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Article: Review paper: cancer stem cells and cancer nonstem cells: from adult stem cells or from reprogramming of differentiated somatic cells.

Trosko, J E

2009 Volume 46, Issue 2, Page(s) 176–193

Abstract: Two opposing hypotheses of the origin of cancer have existed for many decades. One hypothesis postulates that the adult stem cell is needed to initiate the carcinogenic process, whereas the other claims a somatic differentiated cell can dedifferentiate ... ...

Abstract	Two opposing hypotheses of the origin of cancer have existed for many decades. One hypothesis postulates that the adult stem cell is needed to initiate the carcinogenic process, whereas the other claims a somatic differentiated cell can dedifferentiate or be reprogrammed to regain properties associated with cancer cells. Recent reemergence of the cancer stem cell hypothesis and the isolation of presumptive cancer stem cells from many types of cancer have forced a reexamination of these 2 hypotheses of the origin of cancer. In addition, normal embryonic and adult stem cells have now been isolated and partially characterized. Furthermore, the demonstration of embryonic-like stem cells, being isolated from adult-differentiated skin fibroblast cells of mice, monkey, and human beings, provides a newer opportunity to determine which of these 2 hypotheses might explain the cell type for initiating the carcinogenic process. The goal of this review is to integrate these recent findings, concerning the isolation of normal and cancer stem cells, with several of the classical concepts of carcinogenesis (initiation/promotion/progression; mutation/epigenetic; stem cell theory/dedifferentiation hypotheses; oncogene-tumor suppressor theory). Although the weight of the evidence in this review seems to support the stem cell hypothesis, only future studies, probably using comparative animal and human oncologic studies, will determine if targeting the cancer stem cell, with individualized medical approaches, will improve cancer prevention and therapy.
MeSH term(s)	Adult Stem Cells/pathology ; Animals ; Cell Differentiation ; Humans ; Mice ; Neoplasms/pathology
Language	English
Publishing date	2009-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	188012-3
ISSN	1544-2217 ; 0300-9858
ISSN (online)	1544-2217
ISSN	0300-9858
DOI	10.1354/vp.46-2-176
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Article ; Online: Role of diet and nutrition on the alteration of the quality and quantity of stem cells in human aging and the diseases of aging.

Trosko, J E

Current pharmaceutical design

2006 Volume 14, Issue 26, Page(s) 2707–2718

Abstract: An integrative synthesis of concepts and an explosion of experimental and epidemiological findings allow new insights as to how the interactions of genetic, environmental, dietary, cultural (social, psychological, economic) factors can influence the ... ...

Abstract	An integrative synthesis of concepts and an explosion of experimental and epidemiological findings allow new insights as to how the interactions of genetic, environmental, dietary, cultural (social, psychological, economic) factors can influence the aging and diseases of aging processes. Although the net effect of the best dietary maintenance of homeostatic control of cell proliferation, cell differentiation and apoptosis, systems breakdown of the human being and death will inevitably be the ultimate end result. Reduction of the quantity of the stem cell pool in any tissue will affect the "aging" of that organ. This, in turn, will affect the homeostatic maintenance of the organ systems of the human. Clearly, not all organs of the body age uniformly. The quality of the stem cells in any organ, depending on circumstances, can contribute to various disease pathogeneses. In the case where the quality of the stem cells is altered in utero or early postnatal development by some mutagenic mechanism that could lead to the initiation step of carcinogenesis, then the individual can, to some degree, control the fate of those prenatally and early postnatally-derived initiated stem cells by choosing those environmentally and dietary factors that either enhance or prevent the clonal expansion of these initiated stem cells during the promotion phase of carcinogenesis. This might explain the Barker hypothesis which suggests that prenatal and early postnatal exposures to toxic agents can lead to diseases later in life.
MeSH term(s)	Aged ; Aging ; Animals ; Apoptosis/physiology ; Cell Differentiation/physiology ; Cell Proliferation ; Diet ; Female ; Homeostasis/physiology ; Humans ; Neoplasms/etiology ; Neoplasms/prevention & control ; Nutritional Status/physiology ; Pregnancy ; Prenatal Exposure Delayed Effects/etiology ; Prenatal Exposure Delayed Effects/physiopathology ; Stem Cells/metabolism
Language	English
Publishing date	2006-01-23
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161208786264106
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Article: The role of stem cells and gap junctions as targets for cancer chemoprevention and chemotherapy.

Trosko, J E

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2006 Volume 59 Suppl 2, Page(s) S326–31

Abstract: Since carcinogenesis is a multi-stage, multi-mechanism process, involving mutagenic, cell death and epigenetic mechanisms, during the "initiation/promotion/and progression" phases, chemoprevention must be based on understanding the mechanism(s) of each ... ...

Abstract	Since carcinogenesis is a multi-stage, multi-mechanism process, involving mutagenic, cell death and epigenetic mechanisms, during the "initiation/promotion/and progression" phases, chemoprevention must be based on understanding the mechanism(s) of each phase. Prevention of each phase could reduce the risk to cancer. Because reducing the initiation phase to a zero level is impossible, the most effective intervention would be at the promotion phase. Assuming the "target" cells for carcinogenesis are the pluri-potent stem cells and their early progenitor or transit cells, chemoprevention strategies for inhibiting the promotion of these two types of pre-malignant "initiated" cells will require different agents. A hypothesis will be proposed that involves stem cells, which lack gap junctional intercellular communication (GJIC-) or their early progenitor daughter cells, which express GJIC+ and are partially-differentiated, if initiated, will be promoted by agents that either inhibit secreted negative growth regulators or by inhibitors of GJIC. Chemopreventing agents to each of these two types of initiated cells must have different mechanisms of action. Assuming stem cells are target cells for carcinogenesis, an alternative method of chemoprevention would be to reduce the stem cell pool. Anti-tumor promoter chemopreventive agents, such as green tea components, resveratrol, caffeic acid phenethylene ester, that either up-regulate GJIC in stem cells or prevent the down regulation of GJIC by tumor promoters in early progenitor cells, will be provided. Human pluri-potent stem cell systems, that can be induced to form 3-dimensional "organoid" structures, will be discussed as a more realistic model system to screen for relevant chemopreventive agents.
MeSH term(s)	Animals ; Anticarcinogenic Agents/pharmacology ; Antineoplastic Agents/pharmacology ; Cell Communication/drug effects ; Gap Junctions/physiology ; Humans ; Neoplasms/drug therapy ; Neoplasms/physiopathology ; Neoplasms/prevention & control ; Stem Cells/physiology
Chemical Substances	Anticarcinogenic Agents ; Antineoplastic Agents
Language	English
Publishing date	2006-02-13
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/s0753-3322(05)80065-4
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Article: Review Paper: Cancer Stem Cells and Cancer Nonstem Cells: From Adult Stem Cells or from Reprogramming of Differentiated Somatic Cells

Trosko, J. E

Veterinary pathology. , v. 46, no. 2

2009

Abstract	Two opposing hypotheses of the origin of cancer have existed for many decades. One hypothesis postulates that the adult stem cell is needed to initiate the carcinogenic process, whereas the other claims a somatic differentiated cell can dedifferentiate or be reprogrammed to regain properties associated with cancer cells. Recent reemergence of the cancer stem cell hypothesis and the isolation of presumptive cancer stem cells from many types of cancer have forced a reexamination of these 2 hypotheses of the origin of cancer. In addition, normal embryonic and adult stem cells have now been isolated and partially characterized. Furthermore, the demonstration of embryonic-like stem cells, being isolated from adult-differentiated skin fibroblast cells of mice, monkey, and human beings, provides a newer opportunity to determine which of these 2 hypotheses might explain the cell type for initiating the carcinogenic process. The goal of this review is to integrate these recent findings, concerning the isolation of normal and cancer stem cells, with several of the classical concepts of carcinogenesis (initiation/promotion/progression; mutation/epigenetic; stem cell theory/dedifferentiation hypotheses; oncogenetumor suppressor theory). Although the weight of the evidence in this review seems to support the stem cell hypothesis, only future studies, probably using comparative animal and human oncologic studies, will determine if targeting the cancer stem cell, with individualized medical approaches, will improve cancer prevention and therapy.
Keywords	carcinogenesis ; cell dedifferentiation ; cell differentiation ; fibroblasts ; gene expression ; genes ; humans ; mice ; monkeys ; neoplasms ; somatic cells ; stem cells
Language	English
Dates of publication	2009-03
Size	p. 176-193.
Publishing place	SAGE Publications
Document type	Article
ZDB-ID	188012-3
ISSN	1544-2217 ; 0300-9858
ISSN (online)	1544-2217
ISSN	0300-9858
DOI	10.1354/vp.46-2-176
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Article: From bacteria to humans: lessons learned from a reductionist's view of ultraviolet light-induced DNA lesions.

Trosko, J E

Environmental and molecular mutagenesis

2003 Volume 38, Issue 2-3, Page(s) 118–121

Abstract: What follows is a personal remembrance of how Dr. Richard Setlow influenced me as a young postdoctoral fellow at Oak Ridge National laboratory between 1963 and 1966. The narrative tries to place my "maturation" as a young, inexperienced scientist in the ... ...

Abstract	What follows is a personal remembrance of how Dr. Richard Setlow influenced me as a young postdoctoral fellow at Oak Ridge National laboratory between 1963 and 1966. The narrative tries to place my "maturation" as a young, inexperienced scientist in the context of the cultural upheaval caused by the Vietnam war, of a Northerner facing a "culture-shock" living in the South and in a revolution in molecular and radiation biology taking place at Oak Ridge National Laboratory at that time. The unique historic juxtaposition of Dr. Setlow's contribution of the discovery of UV-induced pyrimidine dimers in bacterial DNA, being potentially the molecular lesion responsible for cell killing and mutagenesis, occurring as I was at Oak Ridge, and the wonderful working relationship I had with William Carrier, his technician, led to our discovery with James Regan that normal human cells repaired these lesion from their DNA. Amazingly, because of Dr. Setlow's challenge to me about my thoughts of the implications of his findings in bacteria, the chance visit to Oak Ridge National Laboratory by Dr. James Cleaver and my background as a human geneticist provided me the extraordinary opportunity to carry out a collaboration to test if human cancer prone syndromes might be deficient in the repair of these UV-induced DNA lesions. With our finding that the direct demonstration of a lack of repair of UV-induced pyrimidine dimers in cells from the skin cancer prone syndrome, xeroderma pigmentosum, opened up a new paradigm for the understanding of the molecular mechanism of carcinogenesis of both radiation and chemical carcinogenesis. From this investigator's vantage point in the history of the understanding of carcinogenesis, which has led us to the present point of "oncogenes" and "tumor suppressor genes", the old adage by Newton, "I only saw further because I stood on the shoulder of giants", is so applicable here. Dr. Setlow's shoulders were indeed among those of all of us that have made some small contribution in trying to understand this extremely complex process of human carcinogenesis.
MeSH term(s)	Bacteria/genetics ; Bacteria/radiation effects ; DNA Damage/radiation effects ; DNA Repair ; DNA, Bacterial/genetics ; DNA, Bacterial/radiation effects ; History, 20th Century ; Humans ; Mentors/history ; Radiobiology/history ; Ultraviolet Rays ; United States
Chemical Substances	DNA, Bacterial
Language	English
Publishing date	2003-03-07
Publishing country	United States
Document type	Autobiography ; Biography ; Historical Article ; Journal Article
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.1061
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Article: Bioethics: a philosophical basis for moral decisions.

Trosko, J E

Taiwan yi xue ren wen xue kan

2001 Volume 2, Issue 1-2, Page(s) 29–33

MeSH term(s)	Bioethics ; Ecosystem ; Human Characteristics ; Humans ; Philosophy ; Science
Language	English
Publishing date	2001-10
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ISSN	1606-5727
ISSN	1606-5727
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Article: EFFECT ON GENETIC DAMAGE OF POSTTREATMENTS GIVEN X-RAYED DROSOPHILA MALES.

TROSKO, J E

Genetics

2001 Volume 49, Page(s) 401–409

MeSH term(s)	Animals ; Cold Temperature ; Drosophila ; Radiation Genetics ; Research
Language	English
Publishing date	2001-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1093/genetics/49.3.401
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Article: Commentary: is the concept of "tumor promotion" a useful paradigm?

Trosko, J E

Molecular carcinogenesis

2001 Volume 30, Issue 3, Page(s) 131–137

Abstract: Since the demonstration of the multistage nature of carcinogenesis in experimental work on mouse skin carcinogenesis (and subsequently on various other organ systems in other organisms), the concepts of "initiation", "promotion", and "progression" were ... ...

Abstract	Since the demonstration of the multistage nature of carcinogenesis in experimental work on mouse skin carcinogenesis (and subsequently on various other organ systems in other organisms), the concepts of "initiation", "promotion", and "progression" were operationally generated from empiric data. Because these early observations and concepts had no mechanistic explanations, various hypotheses have been generated to explain the unique characteristics of each phase (e.g., initiation, being irreversible, was ascribed as the result of DNA damage leading to mutagenesis; promotion, being interruptible or reversible, was believed to be caused by epigenetic mechanisms; progression, also being irreversible, was believed to be caused by genetic instability that led to mutagenic and epigenetic changes). In addition, many of the molecular, biochemical, and cellular experiments designed to investigate the mechanistic bases of these phases used technologies that did not always lead to unequivocal interpretations, and because "real-life" carcinogenesis does not mimic controlled experimental conditions of the initiation/promotion/progression experiments, many investigators believe that these concepts have lost their usefulness. In this commentary, I explain some of the confusion concerning the concept of promotion and suggest that, by understanding the limitations of many in vitro assays used to characterize mutagens, by integrating other theories of carcinogenesis (i.e., stem cell theory), and by recognizing the role of epigenetic agents, specifically, modulated gap-junctional intercellular communication, the concept of promotion can provide valuable insights into the carcinogenic process. Mol. Carcinog. 30:131--137, 2001.
MeSH term(s)	Animals ; Carcinogens/pharmacology ; Cell Communication ; Cell Transformation, Neoplastic ; Clone Cells ; Drug Screening Assays, Antitumor ; Gap Junctions/physiology ; Humans ; Models, Biological ; Mutagens/pharmacology ; Oligonucleotide Array Sequence Analysis ; Stem Cells/physiology
Chemical Substances	Carcinogens ; Mutagens
Language	English
Publishing date	2001-03
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
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Article: Dietary modulation of the multistage, multimechanisms of human carcinogenesis: effects on initiated stem cells and cell-cell communication

Trosko, J.E

Nutrition and cancer. 2006, v. 54, no. 1

2006

Abstract: Diet can influence the risk to cancer in both negative and positive ways. Worldwide, more than 10 million persons develop cancer annually. Diet could prevent many cancers. Carcinogenesis is a multistage, multimechanism process, consisting of "initiation," ...

Abstract	Diet can influence the risk to cancer in both negative and positive ways. Worldwide, more than 10 million persons develop cancer annually. Diet could prevent many cancers. Carcinogenesis is a multistage, multimechanism process, consisting of "initiation," "promotion," and "progression" phases. Although diet could affect each phase, an efficacious strategy for dietary chemoprevention would be intervention during the promotion phase. The tumor-promotion process requires sustained exposure to agents that stimulate the growth and inhibition of apoptosis of initiated cells in the absence of antipromoters. Chronic inflammation has been associated with the promotion process. The mechanism affecting the promotion process appears to be the inhibition of cell-cell communication between normal and initiated cells. Most, if not all, tumor-promoting agents and conditions, reversibly, inhibit cell-cell communication, whereas antipromoters, antioxidants, and anti-inflammatory agents have been shown to ameliorate the effects of tumor promoters on cell-cell communication. Additionally, adult stem cells are hypothesized to be the target cells for initiating the carcinogenic process. A new paradigm has been presented that postulates the first function of the carcinogenic process is to block the "mortalization" of a normal, "immortal" adult stem cell rather than the induction of "immortalization" of a normal mortal cell.
Keywords	humans ; carcinogenesis ; disease prevention ; nutritional intervention ; diet ; risk factors ; risk reduction ; stem cells ; signal transduction ; nutrition-genotype interaction ; apoptosis ; cell proliferation ; DNA damage ; DNA repair ; remission
Language	English
Size	p. 102-110.
Document type	Article
Note	Paper presented at the International Symposium on "Berries in Cancer Prevention : From Experimental Findings to Human Studies", held July 2004, Lahti, Finland.
ZDB-ID	424433-3
ISSN	0163-5581
ISSN	0163-5581
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Article: Human health consequences of environmentally-modulated gene expression: potential roles of ELF-EMF induced epigenetic versus mutagenic mechanisms of disease.

Trosko, J E

Bioelectromagnetics

2000 Volume 21, Issue 5, Page(s) 402–406

Abstract: In order to determine if there might be biological and health consequences after exposures to extremely-low frequency electromagnetic fields (ELF-EMF), either experimentally or epidemiologically, mechanistic understanding of the potential means by which ... ...

Abstract	In order to determine if there might be biological and health consequences after exposures to extremely-low frequency electromagnetic fields (ELF-EMF), either experimentally or epidemiologically, mechanistic understanding of the potential means by which any environmental agent can affect cells in a multicellular organism has to be reviewed. The goal of this limited review is to demonstrate that, while the prevailing paradigm of the environmentally-induced acute and chronic diseases involves either cell killing (cytotoxicity) or gene/chromosome mutations (genotoxicity), alteration of the expression of genetic information at the transcriptional (turning genes "on" or "off"), translational (stabilizing or de-stabilizing the genetic message), or posttranslational (altering the gene product or protein) levels has the potential to contribute to various diseases. This latter mechanism, "epigenetic" toxicity, unlike the former two which are irreversible, is characterized by threshold-like action, multiple biochemical pathways and chronic, regular exposures to be effective. Ultimately, epigenetic toxicants affect one of four potential cell states, namely alteration of cell proliferation, cell differentiation, programmed cell death (apoptosis) or adaptive responses of differentiated cells.
MeSH term(s)	DNA Damage ; Disease/etiology ; Electromagnetic Fields/adverse effects ; Environmental Health ; Gene Expression ; Humans ; Models, Biological ; Mutation ; Neoplasms/etiology ; Neoplasms/genetics
Language	English
Publishing date	2000-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	760683-7
ISSN	1521-186X ; 0197-8462
ISSN (online)	1521-186X
ISSN	0197-8462
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