LIVIVO - Search results -

Search results

Result 1 - 10 of total 82

Search options

Article ; Online: Chromatin Remodelers Are Regulators of the Tumor Immune Microenvironment.

Chaudhri, Apoorvi / Lizee, Gregory / Hwu, Patrick / Rai, Kunal

2024 Volume 84, Issue 7, Page(s) 965–976

Abstract: Immune checkpoint inhibitors show remarkable responses in a wide range of cancers, yet patients develop adaptive resistance. This necessitates the identification of alternate therapies that synergize with immunotherapies. Epigenetic modifiers are potent ... ...

Abstract	Immune checkpoint inhibitors show remarkable responses in a wide range of cancers, yet patients develop adaptive resistance. This necessitates the identification of alternate therapies that synergize with immunotherapies. Epigenetic modifiers are potent mediators of tumor-intrinsic mechanisms and have been shown to regulate immune response genes, making them prime targets for therapeutic combinations with immune checkpoint inhibitors. Some success has been observed in early clinical studies that combined immunotherapy with agents targeting DNA methylation and histone modification; however, less is known about chromatin remodeler-targeted therapies. Here, we provide a discussion on the regulation of tumor immunogenicity by the chromatin remodeling SWI/SNF complex through multiple mechanisms associated with immunotherapy response that broadly include IFN signaling, DNA damage, mismatch repair, regulation of oncogenic programs, and polycomb-repressive complex antagonism. Context-dependent targeting of SWI/SNF subunits can elicit opportunities for synthetic lethality and reduce T-cell exhaustion. In summary, alongside the significance of SWI/SNF subunits in predicting immunotherapy outcomes, their ability to modulate the tumor immune landscape offers opportunities for therapeutic intervention.
MeSH term(s)	Humans ; Chromatin ; Transcription Factors/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Neoplasms/genetics ; Neoplasms/therapy ; Chromatin Assembly and Disassembly ; Tumor Microenvironment
Chemical Substances	Chromatin ; Transcription Factors ; Chromosomal Proteins, Non-Histone ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2024-01-24
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-23-2244
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.135/5: 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)

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: APE-Gen2.0: Expanding Rapid Class I Peptide-Major Histocompatibility Complex Modeling to Post-Translational Modifications and Noncanonical Peptide Geometries.

Fasoulis, Romanos / Rigo, Mauricio M / Lizée, Gregory / Antunes, Dinler A / Kavraki, Lydia E

Journal of chemical information and modeling

2024 Volume 64, Issue 5, Page(s) 1730–1750

Abstract: The recognition of peptides bound to class I major histocompatibility complex (MHC-I) receptors by T-cell receptors (TCRs) is a determinant of triggering the adaptive immune response. While the exact molecular features that drive the TCR recognition are ... ...

Abstract	The recognition of peptides bound to class I major histocompatibility complex (MHC-I) receptors by T-cell receptors (TCRs) is a determinant of triggering the adaptive immune response. While the exact molecular features that drive the TCR recognition are still unknown, studies have suggested that the geometry of the joint peptide-MHC (pMHC) structure plays an important role. As such, there is a definite need for methods and tools that accurately predict the structure of the peptide bound to the MHC-I receptor. In the past few years, many pMHC structural modeling tools have emerged that provide high-quality modeled structures in the general case. However, there are numerous instances of non-canonical cases in the immunopeptidome that the majority of pMHC modeling tools do not attend to, most notably, peptides that exhibit non-standard amino acids and post-translational modifications (PTMs) or peptides that assume non-canonical geometries in the MHC binding cleft. Such chemical and structural properties have been shown to be present in neoantigens; therefore, accurate structural modeling of these instances can be vital for cancer immunotherapy. To this end, we have developed APE-Gen2.0, a tool that improves upon its predecessor and other pMHC modeling tools, both in terms of modeling accuracy and the available modeling range of non-canonical peptide cases. Some of the improvements include (i) the ability to model peptides that have different types of PTMs such as phosphorylation, nitration, and citrullination; (ii) a new and improved anchor identification routine in order to identify and model peptides that exhibit a non-canonical anchor conformation; and (iii) a web server that provides a platform for easy and accessible pMHC modeling. We further show that structures predicted by APE-Gen2.0 can be used to assess the effects that PTMs have in binding affinity in a more accurate manner than just using solely the sequence of the peptide. APE-Gen2.0 is freely available at https://apegen.kavrakilab.org.
MeSH term(s)	Animals ; Peptides/chemistry ; Major Histocompatibility Complex ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/metabolism ; Protein Processing, Post-Translational ; Hominidae/metabolism ; Protein Binding
Chemical Substances	Peptides ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	190019-5
ISSN	1549-960X ; 0095-2338
ISSN (online)	1549-960X
ISSN	0095-2338
DOI	10.1021/acs.jcim.3c01667
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1230: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Vestigial-like 1 (VGLL1): An ancient co-transcriptional activator linking wing, placenta, and tumor development.

Sonnemann, Heather M / Pazdrak, Barbara / Antunes, Dinler A / Roszik, Jason / Lizée, Gregory

Biochimica et biophysica acta. Reviews on cancer

2023 Volume 1878, Issue 3, Page(s) 188892

Abstract: Vestigial-like 1 (VGLL1) is a recently discovered driver of proliferation and invasion that is expressed in many aggressive human malignancies and is strongly associated with poor prognosis. The VGLL1 gene encodes for a co-transcriptional activator that ... ...

Abstract	Vestigial-like 1 (VGLL1) is a recently discovered driver of proliferation and invasion that is expressed in many aggressive human malignancies and is strongly associated with poor prognosis. The VGLL1 gene encodes for a co-transcriptional activator that shows intriguing structural similarity to key activators in the hippo pathway, providing important clues to its functional role. VGLL1 binds to TEAD transcription factors in an analogous fashion to YAP1 but appears to activate a distinct set of downstream gene targets. In mammals, VGLL1 expression is found almost exclusively in placental trophoblasts, cells that share many hallmarks of cancer. Due to its role as a driver of tumor progression, VGLL1 has become a target of interest for potential anticancer therapies. In this review, we discuss VGLL1 from an evolutionary perspective, contrast its role in placental and tumor development, summarize the current knowledge of how signaling pathways can modulate VGLL1 function, and discuss potential approaches for targeting VGLL1 therapeutically.
MeSH term(s)	Animals ; Female ; Humans ; Pregnancy ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Placenta/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; TEA Domain Transcription Factors ; Neoplasms/genetics ; Mammals/metabolism
Chemical Substances	DNA-Binding Proteins ; Transcription Factors ; TEA Domain Transcription Factors ; VGLL1 protein, human
Language	English
Publishing date	2023-03-31
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2023.188892
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 7162: 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: Exploiting Tumor Neoantigens to Target Cancer Evolution: Current Challenges and Promising Therapeutic Approaches.

Gupta, Ravi G / Li, Fenge / Roszik, Jason / Lizée, Gregory

Cancer discovery

2021 Volume 11, Issue 5, Page(s) 1024–1039

Abstract: Immunotherapeutic manipulation of the antitumor immune response offers an attractive strategy to target genomic instability in cancer. A subset of tumor-specific somatic mutations can be translated into immunogenic and HLA-bound epitopes called ... ...

Abstract	Immunotherapeutic manipulation of the antitumor immune response offers an attractive strategy to target genomic instability in cancer. A subset of tumor-specific somatic mutations can be translated into immunogenic and HLA-bound epitopes called neoantigens, which can induce the activation of helper and cytotoxic T lymphocytes. However, cancer immunoediting and immunosuppressive mechanisms often allow tumors to evade immune recognition. Recent evidence also suggests that the tumor neoantigen landscape extends beyond epitopes originating from nonsynonymous single-nucleotide variants in the coding exome. Here we review emerging approaches for identifying, prioritizing, and immunologically targeting personalized neoantigens using polyvalent cancer vaccines and T-cell receptor gene therapy. SIGNIFICANCE: Several major challenges currently impede the clinical efficacy of neoantigen-directed immunotherapy, such as the relative infrequency of immunogenic neoantigens, suboptimal potency and priming of
MeSH term(s)	Antigens, Neoplasm/immunology ; Humans ; Immunotherapy ; Neoplasms/drug therapy
Chemical Substances	Antigens, Neoplasm
Language	English
Publishing date	2021-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-1575
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6916: 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: An interpretable ML model to characterize patient-specific HLA-I antigen presentation.

Liang, Shaoheng / Jiang, Xianli / Chiu, Yulun / Xu, Haodong / Kim, Kun Hee / Lizee, Gregory / Chen, Ken

bioRxiv : the preprint server for biology

2023

Abstract: Personalized immunotherapy holds the promise of revolutionizing cancer prevention and treatment. However, selecting HLA-bound peptide targets that are specific to patient tumors has been challenging due to a lack of patient-specific antigen presentation ... ...

Abstract	Personalized immunotherapy holds the promise of revolutionizing cancer prevention and treatment. However, selecting HLA-bound peptide targets that are specific to patient tumors has been challenging due to a lack of patient-specific antigen presentation models. Here, we present epiNB, a white-box, positive-example-only, semi-supervised method based on Naïve Bayes formulation, with information content-based feature selection, to achieve accurate modeling using Mass Spectrometry data eluted from mono-allelic cell lines and patient-derived cell lines. In addition to achieving state-of-the-art accuracy, epiNB yields novel insights into the structural properties, such as interactions of peptide positions, that appear important for modeling personalized, tumor-specific antigen presentation. epiNB uses substantially less parameters than neural networks, does not require hyperparameter tweaking and can efficiently train and run on our web portal (https://epinbweb.streamlit.app/) or a regular PC/laptop, making it easily applicable in translational settings.
Language	English
Publishing date	2023-03-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.12.532264
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Details ▾

Article ; Online: PepSim: T-cell cross-reactivity prediction via comparison of peptide sequence and peptide-HLA structure.

Hall-Swan, Sarah / Slone, Jared / Rigo, Mauricio M / Antunes, Dinler A / Lizée, Gregory / Kavraki, Lydia E

Frontiers in immunology

2023 Volume 14, Page(s) 1108303

Abstract: Introduction: Peptide-HLA class I (pHLA) complexes on the surface of tumor cells can be targeted by cytotoxic T-cells to eliminate tumors, and this is one of the bases for T-cell-based immunotherapies. However, there exist cases where therapeutic T- ... ...

Abstract	Introduction: Peptide-HLA class I (pHLA) complexes on the surface of tumor cells can be targeted by cytotoxic T-cells to eliminate tumors, and this is one of the bases for T-cell-based immunotherapies. However, there exist cases where therapeutic T-cells directed towards tumor pHLA complexes may also recognize pHLAs from healthy normal cells. The process where the same T-cell clone recognizes more than one pHLA is referred to as T-cell cross-reactivity and this process is driven mainly by features that make pHLAs similar to each other. T-cell cross-reactivity prediction is critical for designing T-cell-based cancer immunotherapies that are both effective and safe. Methods: Here we present PepSim, a novel score to predict T-cell cross-reactivity based on the structural and biochemical similarity of pHLAs. Results and discussion: We show our method can accurately separate cross-reactive from non-crossreactive pHLAs in a diverse set of datasets including cancer, viral, and self-peptides. PepSim can be generalized to work on any dataset of class I peptide-HLAs and is freely available as a web server at pepsim.kavrakilab.org.
MeSH term(s)	Amino Acid Sequence ; Peptides ; T-Lymphocytes, Cytotoxic ; Clone Cells
Chemical Substances	Peptides
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1108303
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Personalized Therapy: Tumor Antigen Discovery for Adoptive Cellular Therapy.

Yee, Cassian / Lizee, Gregory A

Cancer journal (Sudbury, Mass.)

2017 Volume 23, Issue 2, Page(s) 144–148

Abstract: Adoptive cell therapy using endogenous T cells involves the ex vivo isolation and expansion of antigen-specific T cells from the peripheral blood and is uniquely suited for validating and translating antigen discovery. Endogenous T-cell therapy does not ... ...

Abstract	Adoptive cell therapy using endogenous T cells involves the ex vivo isolation and expansion of antigen-specific T cells from the peripheral blood and is uniquely suited for validating and translating antigen discovery. Endogenous T-cell therapy does not require accessible tumor as a source of infiltrating T cells and is free of regulatory and logistical constraints associated with engineering T cells. Candidate epitope peptides identified through antigen discovery may be rapidly implemented as targets in clinical trials of endogenous T-cell therapy and even incorporated as an "ad hoc" approach to personalized treatment when autologous tumor is available. Several first-in-human studies using a uniform population of antigen-specific T cells defined by phenotype and specificity have provided a means to confirm candidate antigens as potential tumor rejection antigens and to evaluate the reasons for success or failure using as a "transferrable cellular biomarker" the adoptively transferred T cells.
MeSH term(s)	Antigens, Neoplasm/immunology ; Humans ; Immunotherapy, Adoptive/methods ; Neoplasms/immunology ; Neoplasms/therapy ; Precision Medicine/methods
Chemical Substances	Antigens, Neoplasm
Language	English
Publishing date	2017-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2018400-1
ISSN	1540-336X ; 1528-9117 ; 1081-4442
ISSN (online)	1540-336X
ISSN	1528-9117 ; 1081-4442
DOI	10.1097/PPO.0000000000000255
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4470: 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.MO 163: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Epidermal Growth Factor Receptor-Targeted Neoantigen Peptide Vaccination for the Treatment of Non-Small Cell Lung Cancer and Glioblastoma.

Li, Fenge / Wu, Huancheng / Du, Xueming / Sun, Yimo / Rausseo, Barbara Nassif / Talukder, Amjad / Katailiha, Arjun / Elzohary, Lama / Wang, Yupeng / Wang, Zhiyu / Lizée, Gregory

Vaccines

2023 Volume 11, Issue 9

Abstract: The epidermal growth factor receptor (EGFR) plays crucial roles in several important biological functions such as embryogenesis, epithelial tissue development, and cellular regeneration. However, in multiple solid tumor types overexpression and/or ... ...

Abstract	The epidermal growth factor receptor (EGFR) plays crucial roles in several important biological functions such as embryogenesis, epithelial tissue development, and cellular regeneration. However, in multiple solid tumor types overexpression and/or activating mutations of the
Language	English
Publishing date	2023-09-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2703319-3
ISSN	2076-393X
ISSN	2076-393X
DOI	10.3390/vaccines11091460
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances response to anti-PD-1 immunotherapy.

Chaudhri, Apoorvi / Bu, Xia / Wang, Yunfei / Gomez, Michael / Torchia, James A / Hua, Ping / Hung, Shao-Hsi / Davies, Michael A / Lizee, Gregory A / von Andrian, Ulrich / Hwu, Patrick / Freeman, Gordon J

Frontiers in immunology

2023 Volume 14, Page(s) 1237715

Abstract: CX3CL1 secreted in the tumor microenvironment serves as a chemoattractant playing a critical role in metastasis of CX3CR1 expressing cancer cells. CX3CR1 can be expressed in both cancer and immune-inhibitory myeloid cells to facilitate their migration. ... ...

Abstract	CX3CL1 secreted in the tumor microenvironment serves as a chemoattractant playing a critical role in metastasis of CX3CR1 expressing cancer cells. CX3CR1 can be expressed in both cancer and immune-inhibitory myeloid cells to facilitate their migration. We generated a novel monoclonal antibody against mouse CX3CR1 that binds to CX3CR1 and blocks the CX3CL1-CX3CR1 interaction. We next explored the immune evasion strategies implemented by the CX3CL1-CX3CR1 axis and find that it initiates a resistance program in cancer cells that results in 1) facilitation of tumor cell migration, 2) secretion of soluble mediators to generate a pro-metastatic niche, 3) secretion of soluble mediators to attract myeloid populations, and 4) generation of tumor-inflammasome. The CX3CR1 monoclonal antibody reduces migration of tumor cells and decreases secretion of immune suppressive soluble mediators by tumor cells. In combination with anti-PD-1 immunotherapy, this CX3CR1 monoclonal antibody enhances survival in an immunocompetent mouse colon carcinoma model through a decrease in tumor-promoting myeloid populations. Thus, this axis is involved in the mechanisms of resistance to anti-PD-1 immunotherapy and the combination therapy can overcome a portion of the resistance mechanisms to anti-PD-1.
MeSH term(s)	Mice ; Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Tumor Escape ; Chemokine CX3CL1/metabolism
Chemical Substances	Antibodies, Monoclonal ; Chemokine CX3CL1
Language	English
Publishing date	2023-09-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1237715
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Markov state modeling reveals alternative unbinding pathways for peptide-MHC complexes.

Abella, Jayvee R / Antunes, Dinler / Jackson, Kyle / Lizée, Gregory / Clementi, Cecilia / Kavraki, Lydia E

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 48, Page(s) 30610–30618

Abstract: Peptide binding to major histocompatibility complexes (MHCs) is a central component of the immune system, and understanding the mechanism behind stable peptide-MHC binding will aid the development of immunotherapies. While MHC binding is mostly ... ...

Abstract	Peptide binding to major histocompatibility complexes (MHCs) is a central component of the immune system, and understanding the mechanism behind stable peptide-MHC binding will aid the development of immunotherapies. While MHC binding is mostly influenced by the identity of the so-called anchor positions of the peptide, secondary interactions from nonanchor positions are known to play a role in complex stability. However, current MHC-binding prediction methods lack an analysis of the major conformational states and might underestimate the impact of secondary interactions. In this work, we present an atomically detailed analysis of peptide-MHC binding that can reveal the contributions of any interaction toward stability. We propose a simulation framework that uses both umbrella sampling and adaptive sampling to generate a Markov state model (MSM) for a coronavirus-derived peptide (QFKDNVILL), bound to one of the most prevalent MHC receptors in humans (HLA-A24:02). While our model reaffirms the importance of the anchor positions of the peptide in establishing stable interactions, our model also reveals the underestimated importance of position 4 (p4), a nonanchor position. We confirmed our results by simulating the impact of specific peptide mutations and validated these predictions through competitive binding assays. By comparing the MSM of the wild-type system with those of the D4A and D4P mutations, our modeling reveals stark differences in unbinding pathways. The analysis presented here can be applied to any peptide-MHC complex of interest with a structural model as input, representing an important step toward comprehensive modeling of the MHC class I pathway.
MeSH term(s)	Alanine/genetics ; Binding, Competitive ; Computer Simulation ; DNA Mutational Analysis ; Major Histocompatibility Complex ; Markov Chains ; Models, Molecular ; Mutation/genetics ; Peptides/metabolism ; Proline/metabolism ; Protein Binding
Chemical Substances	Peptides ; Proline (9DLQ4CIU6V) ; Alanine (OF5P57N2ZX)
Keywords	covid19
Language	English
Publishing date	2020-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2007246117
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

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

More links

Kategorien

Inter-library loan at ZB MED

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

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito