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Article: Biomarkers for lung cancer: clinical uses.

Greenberg, Alissa K / Lee, M Sung

2007 Volume 13, Issue 4, Page(s) 249–255

Abstract: Purpose of review: Biomarkers for lung cancer may be used for risk stratification, early detection, treatment selection, prognostication and monitoring for recurrence. All these areas of clinical management would benefit from sensitive and specific, ... ...

Abstract	Purpose of review: Biomarkers for lung cancer may be used for risk stratification, early detection, treatment selection, prognostication and monitoring for recurrence. All these areas of clinical management would benefit from sensitive and specific, noninvasive, cost-effective biomarkers. Recent findings: Significant progress has been made in understanding the steps involved in lung carcinogenesis and in the development of novel technologies for biomarker discovery. Over the last 3 years research into prospective lung cancer biomarkers has proliferated, especially in the areas of early detection and prognostication. The most active areas of research have been in promoter methylation, proteomics and genomics. Many investigators are adopting panels of serum biomarkers in an attempt to increase sensitivity. The development of targeted lung cancer therapy has engendered interest in markers to identify the optimal candidates for these therapies. Summary: Much progress has been made in the last 3 years in the identification and validation of new biomarkers for the early diagnosis of lung cancer. The biomarkers require additional studies before they can be used clinically. Markers to identify lung cancer patients who may benefit from targeted therapy have been developed more rapidly and may be used now in some clinical situations.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; DNA, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm/genetics ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/metabolism ; Neoplasm Recurrence, Local/diagnosis ; Neoplasm Recurrence, Local/metabolism ; Sensitivity and Specificity
Chemical Substances	Biomarkers, Tumor ; DNA, Neoplasm
Language	English
Publishing date	2007-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1285505-4
ISSN	1531-6971 ; 1070-5287 ; 1078-1641
ISSN (online)	1531-6971
ISSN	1070-5287 ; 1078-1641
DOI	10.1097/MCP.0b013e32819f8f06
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Article ; Online: Aryl hydrocarbon receptor and lung cancer.

Tsay, Junchieh J / Tchou-Wong, Kam-Meng / Greenberg, Alissa K / Pass, Harvey / Rom, William N

Anticancer research

2013 Volume 33, Issue 4, Page(s) 1247–1256

Abstract: The leading cause of lung cancer is exposure to cigarette smoke and other environmental pollutants, which include formaldehyde, acrolein, benzene, dioxin, and polycyclic aromatic hydrocarbons (PAHs). PAHs and dioxins are exogenous ligands that directly ... ...

Abstract	The leading cause of lung cancer is exposure to cigarette smoke and other environmental pollutants, which include formaldehyde, acrolein, benzene, dioxin, and polycyclic aromatic hydrocarbons (PAHs). PAHs and dioxins are exogenous ligands that directly bind to the aryl hydrocarbon receptor (AhR), a transcription factor that activates xenobiotic metabolism, histone modification (an important step in DNA methylation) and, ultimately, tumorigenesis. In this review article we summarize the current understanding of AhR and its role in the development of lung cancer, including its influence on cell proliferation, angiogenesis, inflammation, and apoptosis.
MeSH term(s)	Animals ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/etiology ; Lung Neoplasms/metabolism ; Receptors, Aryl Hydrocarbon/metabolism
Chemical Substances	Receptors, Aryl Hydrocarbon
Language	English
Publishing date	2013-04-05
Publishing country	Greece
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
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Article ; Online: Current readings: blood-based biomarkers for lung cancer.

Tsay, Jun-Chieh J / DeCotiis, Christopher / Greenberg, Alissa K / Rom, William N

Seminars in thoracic and cardiovascular surgery

2013 Volume 25, Issue 4, Page(s) 328–334

Abstract: Lung cancer is the leading cause of cancer deaths worldwide largely owing to diagnosis of the disease at an advanced stage. Recent advances in blood-based biomarker research have the potential to reduce mortality by providing a means for detecting lung ... ...

Abstract	Lung cancer is the leading cause of cancer deaths worldwide largely owing to diagnosis of the disease at an advanced stage. Recent advances in blood-based biomarker research have the potential to reduce mortality by providing a means for detecting lung cancer at an earlier stage. Since the publication of the National Lung Cancer Screening Trial demonstrating reduction in mortality with computed tomography (CT) scan screening, the U.S. Preventive Services Task Force has released a draft statement recommending annual low-dose CT scan screening for high-risk patients. However, CT screening has a high false-positive rate leading to the need for additional imaging and invasive procedures. In this article, we review recent literature on blood-based lung cancer biomarkers that we believe will have a significant role in enhancing screening efficacy in the near future.
Language	English
Publishing date	2013-11-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1038278-1
ISSN	1532-9488 ; 1043-0679
ISSN (online)	1532-9488
ISSN	1043-0679
DOI	10.1053/j.semtcvs.2013.11.001
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Article ; Online: Inflammatory cytokines and non-small cell lung cancer in a CT-scan screening cohort: Background review of the literature.

DeCotiis, Christopher / Hu, Yingjie / Greenberg, Alissa K / Huie, Maryann / Tsay, Jun-Chieh J / Pass, Harvey / Goldberg, Judith D / Rom, William N

Cancer biomarkers : section A of Disease markers

2016 Volume 16, Issue 2, Page(s) 219–233

Abstract: Background: Inflammatory cytokines are at the intersection of tumor cell biology and host immune response. Peripheral cytokine expression levels may reflect the microscopic tumor milieu, and specific cytokines play an integral role in tumor initiation, ... ...

Abstract	Background: Inflammatory cytokines are at the intersection of tumor cell biology and host immune response. Peripheral cytokine expression levels may reflect the microscopic tumor milieu, and specific cytokines play an integral role in tumor initiation, growth, and metastasis. High-throughput cytokine analysis may identify panels for early-stage non-small cell lung cancer (NSCLC) diagnosis and identify individuals at high-risk for lung cancer with indeterminate lung nodules 8-20 mm in size. Methods: Thirteen serum cytokines from the NYU Lung Cancer Biomarker Center cohort with early-stage NSCLC were analyzed using bead-based immunoassay technology. Results: In the NYU cohort, a one unit increase in interferon-γ increased risk of lung cancer by 3% (OR = 1.03, 95% CI, 1.02-1.05) and a one unit increase in TNF-α decreased the risk of lung cancer by 53% (OR = 0.47, 95% Cl, 0.31-0.71) when both cytokines were included in a logistic regression model with adjustments for age and pack-years of smoking. The resulting AUC for the Receiver Operating Characteristic (ROC) curve was 0.88; the sensitivity and specificity at the optimal cutpoint were 78.9% and 90.3%, respectively. Conclusions: Cytokines have limited value in the early diagnosis of early-stage NSCLC. Our review of the literature suggests that although inflammation is important for the development of NSCLC, that cytokines are increased in more advanced lung cancer than when the diagnosis occurs at presentation.
MeSH term(s)	Biomarkers ; Carcinoma, Non-Small-Cell Lung/blood ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/surgery ; Comorbidity ; Cytokines/blood ; Humans ; Inflammation Mediators/blood ; Lung Neoplasms/blood ; Lung Neoplasms/diagnosis ; Lung Neoplasms/surgery ; Neoplasm Staging ; ROC Curve ; Risk Factors ; Tomography, X-Ray Computed
Chemical Substances	Biomarkers ; Cytokines ; Inflammation Mediators
Language	English
Publishing date	2016
Publishing country	Netherlands
Document type	Journal Article ; Meta-Analysis ; Review
ZDB-ID	2203517-5
ISSN	1875-8592 ; 1574-0153 ; 1875-8592
ISSN (online)	1875-8592 ; 1574-0153
ISSN	1875-8592
DOI	10.3233/CBM-150559
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Article: Chemoprevention of lung cancer: prospects and disappointments in human clinical trials.

Greenberg, Alissa K / Tsay, Jun-Chieh / Tchou-Wong, Kam-Meng / Jorgensen, Anna / Rom, William N

Cancers

2013 Volume 5, Issue 1, Page(s) 131–148

Abstract: Decreasing the risk of lung cancer, or preventing its development in high-risk individuals, would have a huge impact on public health. The most effective means to decrease lung cancer incidence is to eliminate exposure to carcinogens. However, with ... ...

Abstract	Decreasing the risk of lung cancer, or preventing its development in high-risk individuals, would have a huge impact on public health. The most effective means to decrease lung cancer incidence is to eliminate exposure to carcinogens. However, with recent advances in the understanding of pulmonary carcinogenesis and the identification of intermediate biomarkers, the prospects for the field of chemoprevention research have improved dramatically. Here we review the most recent research in lung cancer chemoprevention-focusing on those agents that have been investigated in human clinical trials. These agents fall into three major categories. First, oxidative stress plays an important role in pulmonary carcinogenesis; and therefore, antioxidants (including vitamins, selenium, green tea extracts, and isothiocyanates) may be particularly effective in preventing the development of lung cancer. Second, inflammation is increasingly accepted as a crucial factor in carcinogenesis, and many investigators have focused on anti-inflammatory agents, such as glucocorticoids, NSAIDs, statins, and PPARγ agonists. Finally, the PI3K/AKT/mTOR pathway is recognized to play a central role in tobacco-induced carcinogenesis, and inhibitors of this pathway, including myoinositol and metformin, are promising agents for lung cancer prevention. Successful chemoprevention will likely require targeting of multiple pathways to carcinogenesis-both to minimize toxicity and maximize efficacy.
Language	English
Publishing date	2013-01-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers5010131
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Article: Basic pathogenetic mechanisms in silicosis: current understanding.

Rimal, Binaya / Greenberg, Alissa K / Rom, William N

Current opinion in pulmonary medicine

2005 Volume 11, Issue 2, Page(s) 169–173

Abstract: Purpose of review: Silicosis continues to be a common cause of chronic lung diseases, despite evidence that these diseases can be prevented by environmental dust control. Silicosis has been studied extensively by basic and clinical scientists, yet ... ...

Abstract	Purpose of review: Silicosis continues to be a common cause of chronic lung diseases, despite evidence that these diseases can be prevented by environmental dust control. Silicosis has been studied extensively by basic and clinical scientists, yet little is known about the crucial cellular and molecular mechanisms that initiate and propagate the process of inflammation and scarring. Recent findings: Recent in vivo, in vitro, and human studies have focused on several main areas of investigation into the causes and processes of the development of silicosis. These areas of investigation include the variability of pathogenic potential of different varieties of silica; the role of activated alveolar macrophages products in the development and progression of silicosis; and the direct role played by the silica particle surface in triggering adverse biologic reactions, such as generating ROS and RNS. The generation of oxidants by silica particles and by silica-activated cells results in cell and lung damage; increased expression of inflammatory cytokines, including TNF-alpha, IL 1 beta, and TGF-beta; activation of cell signaling pathways, including the MAP kinase pathways; and phosphorylation and activation of specific transcription factors (e.g., NFkB). The ROS, RNS, and NO generated by the silica particles also induce apoptosis in macrophages and other cells. Summary: Further research on the molecular mechanisms involved in the inflammatory processes important for progression to fibrotic diseases is needed for the development of effective treatment of silicosis. Potential therapeutic strategies include inhibition of cytokines such as IL-1, TNF alpha, the use of anti-oxidants, and the inhibition of apoptosis.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Lung/pathology ; Mice ; Necrosis ; Oxidative Stress ; Phagocytosis ; Rats ; Silicon Dioxide/toxicity ; Silicosis/etiology ; Silicosis/pathology ; Silicosis/physiopathology
Chemical Substances	Silicon Dioxide (7631-86-9)
Language	English
Publishing date	2005-02-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1285505-4
ISSN	1531-6971 ; 1070-5287 ; 1078-1641
ISSN (online)	1531-6971
ISSN	1070-5287 ; 1078-1641
DOI	10.1097/01.mcp.0000152998.11335.24
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Article ; Online: Chemoprevention of Lung Cancer

William N. Rom / Anna Jorgensen / Kam-Meng Tchou-Wong / Jun-Chieh Tsay / Alissa K. Greenberg

Cancers, Vol 5, Iss 1, Pp 131-

Prospects and Disappointments in Human Clinical Trials

2013 Volume 148

Abstract	Decreasing the risk of lung cancer, or preventing its development in high-risk individuals, would have a huge impact on public health. The most effective means to decrease lung cancer incidence is to eliminate exposure to carcinogens. However, with recent advances in the understanding of pulmonary carcinogenesis and the identification of intermediate biomarkers, the prospects for the field of chemoprevention research have improved dramatically. Here we review the most recent research in lung cancer chemoprevention—focusing on those agents that have been investigated in human clinical trials. These agents fall into three major categories. First, oxidative stress plays an important role in pulmonary carcinogenesis; and therefore, antioxidants (including vitamins, selenium, green tea extracts, and isothiocyanates) may be particularly effective in preventing the development of lung cancer. Second, inflammation is increasingly accepted as a crucial factor in carcinogenesis, and many investigators have focused on anti-inflammatory agents, such as glucocorticoids, NSAIDs, statins, and PPARγ agonists. Finally, the PI3K/AKT/mTOR pathway is recognized to play a central role in tobacco-induced carcinogenesis, and inhibitors of this pathway, including myoinositol and metformin, are promising agents for lung cancer prevention. Successful chemoprevention will likely require targeting of multiple pathways to carcinogenesis—both to minimize toxicity and maximize efficacy.
Keywords	lung cancer ; chemoprevention ; antioxidants ; anti-inflammatories ; carcinogenesis ; biomarkers ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Molecular characterization of the peripheral airway field of cancerization in lung adenocarcinoma.

Tsay, Jun-Chieh J / Li, Zhiguo / Yie, Ting-An / Wu, Feng / Segal, Leopoldo / Greenberg, Alissa K / Leibert, Eric / Weiden, Michael D / Pass, Harvey / Munger, John / Statnikov, Alexander / Tchou-Wong, Kam-Meng / Rom, William N

PloS one

2015 Volume 10, Issue 2, Page(s) e0118132

Abstract: Field of cancerization in the airway epithelium has been increasingly examined to understand early pathogenesis of non-small cell lung cancer. However, the extent of field of cancerization throughout the lung airways is unclear. Here we sought to ... ...

Abstract	Field of cancerization in the airway epithelium has been increasingly examined to understand early pathogenesis of non-small cell lung cancer. However, the extent of field of cancerization throughout the lung airways is unclear. Here we sought to determine the differential gene and microRNA expressions associated with field of cancerization in the peripheral airway epithelial cells of patients with lung adenocarcinoma. We obtained peripheral airway brushings from smoker controls (n=13) and from the lung contralateral to the tumor in cancer patients (n=17). We performed gene and microRNA expression profiling on these peripheral airway epithelial cells using Affymetrix GeneChip and TaqMan Array. Integrated gene and microRNA analysis was performed to identify significant molecular pathways. We identified 26 mRNAs and 5 miRNAs that were significantly (FDR <0.1) up-regulated and 38 mRNAs and 12 miRNAs that were significantly down-regulated in the cancer patients when compared to smoker controls. Functional analysis identified differential transcriptomic expressions related to tumorigenesis. Integration of miRNA-mRNA data into interaction network analysis showed modulation of the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway in the contralateral lung field of cancerization. In conclusion, patients with lung adenocarcinoma have tumor related molecules and pathways in histologically normal appearing peripheral airway epithelial cells, a substantial distance from the tumor itself. This finding can potentially provide new biomarkers for early detection of lung cancer and novel therapeutic targets.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Aged ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Epithelial Cells/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Gene Expression Profiling ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Male ; MicroRNAs/genetics ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics ; Respiratory System/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Smoking
Chemical Substances	MicroRNAs ; RNA, Messenger ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2015-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0118132
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Article ; Online: Preneoplastic lesions of the lung.

Greenberg, Alissa K / Yee, Herman / Rom, William N

Respiratory research

2002 Volume 3, Page(s) 20

Abstract: Lung cancer is the leading cause of cancer deaths worldwide. If we can define and detect preneoplastic lesions, we might have a chance of improving survival. The World Health Organization has defined three preneoplastic lesions of the bronchial ... ...

Abstract	Lung cancer is the leading cause of cancer deaths worldwide. If we can define and detect preneoplastic lesions, we might have a chance of improving survival. The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia/carcinoma in situ; atypical adenomatous hyperplasia; and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively. In this review we summarize the data supporting the preneoplastic nature of these lesions, and delve into some of the genetic changes found in atypical adenomatous hyperplasia and squamous dysplasia/carcinoma in situ.
MeSH term(s)	Animals ; Humans ; Lung/metabolism ; Lung/pathology ; Lung/physiology ; Lung Neoplasms/classification ; Lung Neoplasms/diagnosis ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mutation/genetics ; Precancerous Conditions/classification ; Precancerous Conditions/diagnosis ; Precancerous Conditions/genetics ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Respiratory Mucosa/physiology
Language	English
Publishing date	2002-04-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/rr170
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Article ; Online: Preneoplastic lesions of the lung

Yee Herman / Greenberg Alissa K / Rom William N

Respiratory Research, Vol 3, Iss 1, p

2002 Volume 20

Abstract: Abstract Lung cancer is the leading cause of cancer deaths worldwide. If we can define and detect preneoplastic lesions, we might have a chance of improving survival. The World Health Organization has defined three preneoplastic lesions of the bronchial ... ...

Abstract	Abstract Lung cancer is the leading cause of cancer deaths worldwide. If we can define and detect preneoplastic lesions, we might have a chance of improving survival. The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia/carcinoma in situ atypical adenomatous hyperplasia; and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively. In this review we summarize the data supporting the preneoplastic nature of these lesions, and delve into some of the genetic changes found in atypical adenomatous hyperplasia and squamous dysplasia/carcinoma in situ .
Keywords	bronchial epithelium ; carcinogenesis ; lung cancer ; preneoplasia ; Diseases of the respiratory system ; RC705-779 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2002-04-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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