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Article: A New Immunotherapy Combination Promises to Improve Survival for Patients with Metastatic Prostate Cancer.

Seremak, Juliette R / Lokeshwar, Bal L

2023 Volume 15, Issue 23

Abstract: Prostate cancer (PC) is the second-most prevalent malignancy affecting the male population worldwide [ ... ]. ...

Abstract	Prostate cancer (PC) is the second-most prevalent malignancy affecting the male population worldwide [...].
Language	English
Publishing date	2023-11-29
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15235640
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Article ; Online: Ursolic Acid Analogs as Potential Therapeutics for Cancer.

Panda, Siva S / Thangaraju, Muthusamy / Lokeshwar, Bal L

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 24

Abstract: Ursolic acid (UA) is a pentacyclic triterpene isolated from a large variety of vegetables, fruits and many traditional medicinal plants. It is a structural isomer of Oleanolic Acid. The medicinal application of UA has been explored extensively over the ... ...

Abstract	Ursolic acid (UA) is a pentacyclic triterpene isolated from a large variety of vegetables, fruits and many traditional medicinal plants. It is a structural isomer of Oleanolic Acid. The medicinal application of UA has been explored extensively over the last two decades. The diverse pharmacological properties of UA include anti-inflammatory, antimicrobial, antiviral, antioxidant, anti-proliferative, etc. Especially, UA holds a promising position, potentially, as a cancer preventive and therapeutic agent due to its relatively non-toxic properties against normal cells but its antioxidant and antiproliferative activities against cancer cells. Cell culture studies have shown interference of UA with multiple pharmacological and molecular targets that play a critical role in many cells signaling pathways. Although UA is considered a privileged natural product, its clinical applications are limited due to its low absorption through the gastro-intestinal track and rapid elimination. The low bioavailability of UA limits its use as a therapeutic drug. To overcome these drawbacks and utilize the importance of the scaffold, many researchers have been engaged in designing and developing synthetic analogs of UA via structural modifications. This present review summarizes the synthetic UA analogs and their cytotoxic antiproliferative properties reported in the last two decades.
MeSH term(s)	Humans ; Antioxidants ; Neoplasms/drug therapy ; Antineoplastic Agents/pharmacology ; Anti-Inflammatory Agents/pharmacology ; Triterpenes/pharmacology ; Triterpenes/therapeutic use ; Triterpenes/chemistry ; Ursolic Acid
Chemical Substances	Antioxidants ; Antineoplastic Agents ; Anti-Inflammatory Agents ; Triterpenes
Language	English
Publishing date	2022-12-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27248981
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Article ; Online: Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids.

Mamouni, Kenza / Kallifatidis, Georgios / Lokeshwar, Bal L

International journal of molecular sciences

2021 Volume 22, Issue 5

Abstract: Metabolic reprogramming is a hallmark of malignancy. It implements profound metabolic changes to sustain cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that ...

Abstract	Metabolic reprogramming is a hallmark of malignancy. It implements profound metabolic changes to sustain cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that tumor cells also depend on mitochondrial metabolism. Due to the essential role of mitochondria in metabolism and cell survival, targeting mitochondria in cancer cells is an attractive therapeutic strategy. However, the metabolic flexibility of cancer cells may enable the upregulation of compensatory pathways, such as glycolysis, to support cancer cell survival when mitochondrial metabolism is inhibited. Thus, compounds capable of targeting both mitochondrial metabolism and glycolysis may help overcome such resistance mechanisms. Normal prostate epithelial cells have a distinct metabolism as they use glucose to sustain physiological citrate secretion. During the transformation process, prostate cancer cells consume citrate to mainly power oxidative phosphorylation and fuel lipogenesis. A growing number of studies have assessed the impact of triterpenoids on prostate cancer metabolism, underlining their ability to hit different metabolic targets. In this review, we critically assess the metabolic transformations occurring in prostate cancer cells. We will then address the opportunities and challenges in using triterpenoids as modulators of prostate cancer cell metabolism.
MeSH term(s)	Animals ; Glycolysis ; Humans ; Male ; Mitochondria/drug effects ; Mitochondria/pathology ; Oxidative Phosphorylation ; Oxidative Stress ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Triterpenes/pharmacology
Chemical Substances	Triterpenes
Language	English
Publishing date	2021-02-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22052466
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Article ; Online: The Role of β-Arrestins in Regulating Stem Cell Phenotypes in Normal and Tumorigenic Cells.

Kallifatidis, Georgios / Mamouni, Kenza / Lokeshwar, Bal L

International journal of molecular sciences

2020 Volume 21, Issue 23

Abstract: β-Arrestins (ARRBs) are ubiquitously expressed scaffold proteins that mediate inactivation of G-protein-coupled receptor signaling, and in certain circumstances, G-protein independent pathways. Intriguingly, the two known ARRBs, β-arrestin1 (ARRB1) and β- ...

Abstract	β-Arrestins (ARRBs) are ubiquitously expressed scaffold proteins that mediate inactivation of G-protein-coupled receptor signaling, and in certain circumstances, G-protein independent pathways. Intriguingly, the two known ARRBs, β-arrestin1 (ARRB1) and β-Arrestin2 (ARRB2), seem to have opposing functions in regulating signaling cascades in several models in health and disease. Recent evidence suggests that ARRBs are implicated in regulating stem cell maintenance; however, their role, although crucial, is complex, and there is no universal model for ARRB-mediated regulation of stem cell characteristics. For the first time, this review compiles information on the function of ARRBs in stem cell biology and will discuss the role of ARRBs in regulating cell signaling pathways implicated in stem cell maintenance in normal and malignant stem cell populations. Although promising targets for cancer therapy, the ubiquitous nature of ARRBs and the plethora of functions in normal cell biology brings challenges for treatment selectivity. However, recent studies show promising evidence for specifically targeting ARRBs in myeloproliferative neoplasms.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Cell Self Renewal ; Humans ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/physiology ; Phenotype ; Pluripotent Stem Cells/metabolism ; Pluripotent Stem Cells/physiology ; beta-Arrestins/genetics ; beta-Arrestins/metabolism
Chemical Substances	beta-Arrestins
Language	English
Publishing date	2020-12-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21239310
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Article ; Online: Atypical chemokine receptors in tumor cell growth and metastasis.

Lokeshwar, Bal L / Kallifatidis, Georgios / Hoy, James J

Advances in cancer research

2020 Volume 145, Page(s) 1–27

Abstract: Atypical chemokine receptors (ACKRs) are seven-transmembrane cell surface protein receptors expressed in immune cells, normal mesenchymal cells, and several tumor cells. As of this writing, six ACKRs have been characterized by diverse activities. They ... ...

Abstract	Atypical chemokine receptors (ACKRs) are seven-transmembrane cell surface protein receptors expressed in immune cells, normal mesenchymal cells, and several tumor cells. As of this writing, six ACKRs have been characterized by diverse activities. They bind both cysteine-cysteine (CC) type and cysteine-X-cysteine (CXC)-type chemokines, either alone, or together with a ligand bound-functional G-protein coupled (typical) chemokine receptor. The major structural difference between ACKRs and typical chemokine receptors is the substituted DRYLAIV amino acid motif in the second intracellular loop of the ACKR. Due to this substitution, these receptors cannot bind Gαi-type G-proteins responsible for intracellular calcium mobilization and cellular chemotaxis. Although initially characterized as non-signaling transmembrane receptors (decoy receptors) that attenuate ligand-induced signaling by GPCRs, studies of all ACKRs have shown ligand-independent and ligand-dependent transmembrane signaling in both non-tumor and tumor cells. The precise function and mechanism of the differential expression of ACKRs in many tumors are not understood well. The use of antagonists of ACKRs ligands has shown limited antitumor potential; however, depleting ACKR expression resulted in a reduction in experimental tumor growth and metastasis. The ACKRs represent a unique class of transmembrane signaling proteins that regulate growth, survival, and metastatic processes in tumor cells, affecting multiple pathways of tumor growth. Therefore, closer investigations of ACKRs have a high potential for identifying therapeutics which affect the intracellular signaling, preferentially via the ligand-independent mechanism.
MeSH term(s)	Animals ; Cell Proliferation ; Chemokines/metabolism ; Humans ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Receptors, Chemokine/metabolism ; Signal Transduction
Chemical Substances	Chemokines ; Receptors, Chemokine
Language	English
Publishing date	2020-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	127-2
ISSN	2162-5557 ; 0065-230X
ISSN (online)	2162-5557
ISSN	0065-230X
DOI	10.1016/bs.acr.2019.12.002
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Article: ARRB1 Regulates Metabolic Reprogramming to Promote Glycolysis in Stem Cell-Like Bladder Cancer Cells.

Mamouni, Kenza / Kim, Jeongheun / Lokeshwar, Bal L / Kallifatidis, Georgios

Cancers

2021 Volume 13, Issue 8

Abstract: β-arrestin 1 (ARRB1) is a scaffold protein that regulates signaling downstream of G protein-coupled receptors (GPCRs). In the current work, we investigated the role of ARRB1 in regulating the metabolic preference of cancer stem cell (CSC)-like cells in ... ...

Abstract	β-arrestin 1 (ARRB1) is a scaffold protein that regulates signaling downstream of G protein-coupled receptors (GPCRs). In the current work, we investigated the role of ARRB1 in regulating the metabolic preference of cancer stem cell (CSC)-like cells in bladder cancer (BC). We show that ARRB1 is crucial for spheroid formation and tumorigenic potential. Furthermore, we measured mitochondrial respiration, glucose uptake, glycolytic rate, mitochondrial/glycolytic ATP production and fuel oxidation in previously established ARRB1 knock out (KO) cells and corresponding controls. Our results demonstrate that depletion of ARRB1 decreased glycolytic rate and induced metabolic reprogramming towards oxidative phosphorylation. Mechanistically, the depletion of ARRB1 dramatically increased the mitochondrial pyruvate carrier MPC1 protein levels and reduced the glucose transporter GLUT1 protein levels along with glucose uptake. Overexpression of ARRB1 in ARRB1 KO cells reversed the phenotype and resulted in the upregulation of glycolysis. In conclusion, we show that ARRB1 regulates the metabolic preference of BC CSC-like cells and functions as a molecular switch that promotes reprogramming towards glycolysis by negatively regulating MPC1 and positively regulating GLUT1/ glucose uptake. These observations open new therapeutic avenues for targeting the metabolic preferences of cancer stem cell (CSC)-like BC cells.
Language	English
Publishing date	2021-04-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13081809
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Article ; Online: Chemically modified non-antimicrobial tetracyclines are multifunctional drugs against advanced cancers.

Lokeshwar, Bal L

Pharmacological research

2010 Volume 63, Issue 2, Page(s) 146–150

Abstract: Metastatic cancers account for more than 90% of cancer mortality. The metastasis of all cancers is critically mediated by enzymes that degrade extracellular matrix. Aggressive tumors are characterized by an imbalance between enzymes that degrade ECM and ... ...

Abstract	Metastatic cancers account for more than 90% of cancer mortality. The metastasis of all cancers is critically mediated by enzymes that degrade extracellular matrix. Aggressive tumors are characterized by an imbalance between enzymes that degrade ECM and endogenous inhibitors of the enzymes. Matrix metalloproteinases (MMPs) make up the majority of ECM degrading enzymes implicated in cancer metastasis. The potent MMP inhibitory activities of tetracyclines, especially their chemically modified analogs, combined with their relatively well tolerated pharmacological profile, led several researchers to investigate their anticancer potential in a variety of cancers, including melanoma, lung, breast and prostate cancers. Chemically modified non-antibiotic tetracyclines (CMTs or COL) were tested using tumors of prostate, breast and melanomas. Some of these CMTs, notably, CMT-3 and CMT-308 significantly inhibited not only invasive potential and MMP activity, but also inhibited cell proliferation by inducing cell cycle arrest and apoptosis. CMT-3 and CMT-308 were significantly more potent than doxycycline or minocycline in inhibiting tumor cell-derived MMPs and inducing apoptosis in vitro and in vivo. CMT-3 (COL-3) showed potent inhibition of tumor growth in xenografts and in bone metastatic models of prostate cancer. Similar results were also reported in melanoma and breast cancer models. The mechanism by which CMTs kill tumor cells is via generation of hydroxyl free radicals ([OH](-)) which permeate and depolarize mitochondria, which in turn activates caspase mediated apoptosis. Analysis of tumor tissues from CMT-3 treated rats demonstrated reduction in angiogenesis and increase in apoptosis; both emerged as mechanisms of CMT action. These observations led to testing the efficacy of CMT-3 in human clinical trials against several types of cancer with significant outcomes, which are described in the next chapter of this issue.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Bone Neoplasms/secondary ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Doxycycline/pharmacology ; Doxycycline/therapeutic use ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Humans ; Male ; Matrix Metalloproteinase Inhibitors ; Melanoma/drug therapy ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Off-Label Use ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Rats ; Tetracyclines/chemistry ; Tetracyclines/pharmacology ; Tetracyclines/therapeutic use
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Matrix Metalloproteinase Inhibitors ; Tetracyclines ; Doxycycline (N12000U13O)
Language	English
Publishing date	2010-11-18
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2010.11.003
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Article: Molecular Oncology of Bladder Cancer from Inception to Modern Perspective.

Lokeshwar, Soum D / Lopez, Maite / Sarcan, Semih / Aguilar, Karina / Morera, Daley S / Shaheen, Devin M / Lokeshwar, Bal L / Lokeshwar, Vinata B

Cancers

2022 Volume 14, Issue 11

Abstract: Within the last forty years, seminal contributions have been made in the areas of bladder cancer (BC) biology, driver genes, molecular profiling, biomarkers, and therapeutic targets for improving personalized patient care. This overview includes seminal ... ...

Abstract	Within the last forty years, seminal contributions have been made in the areas of bladder cancer (BC) biology, driver genes, molecular profiling, biomarkers, and therapeutic targets for improving personalized patient care. This overview includes seminal discoveries and advances in the molecular oncology of BC. Starting with the concept of divergent molecular pathways for the development of low- and high-grade bladder tumors, field cancerization versus clonality of bladder tumors, cancer driver genes/mutations, genetic polymorphisms, and bacillus Calmette-Guérin (BCG) as an early form of immunotherapy are some of the conceptual contributions towards improving patient care. Although beginning with a promise of predicting prognosis and individualizing treatments, "-omic" approaches and molecular subtypes have revealed the importance of BC stem cells, lineage plasticity, and intra-tumor heterogeneity as the next frontiers for realizing individualized patient care. Along with urine as the optimal non-invasive liquid biopsy, BC is at the forefront of the biomarker field. If the goal is to reduce the number of cystoscopies but not to replace them for monitoring recurrence and asymptomatic microscopic hematuria, a BC marker may reach clinical acceptance. As advances in the molecular oncology of BC continue, the next twenty-five years should significantly advance personalized care for BC patients.
Language	English
Publishing date	2022-05-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14112578
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Article: Development of a Transparent Transgenic Zebrafish Cellular Phenotype

Rajpurohit, Surendra K / Ouellette, Logan / Sura, Suvarsha / Appiah, Chelsea / O'Keefe, Annabelle / McCarthy, Katherine / Kandepu, Umasai / Ye Mon, May / Kimmerling, Kirk / Arora, Vishal / Lokeshwar, Bal L

Biomedicines

2023 Volume 11, Issue 7

Abstract: NF-κB signaling has broad effects on cell survival, tissue growth, and proliferation activities. It controls many genes that are involved in inflammation and thus is a key player in many inflammatory diseases. The elevation of NF-κB activators is ... ...

Abstract	NF-κB signaling has broad effects on cell survival, tissue growth, and proliferation activities. It controls many genes that are involved in inflammation and thus is a key player in many inflammatory diseases. The elevation of NF-κB activators is associated with elevated mortality, especially in cancer and cardiovascular diseases. The zebrafish has emerged as an important model for whole-organism in vivo modeling in translational research. In vertebrates, in-vivo spatial resolution is limited due to normal opacification of skin and subdermal structure. For in vivo imaging, skin transparency by blocking the pigmentation via chemical inhibition is required and the maintenance of this transparency is vital. The
Language	English
Publishing date	2023-07-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11071985
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Article ; Online: G protein βγ translocation to the Golgi apparatus activates MAPK via p110γ-p101 heterodimers.

Khater, Mostafa / Wei, Zhe / Xu, Xin / Huang, Wei / Lokeshwar, Bal L / Lambert, Nevin A / Wu, Guangyu

The Journal of biological chemistry

2021 Volume 296, Page(s) 100325

Abstract: The Golgi apparatus (GA) is a cellular organelle that plays a critical role in the processing of proteins for secretion. Activation of G protein-coupled receptors at the plasma membrane (PM) induces the translocation of G protein βγ dimers to the GA. ... ...

Abstract	The Golgi apparatus (GA) is a cellular organelle that plays a critical role in the processing of proteins for secretion. Activation of G protein-coupled receptors at the plasma membrane (PM) induces the translocation of G protein βγ dimers to the GA. However, the functional significance of this translocation is largely unknown. Here, we study PM-GA translocation of all 12 Gγ subunits in response to chemokine receptor CXCR4 activation and demonstrate that Gγ9 is a unique Golgi-translocating Gγ subunit. CRISPR-Cas9-mediated knockout of Gγ9 abolishes activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2), two members of the mitogen-activated protein kinase family, by CXCR4. We show that chemically induced recruitment to the GA of Gβγ dimers containing different Gγ subunits activates ERK1/2, whereas recruitment to the PM is ineffective. We also demonstrate that pharmacological inhibition of phosphoinositide 3-kinase γ (PI3Kγ) and depletion of its subunits p110γ and p101 abrogate ERK1/2 activation by CXCR4 and Gβγ recruitment to the GA. Knockout of either Gγ9 or PI3Kγ significantly suppresses prostate cancer PC3 cell migration, invasion, and metastasis. Collectively, our data demonstrate a novel function for Gβγ translocation to the GA, via activating PI3Kγ heterodimers p110γ-p101, to spatiotemporally regulate mitogen-activated protein kinase activation by G protein-coupled receptors and ultimately control tumor progression.
MeSH term(s)	Cell Membrane/genetics ; Class Ib Phosphatidylinositol 3-Kinase/genetics ; Dimerization ; GTP-Binding Protein beta Subunits/genetics ; GTP-Binding Protein gamma Subunits/genetics ; Golgi Apparatus/genetics ; HEK293 Cells ; Humans ; Mitogen-Activated Protein Kinase Kinases/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Protein Transport/genetics ; Receptors, CXCR4/genetics ; Receptors, G-Protein-Coupled/genetics ; Signal Transduction/genetics
Chemical Substances	CXCR4 protein, human ; G-protein Beta gamma ; GTP-Binding Protein beta Subunits ; GTP-Binding Protein gamma Subunits ; Receptors, CXCR4 ; Receptors, G-Protein-Coupled ; Class Ib Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PIK3CG protein, human (EC 2.7.1.137) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2021-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.100325
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