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Article: Targeting Mitochondrial Protein Expression as a Future Approach for Cancer Therapy.

Criscuolo, Daniela / Avolio, Rosario / Matassa, Danilo Swann / Esposito, Franca

2021 Volume 11, Page(s) 797265

Abstract: Extensive metabolic remodeling is a fundamental feature of cancer cells. Although early reports attributed such remodeling to a loss of mitochondrial functions, it is now clear that mitochondria play central roles in cancer development and progression, ... ...

Abstract	Extensive metabolic remodeling is a fundamental feature of cancer cells. Although early reports attributed such remodeling to a loss of mitochondrial functions, it is now clear that mitochondria play central roles in cancer development and progression, from energy production to synthesis of macromolecules, from redox modulation to regulation of cell death. Biosynthetic pathways are also heavily affected by the metabolic rewiring, with protein synthesis dysregulation at the hearth of cellular transformation. Accumulating evidence in multiple organisms shows that the metabolic functions of mitochondria are tightly connected to protein synthesis, being assembly and activity of respiratory complexes highly dependent on
Language	English
Publishing date	2021-11-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.797265
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Article: Decreased Levels of GSH Are Associated with Platinum Resistance in High-Grade Serous Ovarian Cancer.

Criscuolo, Daniela / Avolio, Rosario / Parri, Matteo / Romano, Simona / Chiarugi, Paola / Matassa, Danilo Swann / Esposito, Franca

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 8

Abstract: High-grade serous ovarian cancer (HGSOC) is the most common and aggressive OC histotype. Although initially sensitive to standard platinum-based chemotherapy, most HGSOC patients relapse and become chemoresistant. We have previously demonstrated that ... ...

Abstract	High-grade serous ovarian cancer (HGSOC) is the most common and aggressive OC histotype. Although initially sensitive to standard platinum-based chemotherapy, most HGSOC patients relapse and become chemoresistant. We have previously demonstrated that platinum resistance is driven by a metabolic shift toward oxidative phosphorylation via activation of an inflammatory response, accompanied by reduced cholesterol biosynthesis and increased uptake of exogenous cholesterol. To better understand metabolic remodeling in OC, herein we performed an untargeted metabolomic analysis, which surprisingly showed decreased reduced glutathione (GSH) levels in resistant cells. Accordingly, we found reduced levels of enzymes involved in GSH synthesis and recycling, and compensatory increased expression of thioredoxin reductase. Cisplatin treatment caused an increase of reduced GSH, possibly due to direct binding hindering its oxidation, and consequent accumulation of reactive oxygen species. Notably, expression of the cysteine-glutamate antiporter xCT, which is crucial for GSH synthesis, directly correlates with post-progression survival of HGSOC patients, and is significantly reduced in patients not responding to platinum-based therapy. Overall, our data suggest that cisplatin treatment could positively select cancer cells which are independent from GSH for the maintenance of redox balance, and thus less sensitive to cisplatin-induced oxidative stress, opening new scenarios for the GSH pathway as a therapeutic target in HGSOC.
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11081544
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Article: Cytosolic and mitochondrial translation elongation are coordinated through the molecular chaperone TRAP1 for the synthesis and import of mitochondrial proteins.

Avolio, Rosario / Agliarulo, Ilenia / Criscuolo, Daniela / Sarnataro, Daniela / Auriemma, Margherita / Pennacchio, Sara / Calice, Giovanni / Ng, Martin Y / Giorgi, Carlotta / Pinton, Paolo / Cooperman, Barry / Landriscina, Matteo / Esposito, Franca / Matassa, Danilo Swann

bioRxiv : the preprint server for biology

2023

Abstract: A complex interplay between mRNA translation and cellular respiration has been recently unveiled, but its regulation in humans is poorly characterized in either health or disease. Cancer cells radically reshape both biosynthetic and bioenergetic pathways ...

Abstract	A complex interplay between mRNA translation and cellular respiration has been recently unveiled, but its regulation in humans is poorly characterized in either health or disease. Cancer cells radically reshape both biosynthetic and bioenergetic pathways to sustain their aberrant growth rates. In this regard, we have shown that the molecular chaperone TRAP1 not only regulates the activity of respiratory complexes, behaving alternatively as an oncogene or a tumor suppressor, but also plays a concomitant moonlighting function in mRNA translation regulation. Herein we identify the molecular mechanisms involved, demonstrating that TRAP1: i) binds both mitochondrial and cytosolic ribosomes as well as translation elongation factors, ii) slows down translation elongation rate, and iii) favors localized translation in the proximity of mitochondria. We also provide evidence that TRAP1 is coexpressed in human tissues with the mitochondrial translational machinery, which is responsible for the synthesis of respiratory complex proteins. Altogether, our results show an unprecedented level of complexity in the regulation of cancer cell metabolism, strongly suggesting the existence of a tight feedback loop between protein synthesis and energy metabolism, based on the demonstration that a single molecular chaperone plays a role in both mitochondrial and cytosolic translation, as well as in mitochondrial respiration.
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.19.524708
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Article: Decreased Levels of GSH Are Associated with Platinum Resistance in High-Grade Serous Ovarian Cancer

Criscuolo, Daniela / Avolio, Rosario / Parri, Matteo / Romano, Simona / Chiarugi, Paola / Matassa, Danilo Swann / Esposito, Franca

Antioxidants. 2022 Aug. 10, v. 11, no. 8

2022

Abstract	High-grade serous ovarian cancer (HGSOC) is the most common and aggressive OC histotype. Although initially sensitive to standard platinum-based chemotherapy, most HGSOC patients relapse and become chemoresistant. We have previously demonstrated that platinum resistance is driven by a metabolic shift toward oxidative phosphorylation via activation of an inflammatory response, accompanied by reduced cholesterol biosynthesis and increased uptake of exogenous cholesterol. To better understand metabolic remodeling in OC, herein we performed an untargeted metabolomic analysis, which surprisingly showed decreased reduced glutathione (GSH) levels in resistant cells. Accordingly, we found reduced levels of enzymes involved in GSH synthesis and recycling, and compensatory increased expression of thioredoxin reductase. Cisplatin treatment caused an increase of reduced GSH, possibly due to direct binding hindering its oxidation, and consequent accumulation of reactive oxygen species. Notably, expression of the cysteine-glutamate antiporter xCT, which is crucial for GSH synthesis, directly correlates with post-progression survival of HGSOC patients, and is significantly reduced in patients not responding to platinum-based therapy. Overall, our data suggest that cisplatin treatment could positively select cancer cells which are independent from GSH for the maintenance of redox balance, and thus less sensitive to cisplatin-induced oxidative stress, opening new scenarios for the GSH pathway as a therapeutic target in HGSOC.
Keywords	antiporters ; biosynthesis ; cholesterol ; cisplatin ; drug therapy ; glutathione ; inflammation ; metabolomics ; ovarian neoplasms ; oxidation ; oxidative phosphorylation ; oxidative stress ; oxidoreductases ; platinum ; reactive oxygen species ; relapse ; thioredoxins
Language	English
Dates of publication	2022-0810
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11081544
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Modulation of Mitochondrial Metabolic Reprogramming and Oxidative Stress to Overcome Chemoresistance in Cancer.

Avolio, Rosario / Matassa, Danilo Swann / Criscuolo, Daniela / Landriscina, Matteo / Esposito, Franca

Biomolecules

2020 Volume 10, Issue 1

Abstract: Metabolic reprogramming, carried out by cancer cells to rapidly adapt to stress such as hypoxia and limited nutrient conditions, is an emerging concepts in tumor biology, and is now recognized as one of the hallmarks of cancer. In contrast with ... ...

Abstract	Metabolic reprogramming, carried out by cancer cells to rapidly adapt to stress such as hypoxia and limited nutrient conditions, is an emerging concepts in tumor biology, and is now recognized as one of the hallmarks of cancer. In contrast with conventional views, based on the classical Warburg effect, these metabolic alterations require fully functional mitochondria and finely-tuned regulations of their activity. In turn, the reciprocal regulation of the metabolic adaptations of cancer cells and the microenvironment critically influence disease progression and response to therapy. This is also realized through the function of specific stress-adaptive proteins, which are able to relieve oxidative stress, inhibit apoptosis, and facilitate the switch between metabolic pathways. Among these, the molecular chaperone tumor necrosis factor receptor associated protein 1 (TRAP1), the most abundant heat shock protein 90 (HSP90) family member in mitochondria, is particularly relevant because of its role as an oncogene or a tumor suppressor, depending on the metabolic features of the specific tumor. This review highlights the interplay between metabolic reprogramming and cancer progression, and the role of mitochondrial activity and oxidative stress in this setting, examining the possibility of targeting pathways of energy metabolism as a therapeutic strategy to overcome drug resistance, with particular emphasis on natural compounds and inhibitors of mitochondrial HSP90s.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Energy Metabolism/drug effects ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; Metabolic Networks and Pathways/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Oxidative Stress/drug effects
Chemical Substances	Antineoplastic Agents ; HSP90 Heat-Shock Proteins ; TRAP1 protein, human
Language	English
Publishing date	2020-01-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10010135
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Article ; Online: Cytosolic and mitochondrial translation elongation are coordinated through the molecular chaperone TRAP1 for the synthesis and import of mitochondrial proteins.

Avolio, Rosario / Agliarulo, Ilenia / Criscuolo, Daniela / Sarnataro, Daniela / Auriemma, Margherita / De Lella, Sabrina / Pennacchio, Sara / Calice, Giovanni / Ng, Martin Y / Giorgi, Carlotta / Pinton, Paolo / Cooperman, Barry S / Landriscina, Matteo / Esposito, Franca / Matassa, Danilo Swann

Genome research

2023 Volume 33, Issue 8, Page(s) 1242–1257

Abstract	A complex interplay between mRNA translation and cellular respiration has been recently unveiled, but its regulation in humans is poorly characterized in either health or disease. Cancer cells radically reshape both biosynthetic and bioenergetic pathways to sustain their aberrant growth rates. In this regard, we have shown that the molecular chaperone TRAP1 not only regulates the activity of respiratory complexes, behaving alternatively as an oncogene or a tumor suppressor, but also plays a concomitant moonlighting function in mRNA translation regulation. Herein, we identify the molecular mechanisms involved, showing that TRAP1 (1) binds both mitochondrial and cytosolic ribosomes, as well as translation elongation factors; (2) slows down translation elongation rate; and (3) favors localized translation in the proximity of mitochondria. We also provide evidence that TRAP1 is coexpressed in human tissues with the mitochondrial translational machinery, which is responsible for the synthesis of respiratory complex proteins. Altogether, our results show an unprecedented level of complexity in the regulation of cancer cell metabolism, strongly suggesting the existence of a tight feedback loop between protein synthesis and energy metabolism, based on the demonstration that a single molecular chaperone plays a role in both mitochondrial and cytosolic translation, as well as in mitochondrial respiration.
MeSH term(s)	Humans ; HSP90 Heat-Shock Proteins/genetics ; HSP90 Heat-Shock Proteins/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Protein Biosynthesis/genetics ; Protein Biosynthesis/physiology ; Ribosomes/genetics ; Ribosomes/metabolism ; Peptide Chain Elongation, Translational/genetics ; Peptide Chain Elongation, Translational/physiology ; Mitochondria/genetics ; Mitochondria/metabolism
Chemical Substances	HSP90 Heat-Shock Proteins ; Mitochondrial Proteins ; Molecular Chaperones ; TRAP1 protein, human
Language	English
Publishing date	2023-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.277755.123
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Zs.A 3729: 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)
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Article ; Online: TRAP1 regulates the response of colorectal cancer cells to hypoxia and inhibits ribosome biogenesis under conditions of oxygen deprivation.

Bruno, Giuseppina / Li Bergolis, Valeria / Piscazzi, Annamaria / Crispo, Fabiana / Condelli, Valentina / Zoppoli, Pietro / Maddalena, Francesca / Pietrafesa, Michele / Giordano, Guido / Matassa, Danilo Swann / Esposito, Franca / Landriscina, Matteo

International journal of oncology

2022 Volume 60, Issue 6

Abstract: Metabolic rewiring fuels rapid cancer cell proliferation by promoting adjustments in energetic resources, and increasing glucose uptake and its conversion into lactate, even in the presence of oxygen. Furthermore, solid tumors often contain hypoxic areas ...

Abstract	Metabolic rewiring fuels rapid cancer cell proliferation by promoting adjustments in energetic resources, and increasing glucose uptake and its conversion into lactate, even in the presence of oxygen. Furthermore, solid tumors often contain hypoxic areas and can rapidly adapt to low oxygen conditions by activating hypoxia inducible factor (HIF)‑1α and several downstream pathways, thus sustaining cell survival and metabolic reprogramming. Since TNF receptor‑associated protein 1 (TRAP1) is a HSP90 molecular chaperone upregulated in several human malignancies and is involved in cancer cell adaptation to unfavorable environments and metabolic reprogramming, in the present study, its role was investigated in the adaptive response to hypoxia in human colorectal cancer (CRC) cells and organoids. In the present study, glucose uptake, lactate production and the expression of key metabolic genes were evaluated in TRAP1‑silenced CRC cell models under conditions of hypoxia/normoxia. Whole genome gene expression profiling was performed in TRAP1‑silenced HCT116 cells exposed to hypoxia to establish the role of TRAP1 in adaptive responses to oxygen deprivation. The results revealed that TRAP1 was involved in regulating hypoxia‑induced HIF‑1α stabilization and glycolytic metabolism and that glucose transporter 1 expression, glucose uptake and lactate production were partially impaired in TRAP1‑silenced CRC cells under hypoxic conditions. At the transcriptional level, the gene expression reprogramming of cancer cells driven by HIF‑1α was partially inhibited in TRAP1‑silenced CRC cells and organoids exposed to hypoxia. Moreover, Gene Set Enrichment Analysis of TRAP1‑silenced HCT116 cells exposed to hypoxia demonstrated that TRAP1 was involved in the regulation of ribosome biogenesis and this occurred with the inhibition of the mTOR pathway. Therefore, as demonstrated herein, TRAP1 is a key factor in maintaining HIF‑1α‑induced genetic/metabolic program under hypoxic conditions and may represent a promising target for novel metabolic therapies.
MeSH term(s)	Cell Hypoxia ; Colorectal Neoplasms/pathology ; Glucose/metabolism ; Glycolysis ; HSP90 Heat-Shock Proteins/genetics ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lactates ; Oxygen/metabolism ; Ribosomes/genetics ; Ribosomes/metabolism ; Ribosomes/pathology ; TNF Receptor-Associated Factor 1/metabolism
Chemical Substances	HSP90 Heat-Shock Proteins ; Hypoxia-Inducible Factor 1, alpha Subunit ; Lactates ; TNF Receptor-Associated Factor 1 ; TRAP1 protein, human ; Glucose (IY9XDZ35W2) ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-05-11
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2022.5369
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ab Jg. 2022: Lesesaal (EG)

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Article: TRAP1 Regulation of Cancer Metabolism: Dual Role as Oncogene or Tumor Suppressor.

Matassa, Danilo Swann / Agliarulo, Ilenia / Avolio, Rosario / Landriscina, Matteo / Esposito, Franca

Genes

2018 Volume 9, Issue 4

Abstract: Metabolic reprogramming is an important issue in tumor biology. An unexpected inter- and intra-tumor metabolic heterogeneity has been strictly correlated to tumor outcome. Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) is a molecular ... ...

Abstract	Metabolic reprogramming is an important issue in tumor biology. An unexpected inter- and intra-tumor metabolic heterogeneity has been strictly correlated to tumor outcome. Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) is a molecular chaperone involved in the regulation of energetic metabolism in cancer cells. This protein is highly expressed in several cancers, such as glioblastoma, colon, breast, prostate and lung cancers and is often associated with drug resistance. However, TRAP1 is also downregulated in specific tumors, such as ovarian, bladder and renal cancers, where its lower expression is correlated with the worst prognoses and chemoresistance. TRAP1 is the only mitochondrial member of the Heat Shock Protein 90 (HSP90) family that directly interacts with respiratory complexes, contributing to their stability and activity but it is still unclear if such interactions lead to reduced or increased respiratory capacity. The role of TRAP1 is to enhance or suppress oxidative phosphorylation; the effects of such regulation on tumor development and progression are controversial. These observations encourage the study of the mechanisms responsible for the dualist role of TRAP1 as an oncogene or oncosuppressor in specific tumor types. In this review, TRAP1 puzzling functions were recapitulated with a special focus on the correlation between metabolic reprogramming and tumor outcome. We wanted to investigate whether metabolism-targeting drugs can efficiently interfere with tumor progression and whether they might be combined with chemotherapeutics or molecular-targeted agents to counteract drug resistance and reduce therapeutic failure.
Language	English
Publishing date	2018-04-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes9040195
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Article: HSP90 Molecular Chaperones, Metabolic Rewiring, and Epigenetics: Impact on Tumor Progression and Perspective for Anticancer Therapy.

Condelli, Valentina / Crispo, Fabiana / Pietrafesa, Michele / Lettini, Giacomo / Matassa, Danilo Swann / Esposito, Franca / Landriscina, Matteo / Maddalena, Francesca

Cells

2019 Volume 8, Issue 6

Abstract: Heat shock protein 90 (HSP90) molecular chaperones are a family of ubiquitous proteins participating in several cellular functions through the regulation of folding and/or assembly of large multiprotein complexes and client proteins. Thus, HSP90s ... ...

Abstract	Heat shock protein 90 (HSP90) molecular chaperones are a family of ubiquitous proteins participating in several cellular functions through the regulation of folding and/or assembly of large multiprotein complexes and client proteins. Thus, HSP90s chaperones are, directly or indirectly, master regulators of a variety of cellular processes, such as adaptation to stress, cell proliferation, motility, angiogenesis, and signal transduction. In recent years, it has been proposed that HSP90s play a crucial role in carcinogenesis as regulators of genotype-to-phenotype interplay. Indeed, HSP90 chaperones control metabolic rewiring, a hallmark of cancer cells, and influence the transcription of several of the key-genes responsible for tumorigenesis and cancer progression, through either direct binding to chromatin or through the quality control of transcription factors and epigenetic effectors. In this review, we will revise evidence suggesting how this interplay between epigenetics and metabolism may affect oncogenesis. We will examine the effect of metabolic rewiring on the accumulation of specific metabolites, and the changes in the availability of epigenetic co-factors and how this process can be controlled by HSP90 molecular chaperones. Understanding deeply the relationship between epigenetic and metabolism could disclose novel therapeutic scenarios that may lead to improvements in cancer treatment.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Disease Progression ; Epigenesis, Genetic/drug effects ; HSP90 Heat-Shock Proteins/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Phenotype
Chemical Substances	Antineoplastic Agents ; HSP90 Heat-Shock Proteins
Language	English
Publishing date	2019-06-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8060532
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Article ; Online: Regulation of sub-compartmental targeting and folding properties of the Prion-like protein Shadoo.

Pepe, Anna / Avolio, Rosario / Matassa, Danilo Swann / Esposito, Franca / Nitsch, Lucio / Zurzolo, Chiara / Paladino, Simona / Sarnataro, Daniela

Scientific reports

2017 Volume 7, Issue 1, Page(s) 3731

Abstract: Shadoo (Sho), a member of prion protein family, has been shown to prevent embryonic lethality in ... ...

Abstract	Shadoo (Sho), a member of prion protein family, has been shown to prevent embryonic lethality in Prnp
Language	English
Publishing date	2017-06-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-03969-2
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