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Article ; Online: Ewing sarcoma in a child with neurofibromatosis type 1.

Fernandez, Karen S / Turski, Michelle L / Shah, Avanthi Tayi / Bastian, Boris C / Horvai, Andrew / Hardee, Steven / Sweet-Cordero, E Alejandro

Cold Spring Harbor molecular case studies

2019 Volume 5, Issue 5

Abstract: We report here on a case of Ewing sarcoma (ES) occurring in a child with neurofibromatosis type 1. The sarcoma had an EWSR1-ERG translocation as well as loss of the remaining wild-type allele ... ...

Abstract	We report here on a case of Ewing sarcoma (ES) occurring in a child with neurofibromatosis type 1. The sarcoma had an EWSR1-ERG translocation as well as loss of the remaining wild-type allele of
MeSH term(s)	Child, Preschool ; Family ; Female ; Humans ; Mutation ; Neurofibromatosis 1/complications ; Neurofibromatosis 1/genetics ; Sarcoma, Ewing/diagnosis ; Sarcoma, Ewing/genetics ; ras Proteins/metabolism
Chemical Substances	ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-10-23
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2835759-0
ISSN	2373-2873 ; 2373-2873
ISSN (online)	2373-2873
ISSN	2373-2873
DOI	10.1101/mcs.a004580
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Article: New roles for copper metabolism in cell proliferation, signaling, and disease.

Turski, Michelle L / Thiele, Dennis J

The Journal of biological chemistry

2008 Volume 284, Issue 2, Page(s) 717–721

MeSH term(s)	Animals ; Cation Transport Proteins/metabolism ; Cell Proliferation ; Copper/deficiency ; Copper/metabolism ; Disease ; Homeostasis ; Humans ; Signal Transduction
Chemical Substances	Cation Transport Proteins ; Copper (789U1901C5)
Language	English
Publishing date	2008-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.R800055200
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Article: Drosophila Ctr1A functions as a copper transporter essential for development.

Turski, Michelle L / Thiele, Dennis J

The Journal of biological chemistry

2007 Volume 282, Issue 33, Page(s) 24017–24026

Abstract: Copper is an essential trace element required by all aerobic organisms as a cofactor for enzymes involved in normal growth, development, and physiology. Ctr1 proteins are members of a highly conserved family of copper importers responsible for copper ... ...

Abstract	Copper is an essential trace element required by all aerobic organisms as a cofactor for enzymes involved in normal growth, development, and physiology. Ctr1 proteins are members of a highly conserved family of copper importers responsible for copper uptake across the plasma membrane. Mice lacking Ctr1 die during embryogenesis from widespread developmental defects, demonstrating the need for adequate copper acquisition in the development of metazoan organisms via as yet uncharacterized mechanisms. Whereas the fruit fly, Drosophila melanogaster, expresses three Ctr1 genes, ctr1A, ctr1B, and ctr1C, little is known about their protein isoform-specific roles. Previous studies demonstrated that Ctr1B localizes to the plasma membrane and is not essential for development unless flies are severely copper-deficient or are subjected to copper toxicity. Here we demonstrate that Ctr1A also resides on the plasma membrane and is the primary Drosophila copper transporter. Loss of Ctr1A results in copper-remedial developmental arrest at early larval stages. Ctr1A mutants are deficient in the activity of copper-dependent enzymes, including cytochrome c oxidase and tyrosinase. Amidation of Phe-Met-Arg-Phe-amides, a group of cardiomodulatory neuropeptide hormones that are matured via the action of peptidylglycine alpha-hydroxylating monooxygenase, is defective in neuroendocrine cells of Ctr1A mutant larvae. Moreover, both the Phe-Met-Arg-Phe-amide maturation and heart beat rate defects observed in Ctr1A mutant larvae can be partially rescued by exogenous copper. These studies establish clear physiological distinctions between two Drosophila plasma membrane copper transport proteins and demonstrate that copper import by Ctr1A is required to drive neuropeptide maturation during normal growth and development.
MeSH term(s)	Amino Acid Motifs ; Animals ; Biological Transport ; Cation Transport Proteins/metabolism ; Cation Transport Proteins/physiology ; Copper/metabolism ; Drosophila Proteins/metabolism ; Drosophila Proteins/physiology ; Embryo, Nonmammalian ; Embryonic Development ; Protein Isoforms/physiology
Chemical Substances	Cation Transport Proteins ; Drosophila Proteins ; Protein Isoforms ; Copper (789U1901C5)
Language	English
Publishing date	2007-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M703792200
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Article: New Roles for Copper Metabolism in Cell Proliferation, Signaling, and Disease

Turski, Michelle L / Thiele, Dennis J

Journal of biological chemistry. 2009 Jan. 9, v. 284, no. 2

2009

Language	English
Dates of publication	2009-0109
Size	p. 717-721.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease.

Neef, Daniel W / Turski, Michelle L / Thiele, Dennis J

PLoS biology

2010 Volume 8, Issue 1, Page(s) e1000291

Abstract: Neurodegenerative diseases such as Huntington disease are devastating disorders with no therapeutic approaches to ameliorate the underlying protein misfolding defect inherent to poly-glutamine (polyQ) proteins. Given the mounting evidence that elevated ... ...

Abstract	Neurodegenerative diseases such as Huntington disease are devastating disorders with no therapeutic approaches to ameliorate the underlying protein misfolding defect inherent to poly-glutamine (polyQ) proteins. Given the mounting evidence that elevated levels of protein chaperones suppress polyQ protein misfolding, the master regulator of protein chaperone gene transcription, HSF1, is an attractive target for small molecule intervention. We describe a humanized yeast-based high-throughput screen to identify small molecule activators of human HSF1. This screen is insensitive to previously characterized activators of the heat shock response that have undesirable proteotoxic activity or that inhibit Hsp90, the central chaperone for cellular signaling and proliferation. A molecule identified in this screen, HSF1A, is structurally distinct from other characterized small molecule human HSF1 activators, activates HSF1 in mammalian and fly cells, elevates protein chaperone expression, ameliorates protein misfolding and cell death in polyQ-expressing neuronal precursor cells and protects against cytotoxicity in a fly model of polyQ-mediated neurodegeneration. In addition, we show that HSF1A interacts with components of the TRiC/CCT complex, suggesting a potentially novel regulatory role for this complex in modulating HSF1 activity. These studies describe a novel approach for the identification of new classes of pharmacological interventions for protein misfolding that underlies devastating neurodegenerative disease.
MeSH term(s)	Animals ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA-Binding Proteins/analysis ; DNA-Binding Proteins/metabolism ; Drosophila/genetics ; Drosophila/metabolism ; HSP90 Heat-Shock Proteins/metabolism ; Heat Shock Transcription Factors ; Humans ; Mice ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Phosphorylation ; Protein Folding ; Saccharomyces cerevisiae/genetics ; Transcription Factors/analysis ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; HSF1 protein, human ; HSP90 Heat-Shock Proteins ; Heat Shock Transcription Factors ; Molecular Chaperones ; Transcription Factors
Language	English
Publishing date	2010-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.1000291
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Article ; Online: Genomically Driven Tumors and Actionability across Histologies: BRAF-Mutant Cancers as a Paradigm.

Turski, Michelle L / Vidwans, Smruti J / Janku, Filip / Garrido-Laguna, Ignacio / Munoz, Javier / Schwab, Richard / Subbiah, Vivek / Rodon, Jordi / Kurzrock, Razelle

Molecular cancer therapeutics

2016 Volume 15, Issue 4, Page(s) 533–547

Abstract: The diagnosis, classification, and management of cancer are traditionally dictated by the site of tumor origin, for example, breast or lung, and by specific histologic subtypes of site-of-origin cancers (e.g., non-small cell versus small cell lung cancer) ...

Abstract	The diagnosis, classification, and management of cancer are traditionally dictated by the site of tumor origin, for example, breast or lung, and by specific histologic subtypes of site-of-origin cancers (e.g., non-small cell versus small cell lung cancer). However, with the advent of sequencing technologies allowing for rapid, low cost, and accurate sequencing of clinical samples, new observations suggest an expanded or different approach to the diagnosis and treatment of cancer-one driven by the unique molecular features of the tumor. We discuss a genomically driven strategy for cancer treatment using BRAF as an example. Several key points are highlighted: (i) molecular aberrations can be shared across cancers; (ii) approximately 15% of all cancers harbor BRAF mutations; and (iii) BRAF inhibitors, while approved only for melanoma, have reported activity across numerous cancers and related disease types bearing BRAF aberrations. However, BRAF-mutated colorectal cancer has shown poor response rate to BRAF inhibitor monotherapy, striking a cautionary note. Yet, even in this case, emerging data suggest BRAF-mutated colorectal cancers can respond well to BRAF inhibitors, albeit when administered in combination with other agents that impact resistance pathways. Taken together, these data suggest that molecular aberrations may be the basis for a new nosology for cancer. Mol Cancer Ther; 15(4); 533-47. ©2016 AACR.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genetic Testing/methods ; Genetic Variation ; Humans ; MAP Kinase Signaling System/drug effects ; Molecular Targeted Therapy ; Mutation ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Neoplasms/genetics ; Prognosis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2016-03-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-15-0643
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Article ; Online: A recurrent missense variant in the E3 ubiquitin ligase substrate recognition subunit FEM1B causes a rare syndromic neurodevelopmental disorder.

Lecoquierre, François / Punt, A Mattijs / Ebstein, Frédéric / Wallaard, Ilse / Verhagen, Rob / Studencka-Turski, Maja / Duffourd, Yannis / Moutton, Sébastien / Tran Mau-Them, Frédédic / Philippe, Christophe / Dean, John / Tennant, Stephen / Brooks, Alice S / van Slegtenhorst, Marjon A / Jurgens, Julie A / Barry, Brenda J / Chan, Wai-Man / England, Eleina M / Martinez Ojeda, Mayra /

Engle, Elizabeth C / Robson, Caroline D / Morrow, Michelle / Innes, A Micheil / Lamont, Ryan / Sanderson, Matthea / Krüger, Elke / Thauvin, Christel / Distel, Ben / Faivre, Laurence / Elgersma, Ype / Vitobello, Antonio

Genetics in medicine : official journal of the American College of Medical Genetics

2024 Volume 26, Issue 6, Page(s) 101119

Abstract: Purpose: Fem1 homolog B (FEM1B) acts as a substrate recognition subunit for ubiquitin ligase complexes belonging to the CULLIN 2-based E3 family. Several biological functions have been proposed for FEM1B, including a structurally resolved function as a ... ...

Abstract	Purpose: Fem1 homolog B (FEM1B) acts as a substrate recognition subunit for ubiquitin ligase complexes belonging to the CULLIN 2-based E3 family. Several biological functions have been proposed for FEM1B, including a structurally resolved function as a sensor for redox cell status by controlling mitochondrial activity, but its implication in human disease remains elusive. Methods: To understand the involvement of FEM1B in human disease, we made use of Matchmaker exchange platforms to identify individuals with de novo variants in FEM1B and performed their clinical evaluation. We performed functional validation using primary neuronal cultures and in utero electroporation assays, as well as experiments on patient's cells. Results: Five individuals with a recurrent de novo missense variant in FEM1B were identified: NM_015322.5:c.377G>A NP_056137.1:p.(Arg126Gln) (FEM1B Conclusion: Overall, our data indicate that p.(Arg126Gln) induces aberrant FEM1B activation, resulting in a gain-of-function mechanism associated with a severe syndromic developmental disorder in humans.
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1016/j.gim.2024.101119
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Article ; Online: Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs.

Kim, Byung-Eun / Turski, Michelle L / Nose, Yasuhiro / Casad, Michelle / Rockman, Howard A / Thiele, Dennis J

Cell metabolism

2010 Volume 11, Issue 5, Page(s) 353–363

Abstract: Copper (Cu) is an essential cofactor for a variety of metabolic functions, and the regulation of systemic Cu metabolism is critical to human health. Dietary Cu is absorbed through the intestine, stored in the liver, and mobilized into the circulation; ... ...

Abstract	Copper (Cu) is an essential cofactor for a variety of metabolic functions, and the regulation of systemic Cu metabolism is critical to human health. Dietary Cu is absorbed through the intestine, stored in the liver, and mobilized into the circulation; however, systemic Cu homeostasis is poorly understood. We generated mice with a cardiac-specific knockout of the Ctr1 Cu transporter (Ctr1(hrt/hrt)), resulting in cardiac Cu deficiency and severe cardiomyopathy. Unexpectedly, Ctr1(hrt/hrt) mice exhibited increased serum Cu levels and a concomitant decrease in hepatic Cu stores. Expression of the ATP7A Cu exporter, thought to function predominantly in intestinal Cu acquisition, was strongly increased in liver and intestine of Ctr1(hrt/hrt) mice. These studies identify ATP7A as a candidate for hepatic Cu mobilization in response to peripheral tissue demand, and illuminate a systemic regulation in which the Cu status of the heart is signaled to organs that take up and store Cu.
MeSH term(s)	Adenosine Triphosphatases/metabolism ; Animals ; Cardiomyopathy, Dilated/etiology ; Cation Transport Proteins/deficiency ; Cation Transport Proteins/genetics ; Cation Transport Proteins/metabolism ; Copper/deficiency ; Copper/metabolism ; Copper Transporter 1 ; Copper-Transporting ATPases ; Drosophila/metabolism ; Intestinal Mucosa/metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Myocardium/metabolism ; Signal Transduction
Chemical Substances	Atp7a protein, mouse ; Cation Transport Proteins ; Copper Transporter 1 ; Slc31a1 protein, mouse ; Copper (789U1901C5) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Copper-Transporting ATPases (EC 7.2.2.8)
Language	English
Publishing date	2010-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2010.04.003
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Article: A framework for genomic biomarker actionability and its use in clinical decision making.

Vidwans, Smruti J / Turski, Michelle L / Janku, Filip / Garrido-Laguna, Ignacio / Munoz, Javier / Schwab, Richard / Subbiah, Vivek / Rodon, Jordi / Kurzrock, Razelle

Oncoscience

2014 Volume 1, Issue 10, Page(s) 614–623

Abstract: The increasing scope and availability of genetic testing options for patients suffering from cancer has raised questions about how to use results of molecular diagnostics to inform patient care. For some biomarkers (e.g. BRAF mutations in melanoma), ... ...

Abstract	The increasing scope and availability of genetic testing options for patients suffering from cancer has raised questions about how to use results of molecular diagnostics to inform patient care. For some biomarkers (e.g. BRAF mutations in melanoma), standards exist that outline treatments for individuals harboring aberrations in the biomarker; however for the vast majority of genomic abnormalities, few guidelines exist. Clinical decision making and the therapeutic approach for a patient with a given cancer characterized by aberrations in different genes may be aided by the use of a biomarker actionability framework that provides levels of evidence regarding whether and how a molecular abnormality can be considered a therapeutically relevant biomarker. A gene may be considered theoretically actionable if it has a basis of actionability, such that clinically available drugs can target a gene product that drives the cancer or is differentially expressed in tumor versus normal elements. Herein, we discuss a possible framework for developing guidelines for actionability, as they relate to genomically-based cancer therapeutics.
Language	English
Publishing date	2014-10-22
Publishing country	United States
Document type	Journal Article
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.90
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Article: APOBEC Mutational Signature and Tumor Mutational Burden as Predictors of Clinical Outcomes and Treatment Response in Patients With Advanced Urothelial Cancer.

Natesan, Divya / Zhang, Li / Martell, Henry J / Jindal, Tanya / Devine, Patrick / Stohr, Bradley / Espinosa-Mendez, Carlos / Grenert, James / Van Ziffle, Jessica / Joseph, Nancy / Umetsu, Sarah / Onodera, Courtney / Turski, Michelle / Chan, Emily / Desai, Arpita / Aggarwal, Rahul / Wong, Anthony / Porten, Sima / Chou, Jonathan /

Friedlander, Terence / Fong, Lawrence / Small, Eric J / Sweet-Cordero, Alejandro / Koshkin, Vadim S

Frontiers in oncology

2022 Volume 12, Page(s) 816706

Abstract: Introduction: Tumor mutational burden (TMB) and APOBEC mutational signatures are potential prognostic markers in patients with advanced urothelial carcinoma (aUC). Their utility in predicting outcomes to specific therapies in aUC warrants additional ... ...

Abstract	Introduction: Tumor mutational burden (TMB) and APOBEC mutational signatures are potential prognostic markers in patients with advanced urothelial carcinoma (aUC). Their utility in predicting outcomes to specific therapies in aUC warrants additional study. Methods: We retrospectively reviewed consecutive UC cases assessed with UCSF500, an institutional assay that uses hybrid capture enrichment of target DNA to interrogate 479 common cancer genes. Hypermutated tumors (HM), defined as having TMB ≥10 mutations/Mb, were also assessed for APOBEC mutational signatures, while non-HM (NHM) tumors were not assessed due to low TMB. The logrank test was used to determine if there were differences in overall survival (OS) and progression-free survival (PFS) among patient groups of interest. Results: Among 75 aUC patients who had UCSF500 testing, 46 patients were evaluable for TMB, of which 19 patients (41%) had HM tumors and the rest had NHM tumors (27 patients). An additional 29 patients had unknown TMB status. Among 19 HM patients, all 16 patients who were evaluable for analysis had APOBEC signatures. HM patients (N=19) were compared with NHM patients (N=27) and had improved OS from diagnosis (125.3 months Conclusions: In a large, single-institution aUC cohort assessed with UCSF500, an institutional NGS panel, HM tumors were common and all such tumors that were evaluated for mutational signature analysis had APOBEC signatures. APOBEC signatures and high TMB were prognostic of improved OS from diagnosis and both analyses also predicted inferior outcomes with chemotherapy treatment.
Language	English
Publishing date	2022-03-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.816706
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