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Article ; Online: The importance of being CAFs (in cancer resistance to targeted therapies).

Rizzolio, Sabrina / Giordano, Silvia / Corso, Simona

Journal of experimental & clinical cancer research : CR

2022 Volume 41, Issue 1, Page(s) 319

Abstract: In the last two decades, clinical oncology has been revolutionized by the advent of targeted drugs. However, the efficacy of these therapies is significantly limited by primary and acquired resistance, that relies not only on cell-autonomous mechanisms ... ...

Abstract	In the last two decades, clinical oncology has been revolutionized by the advent of targeted drugs. However, the efficacy of these therapies is significantly limited by primary and acquired resistance, that relies not only on cell-autonomous mechanisms but also on tumor microenvironment cues. Cancer-associated fibroblasts (CAFs) are extremely plastic cells of the tumor microenvironment. They not only produce extracellular matrix components that build up the structure of tumor stroma, but they also release growth factors, chemokines, exosomes, and metabolites that affect all tumor properties, including response to drug treatment. The contribution of CAFs to tumor progression has been deeply investigated and reviewed in several works. However, their role in resistance to anticancer therapies, and in particular to molecular therapies, has been largely overlooked. This review specifically dissects the role of CAFs in driving resistance to targeted therapies and discusses novel CAF targeted therapeutic strategies to improve patient survival.
MeSH term(s)	Humans ; Cancer-Associated Fibroblasts/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Tumor Microenvironment ; Exosomes/metabolism
Language	English
Publishing date	2022-11-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-022-02524-w
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Article: Autocrine Signaling of NRP1 Ligand Galectin-1 Elicits Resistance to BRAF-Targeted Therapy in Melanoma Cells.

Rizzolio, Sabrina / Corso, Simona / Giordano, Silvia / Tamagnone, Luca

Cancers

2020 Volume 12, Issue 8

Abstract: Melanoma cells addicted to mutated BRAF oncogene activity can be targeted by specific kinase inhibitors until they develop resistance to therapy. We observed that the expression of Galectin-1 (Gal-1), a soluble ligand of Neuropilin-1 (NRP1), is ... ...

Abstract	Melanoma cells addicted to mutated BRAF oncogene activity can be targeted by specific kinase inhibitors until they develop resistance to therapy. We observed that the expression of Galectin-1 (Gal-1), a soluble ligand of Neuropilin-1 (NRP1), is upregulated in melanoma tumor samples and melanoma cells resistant to BRAF-targeted therapy. We then demonstrated that Gal-1 is a novel driver of resistance to BRAF inhibitors in melanoma and that its activity is linked to the concomitant upregulation of the NRP1 receptor observed in drug-resistant cells. Mechanistically, Gal-1 sustains increased expression of NRP1 and EGFR in drug-resistant melanoma cells. Moreover, consistent with its role as a NRP1 ligand, Gal-1 negatively controls p27 levels, a mechanism previously found to enable EGFR upregulation in cancer cells. Finally, the combined treatment with a Gal-1 inhibitor and a NRP1 blocking drug enabled resistant melanoma cell resensitization to BRAF-targeted therapy. In summary, we found that the activation of Galectin-1/NRP1 autocrine signaling is a new mechanism conferring independence from BRAF kinase activity to oncogene-addicted melanoma cells.
Language	English
Publishing date	2020-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12082218
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Article ; Online: Antibody-Feeding Assay: A Method to Track the Internalization of Neuropilin-1 and Other Cell Surface Receptors.

Rizzolio, Sabrina / Tamagnone, Luca

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1493, Page(s) 311–319

Abstract: Ligand-induced endocytosis of receptors exposed on the plasma membrane is a fundamental regulatory step for their functional activation and interaction with intracellular signal transducers. Thus, elucidating the timing of endocytosis and tracing the ... ...

Abstract	Ligand-induced endocytosis of receptors exposed on the plasma membrane is a fundamental regulatory step for their functional activation and interaction with intracellular signal transducers. Thus, elucidating the timing of endocytosis and tracing the intracellular fate of receptors is instrumental to understand their signaling cascade in different conditions. Here we describe an assay for the study of endocytosis and intracellular trafficking of individual surface receptors, in living cells subject to different experimental challenges. We applied this method for studying the functional interaction between semaphorin coreceptor Neuropilin-1 and a tyrosine kinase receptor exposed on the cell surface.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6448-2_23
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Article ; Online: Autocrine Signaling of NRP1 Ligand Galectin-1 Elicits Resistance to BRAF-Targeted Therapy in Melanoma Cells

Sabrina Rizzolio / Simona Corso / Silvia Giordano / Luca Tamagnone

Cancers, Vol 12, Iss 2218, p

2020 Volume 2218

Abstract	Melanoma cells addicted to mutated BRAF oncogene activity can be targeted by specific kinase inhibitors until they develop resistance to therapy. We observed that the expression of Galectin-1 (Gal-1), a soluble ligand of Neuropilin-1 (NRP1), is upregulated in melanoma tumor samples and melanoma cells resistant to BRAF-targeted therapy. We then demonstrated that Gal-1 is a novel driver of resistance to BRAF inhibitors in melanoma and that its activity is linked to the concomitant upregulation of the NRP1 receptor observed in drug-resistant cells. Mechanistically, Gal-1 sustains increased expression of NRP1 and EGFR in drug-resistant melanoma cells. Moreover, consistent with its role as a NRP1 ligand, Gal-1 negatively controls p27 levels, a mechanism previously found to enable EGFR upregulation in cancer cells. Finally, the combined treatment with a Gal-1 inhibitor and a NRP1 blocking drug enabled resistant melanoma cell resensitization to BRAF-targeted therapy. In summary, we found that the activation of Galectin-1/NRP1 autocrine signaling is a new mechanism conferring independence from BRAF kinase activity to oncogene-addicted melanoma cells.
Keywords	galectin ; neuropilin ; melanoma ; cancer therapy ; molecular biology ; cell signaling ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SEMA6C: a novel adhesion-independent FAK and YAP activator, required for cancer cell viability and growth.

Fard, Damon / Testa, Erika / Panzeri, Valentina / Rizzolio, Sabrina / Bianchetti, Giada / Napolitano, Virginia / Masciarelli, Silvia / Fazi, Francesco / Maulucci, Giuseppe / Scicchitano, Bianca Maria / Sette, Claudio / Viscomi, Maria Teresa / Tamagnone, Luca

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 4, Page(s) 111

Abstract: Transmembrane semaphorins are signaling molecules, controlling axonal wiring and embryo development, which are increasingly implicated in human diseases. Semaphorin 6C (Sema6C) is a poorly understood family member and its functional role is still unclear. ...

Abstract	Transmembrane semaphorins are signaling molecules, controlling axonal wiring and embryo development, which are increasingly implicated in human diseases. Semaphorin 6C (Sema6C) is a poorly understood family member and its functional role is still unclear. Upon targeting Sema6C expression in a range of cancer cells, we observed dramatic growth suppression, decreased ERK phosphorylation, upregulation of cell cycle inhibitor proteins p21, p27 and p53, and the onset of cell senescence, associated with activation of autophagy. These data are consistent with a fundamental requirement for Sema6C to support viability and growth in cancer cells. Mechanistically, we unveiled a novel signaling pathway elicited by Sema6C, and dependent on its intracellular domain, mediated by tyrosine kinases c-Abl and Focal Adhesion Kinase (FAK). Sema6C was found in complex with c-Abl, and induced its phosphorylation, which in turn led to FAK activation, independent of cell-matrix adhesion. Sema6C-induced FAK activity was furthermore responsible for increased nuclear localization of YAP transcriptional regulator. Moreover, Sema6C conferred YAP signaling-dependent long-term cancer cell survival upon nutrient deprivation. In conclusion, our findings demonstrate that Sema6C elicits a cancer promoting-signaling pathway sustaining cell viability and self-renewal, independent of growth factors and nutrients availability.
MeSH term(s)	Humans ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Cell Survival ; Focal Adhesion Kinase 1/genetics ; Focal Adhesion Kinase 1/metabolism ; Signal Transduction ; Phosphorylation ; Cell Cycle Proteins/metabolism ; Neoplasms/genetics
Chemical Substances	Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; Cell Cycle Proteins
Language	English
Publishing date	2023-03-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04756-1
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Article: Distinct Mechanisms Are Responsible for Nrf2-Keap1 Pathway Activation at Different Stages of Rat Hepatocarcinogenesis.

Orrù, Claudia / Perra, Andrea / Kowalik, Marta Anna / Rizzolio, Sabrina / Puliga, Elisabetta / Cabras, Lavinia / Giordano, Silvia / Columbano, Amedeo

Cancers

2020 Volume 12, Issue 8

Abstract: Activation of the Nrf2-Keap1 pathway, the main intracellular defense against environmental stress, has been observed in several human cancers, including hepatocellular carcinoma (HCC). Here, we assessed whether distinct mechanisms of activation may be ... ...

Abstract	Activation of the Nrf2-Keap1 pathway, the main intracellular defense against environmental stress, has been observed in several human cancers, including hepatocellular carcinoma (HCC). Here, we assessed whether distinct mechanisms of activation may be involved at different stages of hepatocarcinogenesis. We adopted an experimental model consisting of treatment with diethylnitrosamine (DENA) followed by a choline-devoid methionine-deficient (CMD) diet for 4 months. The CMD diet was then replaced with a basal diet, and the animals were killed at 6, 10 or 13 months after DENA injection. Nrf2 activation occurred at early steps of hepatocarcinogenesis and persisted throughout the tumorigenic process. While
Language	English
Publishing date	2020-08-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12082305
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Article ; Online: SEMA6C: a novel adhesion-independent FAK and YAP activator, required for cancer cell viability and growth

Cell. Mol. Life Sci.. 2023 Apr., v. 80, no. 4 p.111-111

2023

Abstract	Transmembrane semaphorins are signaling molecules, controlling axonal wiring and embryo development, which are increasingly implicated in human diseases. Semaphorin 6C (Sema6C) is a poorly understood family member and its functional role is still unclear. Upon targeting Sema6C expression in a range of cancer cells, we observed dramatic growth suppression, decreased ERK phosphorylation, upregulation of cell cycle inhibitor proteins p21, p27 and p53, and the onset of cell senescence, associated with activation of autophagy. These data are consistent with a fundamental requirement for Sema6C to support viability and growth in cancer cells. Mechanistically, we unveiled a novel signaling pathway elicited by Sema6C, and dependent on its intracellular domain, mediated by tyrosine kinases c-Abl and Focal Adhesion Kinase (FAK). Sema6C was found in complex with c-Abl, and induced its phosphorylation, which in turn led to FAK activation, independent of cell–matrix adhesion. Sema6C-induced FAK activity was furthermore responsible for increased nuclear localization of YAP transcriptional regulator. Moreover, Sema6C conferred YAP signaling-dependent long-term cancer cell survival upon nutrient deprivation. In conclusion, our findings demonstrate that Sema6C elicits a cancer promoting-signaling pathway sustaining cell viability and self-renewal, independent of growth factors and nutrients availability.
Keywords	autophagy ; cell adhesion ; cell cycle ; cell senescence ; cell viability ; embryogenesis ; humans ; neoplasm cells ; non-specific protein-tyrosine kinase ; phosphorylation ; transcription factors ; tyrosine
Language	English
Dates of publication	2023-04
Size	p. 111.
Publishing place	Springer International Publishing
Document type	Article ; Online
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04756-1
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Downregulating Neuropilin-2 Triggers a Novel Mechanism Enabling EGFR-Dependent Resistance to Oncogene-Targeted Therapies.

Rizzolio, Sabrina / Battistini, Chiara / Cagnoni, Gabriella / Apicella, Maria / Vella, Viviana / Giordano, Silvia / Tamagnone, Luca

Cancer research

2017 Volume 78, Issue 4, Page(s) 1058–1068

Abstract: Neuropilins are a class of cell surface proteins implicated in cell migration and angiogenesis, with aberrant expression in human tumors. Here, we show that the expression of Neuropilin-2 (NRP2) controls EGFR protein levels, thereby impinging on ... ...

Abstract	Neuropilins are a class of cell surface proteins implicated in cell migration and angiogenesis, with aberrant expression in human tumors. Here, we show that the expression of Neuropilin-2 (NRP2) controls EGFR protein levels, thereby impinging on intracellular signaling, viability, and response to targeted therapies of oncogene-addicted cells. Notably, increased NRP2 expression in EGFR-addicted tumor cells led to downregulation of EGFR protein and tumor cell growth inhibition. NRP2 also blunted upregulation of an EGFR "rescue" pathway induced by targeted therapy in Met-addicted carcinoma cells. Cancer cells acquiring resistance to MET oncogene-targeted drugs invariably underwent NRP2 loss, a step required for EGFR upregulation. Mechanistic investigations revealed that NRP2 loss activated NFkB and upregulated the EGFR-associated protein KIAA1199/CEMIP, which is known to oppose the degradation of activated EGFR kinase. Notably, KIAA1199 silencing in oncogene-addicted tumor cells improved therapeutic responses and counteracted acquired drug resistance. Our findings define NRP2 as the pivotal switch of a novel broad-acting and actionable pathway controlling EGFR signaling, and driving resistance to therapies targeting oncogene-addiction.
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Humans ; Neuropilin-2/genetics ; Neuropilin-2/metabolism ; Oncogenes ; Signal Transduction
Chemical Substances	Neuropilin-2 ; neuropilin-2, human
Language	English
Publishing date	2017-12-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-2020
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Article ; Online: BRCA2 Germline Mutations Identify Gastric Cancers Responsive to PARP Inhibitors.

Petrelli, Annalisa / Rizzolio, Sabrina / Pietrantonio, Filippo / Bellomo, Sara E / Benelli, Matteo / De Cecco, Loris / Romagnoli, Dario / Berrino, Enrico / Orrù, Claudia / Ribisi, Salvatore / Moya-Rull, Daniel / Migliore, Cristina / Conticelli, Daniela / Maina, Irene M / Puliga, Elisabetta / Serra, Violeta / Pellegrino, Benedetta / Llop-Guevara, Alba / Musolino, Antonino /

Siena, Salvatore / Sartore-Bianchi, Andrea / Prisciandaro, Michele / Morano, Federica / Antista, Maria / Fumagalli, Uberto / De Manzoni, Giovanni / Degiuli, Maurizio / Baiocchi, Gian Luca / Amisano, Marco F / Ferrero, Alessandro / Marchiò, Caterina / Corso, Simona / Giordano, Silvia

Cancer research

2023 Volume 83, Issue 10, Page(s) 1699–1710

Abstract: Despite negative results of clinical trials conducted on the overall population of patients with gastric cancer, PARP inhibitor (PARPi) therapeutic strategy still might represent a window of opportunity for a subpopulation of patients with gastric cancer. ...

Abstract	Despite negative results of clinical trials conducted on the overall population of patients with gastric cancer, PARP inhibitor (PARPi) therapeutic strategy still might represent a window of opportunity for a subpopulation of patients with gastric cancer. An estimated 7% to 12% of gastric cancers exhibit a mutational signature associated with homologous recombination (HR) failure, suggesting that these patients could potentially benefit from PARPis. To analyze responsiveness of gastric cancer to PARPi, we exploited a gastroesophageal adenocarcinoma (GEA) platform of patient-derived xenografts (PDX) and PDX-derived primary cells and selected 10 PDXs with loss-of-function mutations in HR pathway genes. Cell viability assays and preclinical trials showed that olaparib treatment was effective in PDXs harboring BRCA2 germline mutations and somatic inactivation of the second allele. Olaparib responsive tumors were sensitive to oxaliplatin as well. Evaluation of HR deficiency (HRD) and mutational signatures efficiently stratified responder and nonresponder PDXs. A retrospective analysis on 57 patients with GEA showed that BRCA2 inactivating variants were associated with longer progression-free survival upon platinum-based regimens. Five of 7 patients with BRCA2 germline mutations carried the p.K3326* variant, classified as "benign." However, familial history of cancer, the absence of RAD51 foci in tumor cells, and a high HRD score suggest a deleterious effect of this mutation in gastric cancer. In conclusion, PARPis could represent an effective therapeutic option for BRCA2-mutated and/or high HRD score patients with GEA, including patients with familial intestinal gastric cancer. Significance: PARP inhibition is a potential strategy for treating patients with gastric cancer with mutated BRCA2 or homologous repair deficiency, including patients with familial intestinal gastric cancer, for whom BRCA2 germline testing should be recommended.
MeSH term(s)	Humans ; Female ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; Germ-Line Mutation ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Retrospective Studies ; BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Ovarian Neoplasms/drug therapy
Chemical Substances	Poly(ADP-ribose) Polymerase Inhibitors ; BRCA1 Protein ; BRCA2 Protein ; Antineoplastic Agents ; BRCA2 protein, human
Language	English
Publishing date	2023-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-2620
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Article ; Online: Semaphorin signals on the road to cancer invasion and metastasis.

Rizzolio, Sabrina / Tamagnone, Luca

Cell adhesion & migration

2007 Volume 1, Issue 2, Page(s) 62–68

Abstract: Semaphorins are a large family of secreted and membrane-bound molecules initially implicated in the development of the nervous system and in axon guidance. More recently, they have been found to regulate cell adhesion and cell motility, angiogenesis, ... ...

Abstract	Semaphorins are a large family of secreted and membrane-bound molecules initially implicated in the development of the nervous system and in axon guidance. More recently, they have been found to regulate cell adhesion and cell motility, angiogenesis, immune function and tumour progression. Notably, Semaphorins have been implicated with opposite functions in cancer: either as putative tumor suppressors and anti-angiogenic factors, or as mediating tumour angiogenesis, invasion and metastasis. Interestingly, Semaphorins may display divergent activities in different cell types. These multifaceted functions may be explained by the involvement of different kinds of semaphorin receptor complexes, and by the consequent activation of multiple signaling pathways, in different cells or different functional stages. Semaphorin signaling is largely mediated by the Plexins. However, semaphorin receptor complexes may also include Neuropilins and tyrosine kinases implicated in cancer. In this review, we will focus on major open questions concerning the potential role of Semaphorin signals in cancer.
MeSH term(s)	Animals ; Humans ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Receptors, Cell Surface/metabolism ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction
Chemical Substances	Receptors, Cell Surface ; Semaphorins
Language	English
Publishing date	2007-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2268518-2
ISSN	1933-6926 ; 1933-6918
ISSN (online)	1933-6926
ISSN	1933-6918
DOI	10.4161/cam.1.2.4570
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