infection can be effectively cured with the advent of direct acting antivirals (DAA). Nevertheless, patients cured of their HCV infection still have a high risk of developing hepatocellular carcinoma (HCC). Importantly, it has been shown that some of the deregulations induced by HCV are maintained despite a sustained virologic response (SVR), including the down-regulation of some hepatocyte functions such as bile acid metabolism, exemplifying cell dedifferentiation, and the up-regulation of the epithelial–mesenchymal transition (EMT). EMT is a process by which epithelial cells lose their differentiation and their specific polarity to acquire mesenchymal cell properties, including migration and extracellular matrix remodeling capabilities. Of note, epithelial cell polarity acts as a gatekeeper against EMT. Thus, it remains important to elucidate the mechanisms by which HCV alters polarity and promotes EMT that could participate in viral-induced hepatic carcinogenesis. In this review, we define the main steps involved in the polarization process of epithelial cells and recall the essential cellular actors involved. We also highlight the particularities of hepatocyte polarity, responsible for their unique morphology. We then focus on the alterations by HCV of epithelial cell polarity and the consequences of the transformation of hepatocytes involved in the carcinogenesis process.
Keywords	HCV ; hepatocytes ; polarity ; EMT ; cell junctions ; traffic ; Medicine ; R
Subject code	571
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Protein-protein interaction analysis highlights the role of septins in membrane enclosed lumen and mRNA processing.

Desterke, Christophe / Gassama-Diagne, Ama

Advances in biological regulation

2019 Volume 73, Page(s) 100635

Abstract: Septins are a family of GTP-binding proteins that assemble into non-polar filaments which can be recruited to negatively charged membranes and serve as a scaffold to recruit cytosolic proteins and cytoskeletal elements such as microtubules and actin so ... ...

Abstract	Septins are a family of GTP-binding proteins that assemble into non-polar filaments which can be recruited to negatively charged membranes and serve as a scaffold to recruit cytosolic proteins and cytoskeletal elements such as microtubules and actin so that they can perform their important biological functions. Human septins consist of four groups, each with 13 members, and filaments formation usually involve members from each group in specific positions. However, little is known about the molecular mechanisms that drive the binding of septins to membranes and its importance to their biological functions. Here we have built a protein-protein interaction (PPI) network around human septins and highlighted the connections with 170 partners. Functional enrichment by inference of the network of septins and their partners revealed their participation in functions consistent with some of the roles described for septins, including cell cycle, cell division and cell shape, but we also identified septin partners in these functions that had not previously been described. Interestingly, we identified important and multiple connections between septins and mRNA processing and their export from the nucleus. Analysis of the enrichment of gene ontology cellular components highlighted some important interactions between molecules involved in the spliceosome with septin 2 and septin 7 in particular. RNA splicing regulates gene expression, and through it, cell fate, development and physiology. Mutations in components of the in the splicing machinery is linked to several diseases including cancer, thus taken together, the different analyses presented here open new perspectives to elucidate the pathobiological role of septins.
MeSH term(s)	Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Division ; Cell Membrane/genetics ; Cell Membrane/metabolism ; Humans ; Protein Interaction Maps ; RNA Splicing ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Septins/genetics ; Septins/metabolism
Chemical Substances	Cell Cycle Proteins ; RNA, Messenger ; SEPTIN2 protein, human (EC 3.6.1.-) ; SEPTIN7 protein, human (EC 3.6.1.-) ; Septins (EC 3.6.1.-)
Language	English
Publishing date	2019-07-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2667413-0
ISSN	2212-4934 ; 2212-4926
ISSN (online)	2212-4934
ISSN	2212-4926
DOI	10.1016/j.jbior.2019.100635
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