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Article: NEDD9 sustains hexokinase expression to promote glycolysis.

Deneka, Alexander Y / Nikonova, Anna S / Lee, Hyung-Ok / Kruger, Warren D / Golemis, Erica A

2022 Volume 11, Issue 1, Page(s) 15

Abstract: Elevated rates of glycolysis in cancer cells support tumor growth, in a process that typically depends on oncogene-induced increases in the expression and/or activity of enzymes in the glycolytic pathway. The NEDD9 scaffolding protein is upregulated in ... ...

Abstract	Elevated rates of glycolysis in cancer cells support tumor growth, in a process that typically depends on oncogene-induced increases in the expression and/or activity of enzymes in the glycolytic pathway. The NEDD9 scaffolding protein is upregulated in many advanced tumors, with increased NEDD9 promoting the activity of SRC and other effectors that promote invasion and metastasis. We here define a new role for NEDD9 in support of glycolysis. NEDD9 knockdown significantly impaired glycolysis in multiple lung cancer cell lines This was accompanied by post-transcriptional downregulation of steady-state levels of hexokinases (HK1 and HK2), which catalyze early steps in the glycolytic cascade, key rate limiting enzyme phosphofructokinase (PFK1), and downstream glyceraldehyde phosphate dehydrogenase (GAPDH). In mice, protein levels of HK1, HK2, PFK1, and GAPDH were depressed in Kras
Language	English
Publishing date	2022-04-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-022-00391-w
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Article: NEDD9 Restrains dsDNA Damage Response during Non-Small Cell Lung Cancer (NSCLC) Progression.

Tikhomirova, Mariya / Topchu, Iuliia / Mazitova, Aleksandra / Barmin, Vitaly / Ratner, Ekaterina / Sabirov, Alexey / Abramova, Zinaida / Deneka, Alexander Y

Cancers

2022 Volume 14, Issue 10

Abstract: DNA damaging modalities are the backbone of treatments for non-small cell lung cancer (NSCLC). Alterations in DNA damage response (DDR) in tumor cells commonly contribute to emerging resistance to platinating agents, other targeted therapies, and ... ...

Abstract	DNA damaging modalities are the backbone of treatments for non-small cell lung cancer (NSCLC). Alterations in DNA damage response (DDR) in tumor cells commonly contribute to emerging resistance to platinating agents, other targeted therapies, and radiation. The goal of this study is to identify the previously unreported role of NEDD9 scaffolding protein in controlling DDR processes and sensitivity to DNA damaging therapies. Using a siRNA-mediated approach to deplete NEDD9 in a group of human and murine
Language	English
Publishing date	2022-05-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14102517
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Article: Tumor-Targeted Drug Conjugates as an Emerging Novel Therapeutic Approach in Small Cell Lung Cancer (SCLC).

Deneka, Alexander Y / Boumber, Yanis / Beck, Tim / Golemis, Erica A

Cancers

2019 Volume 11, Issue 9

Abstract: There are few effective therapies for small cell lung cancer (SCLC), a highly aggressive disease representing 15% of total lung cancers. With median survival <2 years, SCLC is one of the most lethal cancers. At present, chemotherapies and radiation ... ...

Abstract	There are few effective therapies for small cell lung cancer (SCLC), a highly aggressive disease representing 15% of total lung cancers. With median survival <2 years, SCLC is one of the most lethal cancers. At present, chemotherapies and radiation therapy are commonly used for SCLC management. Few protein-targeted therapies have shown efficacy in improving overall survival; immune checkpoint inhibitors (ICIs) are promising agents, but many SCLC tumors do not express ICI targets such as PD-L1. This article presents an alternative approach to the treatment of SCLC: the use of drug conjugates, where a targeting moiety concentrates otherwise toxic agents in the vicinity of tumors, maximizing the differential between tumor killing and the cytotoxicity of normal tissues. Several tumor-targeted drug conjugate delivery systems exist and are currently being actively tested in the setting of SCLC. These include antibody-drug conjugates (ADCs), radioimmunoconjugates (RICs), small molecule-drug conjugates (SMDCs), and polymer-drug conjugates (PDCs). We summarize the basis of action for these targeting compounds, discussing principles of construction and providing examples of effective versus ineffective compounds, as established by preclinical and clinical testing. Such agents may offer new therapeutic options for the clinical management of this challenging disease in the future.
Language	English
Publishing date	2019-09-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11091297
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Article ; Online: Mechanisms for nonmitotic activation of Aurora-A at cilia.

Korobeynikov, Vladislav / Deneka, Alexander Y / Golemis, Erica A

Biochemical Society transactions

2017 Volume 45, Issue 1, Page(s) 37–49

Abstract: Overexpression of the Aurora kinase A (AURKA) is oncogenic in many tumors. Many studies of AURKA have focused on activities of this kinase in mitosis, and elucidated the mechanisms by which AURKA activity is induced at the G2/M boundary through ... ...

Abstract	Overexpression of the Aurora kinase A (AURKA) is oncogenic in many tumors. Many studies of AURKA have focused on activities of this kinase in mitosis, and elucidated the mechanisms by which AURKA activity is induced at the G2/M boundary through interactions with proteins such as TPX2 and NEDD9. These studies have informed the development of small molecule inhibitors of AURKA, of which a number are currently under preclinical and clinical assessment. While the first activities defined for AURKA were its control of centrosomal maturation and organization of the mitotic spindle, an increasing number of studies over the past decade have recognized a separate biological function of AURKA, in controlling disassembly of the primary cilium, a small organelle protruding from the cell surface that serves as a signaling platform. Importantly, these activities require activation of AURKA in early G1, and the mechanisms of activation are much less well defined than those in mitosis. A better understanding of the control of AURKA activity and the role of AURKA at cilia are both important in optimizing the efficacy and interpreting potential downstream consequences of AURKA inhibitors in the clinic. We here provide a current overview of proteins and mechanisms that have been defined as activating AURKA in G1, based on the study of ciliary disassembly.
MeSH term(s)	Animals ; Aurora Kinase A/metabolism ; Cilia/enzymology ; Enzyme Activation ; G1 Phase ; Humans ; Mitosis ; Models, Biological ; Neoplasms/enzymology ; Signal Transduction
Chemical Substances	Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2017-02-15
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20160142
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Zs.A 944: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Loss of Pkd1 limits susceptibility to colitis and colorectal cancer.

Nikonova, Anna S / Deneka, Alexander Y / Silva, Flaviane N / Pirestani, Shabnam / Tricarico, Rossella / Kiseleva, Anna A / Zhou, Yan / Nicolas, Emmanuelle / Flieder, Douglas B / Grivennikov, Sergei I / Golemis, Erica A

Oncogenesis

2023 Volume 12, Issue 1, Page(s) 40

Abstract: Colorectal cancer (CRC) is one of the most common cancers, with an annual incidence of ~135,000 in the US, associated with ~50,000 deaths. Autosomal dominant polycystic kidney disease (ADPKD), associated with mutations disabling the PKD1 gene, affects as ...

Abstract	Colorectal cancer (CRC) is one of the most common cancers, with an annual incidence of ~135,000 in the US, associated with ~50,000 deaths. Autosomal dominant polycystic kidney disease (ADPKD), associated with mutations disabling the PKD1 gene, affects as many as 1 in 1000. Intriguingly, some studies have suggested that individuals with germline mutations in PKD1 have reduced incidence of CRC, suggesting a genetic modifier function. Using mouse models, we here establish that loss of Pkd1 greatly reduces CRC incidence and tumor growth induced by loss of the tumor suppressor Apc. Growth of Pkd1
Language	English
Publishing date	2023-08-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-023-00486-y
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Article ; Online: Association of TP53 and CDKN2A Mutation Profile with Tumor Mutation Burden in Head and Neck Cancer.

Deneka, Alexander Y / Baca, Yasmine / Serebriiskii, Ilya G / Nicolas, Emmanuelle / Parker, Mitchell I / Nguyen, Theodore T / Xiu, Joanne / Korn, W Michael / Demeure, Michael J / Wise-Draper, Trisha / Sukari, Ammar / Burtness, Barbara / Golemis, Erica A

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 28, Issue 9, Page(s) 1925–1937

Abstract: Purpose: Head and neck squamous cell carcinoma (HNSCC) is a frequently devastating cancer that affects more than a half million people annually worldwide. Although some cases arise from infection with human papillomavirus (HPV), HPV-negative HNSCC is ... ...

Abstract	Purpose: Head and neck squamous cell carcinoma (HNSCC) is a frequently devastating cancer that affects more than a half million people annually worldwide. Although some cases arise from infection with human papillomavirus (HPV), HPV-negative HNSCC is more common, and associated with worse outcome. Advanced HPV-negative HNSCC may be treated with surgery, chemoradiation, targeted therapy, or immune checkpoint inhibition (ICI). There is considerable need for predictive biomarkers for these treatments. Defects in DNA repair capacity and loss of cell-cycle checkpoints sensitize tumors to cytotoxic therapies, and can contribute to phenotypes such as elevated tumor mutation burden (TMB), associated with response to ICI. Mutation of the tumor suppressors and checkpoint mediators TP53 and CDKN2A is common in HPV-negative HNSCC. Experimental design: To gain insight into the relation of the interaction of TP53 and CDKN2A mutations with TMB in HNSCC, we have analyzed genomic data from 1,669 HPV-negative HNSCC tumors with multiple criteria proposed for assessing the damaging effect of TP53 mutations. Results: Data analysis established the TP53 and CDKN2A mutation profiles in specific anatomic subsites and suggested that specific categories of TP53 mutations are more likely to associate with CDKN2A mutation or high TMB based on tumor subsite. Intriguingly, the pattern of hotspot mutations in TP53 differed depending on the presence or absence of a cooccurring CDKN2A mutation. Conclusions: These data emphasize the role of tumor subsite in evaluation of mutational profiles in HNSCC, and link defects in TP53 and CDKN2A to elevated TMB levels in some tumor subgroups.
MeSH term(s)	Biomarkers, Tumor/genetics ; Carcinoma, Squamous Cell/pathology ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Head and Neck Neoplasms/genetics ; Humans ; Mutation ; Papillomavirus Infections/complications ; Papillomavirus Infections/genetics ; Squamous Cell Carcinoma of Head and Neck/genetics ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Biomarkers, Tumor ; CDKN2A protein, human ; Cyclin-Dependent Kinase Inhibitor p16 ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-4316
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Zs.A 4223: Show issues

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Article ; Online: Nedd9

Deneka, Alexander Y / Kopp, Meghan C / Nikonova, Anna S / Gaponova, Anna V / Kiseleva, Anna A / Hensley, Harvey H / Flieder, Douglas B / Serebriiskii, Ilya G / Golemis, Erica A

Cancer research

2021 Volume 81, Issue 13, Page(s) 3717–3726

Abstract: Non-small cell lung cancer (NSCLC) is the most common cancer worldwide. With overall 5-year survival estimated at <17%, it is critical to identify factors that regulate NSCLC disease prognosis. NSCLC is commonly driven by mutations ... ...

Abstract	Non-small cell lung cancer (NSCLC) is the most common cancer worldwide. With overall 5-year survival estimated at <17%, it is critical to identify factors that regulate NSCLC disease prognosis. NSCLC is commonly driven by mutations in
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Adaptor Proteins, Signal Transducing/physiology ; Animals ; Autophagy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Proliferation ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Prognosis ; Proto-Oncogene Proteins p21(ras)/physiology ; Survival Rate ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology
Chemical Substances	Adaptor Proteins, Signal Transducing ; NEDD9 protein, mouse ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Stk11 protein, mouse (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2021-05-18
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	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-3626
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Uh III Zs.135/5: Show issues

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Article: Synthetic Lethal Targeting of Mitotic Checkpoints in HPV-Negative Head and Neck Cancer.

Deneka, Alexander Y / Einarson, Margret B / Bennett, John / Nikonova, Anna S / Elmekawy, Mohamed / Zhou, Yan / Lee, Jong Woo / Burtness, Barbara A / Golemis, Erica A

Cancers

2020 Volume 12, Issue 2

Abstract: Head and neck squamous cell carcinomas (HNSCC) affect more than 800,000 people annually worldwide, causing over 15,000 deaths in the US. Among HNSCC cancers, human papillomavirus (HPV)-negative HNSCC has the worst outcome, motivating efforts to improve ... ...

Abstract	Head and neck squamous cell carcinomas (HNSCC) affect more than 800,000 people annually worldwide, causing over 15,000 deaths in the US. Among HNSCC cancers, human papillomavirus (HPV)-negative HNSCC has the worst outcome, motivating efforts to improve therapy for this disease. The most common mutational events in HPV-negative HNSCC are inactivation of the tumor suppressors
Language	English
Publishing date	2020-01-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12020306
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Article ; Online: Evaluation of the Small-molecule BRD4 Degrader CFT-2718 in Small-cell Lung Cancer and Pancreatic Cancer Models.

Sun, Danlin / Nikonova, Anna S / Zhang, Peishan / Deneka, Alexander Y / Fitzgerald, Mark E / Michael, Ryan E / Lee, Linda / Lilly, Anna C / Fisher, Stewart L / Phillips, Andrew J / Nasveschuk, Christopher G / Proia, David A / Tu, Zhigang / Golemis, Erica A

Molecular cancer therapeutics

2021 Volume 20, Issue 8, Page(s) 1367–1377

Abstract: Targeted, catalytic degradation of oncoproteins using heterobifunctional small molecules is an attractive modality, particularly for hematologic malignancies, which are often initiated by aberrant transcription factors and are challenging to drug with ... ...

Abstract	Targeted, catalytic degradation of oncoproteins using heterobifunctional small molecules is an attractive modality, particularly for hematologic malignancies, which are often initiated by aberrant transcription factors and are challenging to drug with inhibitors. BRD4, a member of the bromodomain and extraterminal family, is a core transcriptional and epigenetic regulator that recruits the P-TEFb complex, which includes Cdk9 and cyclin T, to RNA polymerase II (pol II). Together, BRD4 and CDK9 phosphorylate serine 2 (pSer2) of heptad repeats in the C-terminal domain of RPB1, the large subunit of pol II, promote transcriptional elongation. Small-molecule degraders of BRD4 have shown encouraging efficacy in preclinical models for several tumor types but less efficacy in other cancers including small-cell lung cancer (SCLC) and pancreatic cancer. Here, we evaluated CFT-2718, a new BRD4-targeting degrader with enhanced catalytic activity and in vivo properties.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis ; Cell Cycle Proteins/metabolism ; Cell Movement ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice ; Mice, SCID ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/metabolism ; Small Cell Lung Carcinoma/pathology ; Small Molecule Libraries/pharmacology ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; BRD4 protein, human ; Cell Cycle Proteins ; Small Molecule Libraries ; Transcription Factors
Language	English
Publishing date	2021-05-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-20-0831
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Zs.A 5750: Show issues

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Article: Trogocytosis of cancer-associated fibroblasts promotes pancreatic cancer growth and immune suppression via phospholipid scramblase anoctamin 6 (ANO6).

Ogier, Charline / Solomon, Akino Mercy Charles / Lu, Zhen / Recoules, Ludmila / Klochkova, Alena / Gabitova-Cornell, Linara / Bayarmagnai, Battuya / Restifo, Diana / Surumbayeva, Aizhan / Vendramini-Costa, Débora B / Deneka, Alexander Y / Francescone, Ralph / Lilly, Anna C / Sipman, Alyssa / Gardiner, Jaye C / Luong, Tiffany / Franco-Barraza, Janusz / Ibeme, Nina / Cai, Kathy Q /

Einarson, Margret B / Nicolas, Emmanuelle / Efimov, Andrei / Megill, Emily / Snyder, Nathaniel W / Bousquet, Corinne / Cros, Jerome / Zhou, Yunyun / Golemis, Erica A / Gligorijevic, Bojana / Soboloff, Jonathan / Fuchs, Serge Y / Cukierman, Edna / Astsaturov, Igor

bioRxiv : the preprint server for biology

2023

Abstract: In pancreatic ductal adenocarcinoma (PDAC), the fibroblastic stroma constitutes most of the tumor mass and is remarkably devoid of functional blood vessels. This raises an unresolved question of how PDAC cells obtain essential metabolites and water- ... ...

Abstract	In pancreatic ductal adenocarcinoma (PDAC), the fibroblastic stroma constitutes most of the tumor mass and is remarkably devoid of functional blood vessels. This raises an unresolved question of how PDAC cells obtain essential metabolites and water-insoluble lipids. We have found a critical role for cancer-associated fibroblasts (CAFs) in obtaining and transferring lipids from blood-borne particles to PDAC cells via trogocytosis of CAF plasma membranes. We have also determined that CAF-expressed phospholipid scramblase anoctamin 6 (ANO6) is an essential CAF trogocytosis regulator required to promote PDAC cell survival. During trogocytosis, cancer cells and CAFs form synapse-like plasma membranes contacts that induce cytosolic calcium influx in CAFs via Orai channels. This influx activates ANO6 and results in phosphatidylserine exposure on CAF plasma membrane initiating trogocytosis and transfer of membrane lipids, including cholesterol, to PDAC cells. Importantly, ANO6-dependent trogocytosis also supports the immunosuppressive function of pancreatic CAFs towards cytotoxic T cells by promoting transfer of excessive amounts of cholesterol. Further, blockade of ANO6 antagonizes tumor growth via disruption of delivery of exogenous cholesterol to cancer cells and reverses immune suppression suggesting a potential new strategy for PDAC therapy.
Language	English
Publishing date	2023-09-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.15.557802
Database	MEDical Literature Analysis and Retrieval System OnLINE

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