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Article ; Online: Rapid and sustained improvements in itch and quality of life with upadacitinib plus topical corticosteroids in adults and adolescents with atopic dermatitis: 52-week outcomes from the phase 3 AD Up study.

Magnolo, Nina / Cameron, Michael C / Shahriari, Mona / Geng, Bob / Calimlim, Brian M / Teixeira, Henrique / Hu, Xiaofei / Yang, Yang / Liu, Yingyi / Zhang, Shiyu / Sancho Sanchez, Cristina / Altman, Katherine / Langley, Richard G

The Journal of dermatological treatment

2024 Volume 35, Issue 1, Page(s) 2344589

Abstract: Purpose:: Materials and methods:: Results:: Conclusions: ...

Abstract	Purpose: Materials and methods: Results: Conclusions:
MeSH term(s)	Humans ; Quality of Life ; Dermatitis, Atopic/drug therapy ; Pruritus/drug therapy ; Pruritus/etiology ; Female ; Male ; Adolescent ; Adult ; Heterocyclic Compounds, 3-Ring/administration & dosage ; Drug Therapy, Combination ; Treatment Outcome ; Patient Reported Outcome Measures ; Young Adult ; Middle Aged ; Severity of Illness Index ; Double-Blind Method ; Adrenal Cortex Hormones/administration & dosage ; Administration, Cutaneous
Chemical Substances	upadacitinib (4RA0KN46E0) ; Heterocyclic Compounds, 3-Ring ; Adrenal Cortex Hormones
Language	English
Publishing date	2024-05-02
Publishing country	England
Document type	Journal Article ; Clinical Trial, Phase III ; Randomized Controlled Trial ; Multicenter Study
ZDB-ID	1036299-x
ISSN	1471-1753 ; 0954-6634
ISSN (online)	1471-1753
ISSN	0954-6634
DOI	10.1080/09546634.2024.2344589
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Article ; Online: Interleukin-1β promotes skeletal colonization and progression of metastatic prostate cancer cells with neuroendocrine features.

Liu, Qingxin / Russell, Mike R / Shahriari, Kristina / Jernigan, Danielle L / Lioni, Mercedes I / Garcia, Fernando U / Fatatis, Alessandro

Cancer research

2013 Volume 73, Issue 11, Page(s) 3297–3305

Abstract: Despite the progress made in the early detection and treatment of prostate adenocarcinoma, the metastatic lesions from this tumor are incurable. We used genome-wide expression analysis of human prostate cancer cells with different metastatic behavior in ... ...

Abstract	Despite the progress made in the early detection and treatment of prostate adenocarcinoma, the metastatic lesions from this tumor are incurable. We used genome-wide expression analysis of human prostate cancer cells with different metastatic behavior in animal models to reveal that bone-tropic phenotypes upregulate three genes encoding for the cytokine interleukin-1β (IL-1β), the chemokine CXCL6 (GCP-2), and the protease inhibitor elafin (PI3). The Oncomine database revealed that these three genes are significantly upregulated in human prostate cancer versus normal tissue and correlate with Gleason scores ≥7. This correlation was further validated for IL-1β by immunodetection in prostate tissue arrays. Our study also shows that the exogenous overexpression of IL-1β in nonmetastatic cancer cells promotes their growth into large skeletal lesions in mice, whereas its knockdown significantly impairs the bone progression of highly metastatic cells. In addition, IL-1β secreted by metastatic cells induced the overexpression of COX-2 (PTGS2) in human bone mesenchymal cells treated with conditioned media from bone metastatic prostate cancer cells. Finally, we inspected human tissue specimens from skeletal metastases and detected prostate cancer cells positive for both IL-1β and synaptophysin while concurrently lacking prostate-specific antigen (PSA, KLK3) expression. Collectively, these findings indicate that IL-1β supports the skeletal colonization and metastatic progression of prostate cancer cells with an acquired neuroendocrine phenotype.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Animals ; Bone Neoplasms/genetics ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Carcinoma, Neuroendocrine/genetics ; Carcinoma, Neuroendocrine/metabolism ; Carcinoma, Neuroendocrine/pathology ; Cell Line, Tumor ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Heterografts ; Humans ; Immunocompromised Host ; Interleukin-1beta/biosynthesis ; Interleukin-1beta/genetics ; Male ; Mice ; NIH 3T3 Cells ; Neuroendocrine Cells/metabolism ; Neuroendocrine Cells/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Receptor, Platelet-Derived Growth Factor alpha/genetics ; Receptor, Platelet-Derived Growth Factor alpha/metabolism ; Synaptophysin/biosynthesis ; Up-Regulation
Chemical Substances	Interleukin-1beta ; SYP protein, human ; Synaptophysin ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1)
Language	English
Publishing date	2013-06-01
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-12-3970
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Article ; Online: Critical role of O-Linked β-N-acetylglucosamine transferase in prostate cancer invasion, angiogenesis, and metastasis.

Lynch, Thomas P / Ferrer, Christina M / Jackson, S RaElle / Shahriari, Kristina S / Vosseller, Keith / Reginato, Mauricio J

The Journal of biological chemistry

2012 Volume 287, Issue 14, Page(s) 11070–11081

Abstract: Cancer cells universally increase glucose and glutamine consumption, leading to the altered metabolic state known as the Warburg effect; one metabolic pathway, highly dependent on glucose and glutamine, is the hexosamine biosynthetic pathway. Increased ... ...

Abstract	Cancer cells universally increase glucose and glutamine consumption, leading to the altered metabolic state known as the Warburg effect; one metabolic pathway, highly dependent on glucose and glutamine, is the hexosamine biosynthetic pathway. Increased flux through the hexosamine biosynthetic pathway leads to increases in the post-translational addition of O-linked β-N-acetylglucosamine (O-GlcNAc) to various nuclear and cytosolic proteins. A number of these target proteins are implicated in cancer, and recently, O-GlcNAcylation was shown to play a role in breast cancer; however, O-GlcNAcylation in other cancers remains poorly defined. Here, we show that O-GlcNAc transferase (OGT) is overexpressed in prostate cancer compared with normal prostate epithelium and that OGT protein and O-GlcNAc levels are elevated in prostate carcinoma cell lines. Reducing O-GlcNAcylation in PC3-ML cells was associated with reduced expression of matrix metalloproteinase (MMP)-2, MMP-9, and VEGF, resulting in inhibition of invasion and angiogenesis. OGT-mediated regulation of invasion and angiogenesis was dependent upon regulation of the oncogenic transcription factor FoxM1, a key regulator of invasion and angiogenesis, as reducing OGT expression led to increased FoxM1 protein degradation. Conversely, overexpression of a degradation-resistant FoxM1 mutant abrogated OGT RNAi-mediated effects on invasion, MMP levels, angiogenesis, and VEGF expression. Using a mouse model of metastasis, we found that reduction of OGT expression blocked bone metastasis. Altogether, these data suggest that as prostate cancer cells alter glucose and glutamine levels, O-GlcNAc modifications and OGT levels become elevated and are required for regulation of malignant properties, implicating OGT as a novel therapeutic target in the treatment of cancer.
MeSH term(s)	Acetylglucosamine/metabolism ; Animals ; Bone Neoplasms/prevention & control ; Bone Neoplasms/secondary ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Forkhead Box Protein M1 ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation, Neoplastic ; Male ; Matrix Metalloproteinase 2/genetics ; Matrix Metalloproteinase 9/genetics ; Mice ; Mutation ; N-Acetylglucosaminyltransferases/deficiency ; N-Acetylglucosaminyltransferases/genetics ; N-Acetylglucosaminyltransferases/metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neovascularization, Pathologic/enzymology ; Prostatic Neoplasms/blood supply ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Proteolysis ; RNA Interference ; Vascular Endothelial Growth Factor A/genetics
Chemical Substances	FOXM1 protein, human ; Forkhead Box Protein M1 ; Forkhead Transcription Factors ; Vascular Endothelial Growth Factor A ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase (EC 2.4.1.150) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Acetylglucosamine (V956696549)
Language	English
Publishing date	2012-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M111.302547
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Article ; Online: Hypoxia suppression of Bim and Bmf blocks anoikis and luminal clearing during mammary morphogenesis.

Whelan, Kelly A / Caldwell, Sarah A / Shahriari, Kristina S / Jackson, S RaElle / Franchetti, Lisa D / Johannes, Gregg J / Reginato, Mauricio J

Molecular biology of the cell

2010 Volume 21, Issue 22, Page(s) 3829–3837

Abstract: Proper adhesion to extracellular matrix is critical for epithelial cell survival. Detachment from matrix signals results in apoptosis, referred to as anoikis. Selective apoptosis of cells that become detached from matrix is associated with the formation ... ...

Abstract	Proper adhesion to extracellular matrix is critical for epithelial cell survival. Detachment from matrix signals results in apoptosis, referred to as anoikis. Selective apoptosis of cells that become detached from matrix is associated with the formation of a lumen in three-dimensional mammary epithelial acinar structures in vitro. Because early breast cancer lesions such as carcinoma in situ, characterized by ducts exhibiting lumens filled with cells, are often associated with hypoxic markers, we sought to examine the role of hypoxia in anoikis and lumen formation in mammary epithelial cells. Here, we show that hypoxic conditions inhibit anoikis and block expression of proapoptotic BH3-only family members Bim and Bmf in epithelial cells. Hypoxia-mediated anoikis protection is associated with increased activation of the epidermal growth factor receptor-mitogen-activated protein kinase kinase-extracellular signal-regulated kinase (Erk) kinase pathway and requires the hypoxia-activated transcription factor. Consistent with these data, hypoxic conditions inhibit luminal clearing during morphogenesis in human mammary epithelial acini when grown in three-dimensional cultures and are associated with decreased expression of Bim and Bmf as well as Erk activation. We show that hypoxia regulates specific cell survival pathways that disrupt tissue architecture related to clearing of luminal space during mammary morphogenesis and suggest that hypoxia-mediated anoikis resistance may contribute to cancer progression.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Anoikis ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Bcl-2-Like Protein 11 ; Butadienes/pharmacology ; Cell Culture Techniques ; Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Immunoblotting ; MAP Kinase Kinase 1/antagonists & inhibitors ; MAP Kinase Kinase 1/metabolism ; Mammary Glands, Human/cytology ; Mammary Glands, Human/growth & development ; Mammary Glands, Human/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Mitogen-Activated Protein Kinases/metabolism ; Morphogenesis ; Nitriles/pharmacology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BCL2L11 protein, human ; BMF protein, human ; Bcl-2-Like Protein 11 ; Butadienes ; Enzyme Inhibitors ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Membrane Proteins ; Nitriles ; Proto-Oncogene Proteins ; U 0126 ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2)
Language	English
Publishing date	2010-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E10-04-0353
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Zs.A 2853: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: ErbB2 requires integrin alpha5 for anoikis resistance via Src regulation of receptor activity in human mammary epithelial cells.

Haenssen, Keneshia K / Caldwell, Sarah A / Shahriari, Kristina S / Jackson, S Raelle / Whelan, Kelly A / Klein-Szanto, Andres J / Reginato, Mauricio J

Journal of cell science

2010 Volume 123, Issue Pt 8, Page(s) 1373–1382

Abstract: ErbB2, a receptor tyrosine kinase highly expressed in many tumors, is known to inhibit apoptotic signals. Overexpression of ErbB2 causes anoikis resistance that contributes to luminal filling in three-dimensional mammary epithelial acinar structures in ... ...

Abstract	ErbB2, a receptor tyrosine kinase highly expressed in many tumors, is known to inhibit apoptotic signals. Overexpression of ErbB2 causes anoikis resistance that contributes to luminal filling in three-dimensional mammary epithelial acinar structures in vitro. Given that integrins and growth factor receptors are highly interdependent for function, we examined the role of integrin subunits in ErbB2-mediated survival signaling. Here, we show that MCF-10A cells overexpressing ErbB2 upregulate integrin alpha5 via the MAP-kinase pathway in three-dimensional acini and found elevated integrin alpha5 levels associated with ErbB2 status in human breast cancer. Integrin alpha5 is required for ErbB2-mediated anoikis resistance and for optimal ErbB2 signaling to the Mek-Erk-Bim axis as depletion of integrin alpha5 reverses anoikis resistance and Bim inhibition. Integrin alpha5 is required for full activation of ErbB2 tyrosine phosphorylation on Y877 and ErbB2 phosphorylation is associated with increased activity of Src in the absence of adhesion. Indeed, we show that blocking elevated Src activity during cell detachment reverses ErbB2-mediated survival and Bim repression. Thus, integrin alpha5 serves as a key mediator of Src and ErbB2-survival signaling in low adhesion states, which are necessary to block the pro-anoikis mediator Bim, and we suggest that this pathway represents a potential novel therapeutic target in ErbB2-positive tumors.
MeSH term(s)	Anoikis ; Apoptosis Regulatory Proteins/metabolism ; Bcl-2-Like Protein 11 ; Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Adhesion ; Cell Survival ; Enzyme Activation ; Epithelial Cells/enzymology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Integrin alpha5/genetics ; Integrin alpha5/metabolism ; MAP Kinase Signaling System ; Mammary Glands, Human/cytology ; Mammary Glands, Human/growth & development ; Membrane Proteins/metabolism ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Morphogenesis ; Proto-Oncogene Proteins/metabolism ; Receptor, ErbB-2/metabolism ; Up-Regulation/genetics ; src-Family Kinases/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; BCL2L11 protein, human ; Bcl-2-Like Protein 11 ; Integrin alpha5 ; Membrane Proteins ; Proto-Oncogene Proteins ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; src-Family Kinases (EC 2.7.10.2) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2010-03-23
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.050906
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Zs.A 1200: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: ErbB2 requires integrin α5 for anoikis resistance via Src regulation of receptor activity in human mammary epithelial cells

Haenssen, Keneshia K / Caldwell, Sarah A / Shahriari, Kristina S / Jackson, S. RaElle / Whelan, Kelly A / Klein-Szanto, Andres J / Reginato, Mauricio J

Journal of cell science. 2010 Apr. 15, v. 123, no. 8

2010

Abstract	ErbB2, a receptor tyrosine kinase highly expressed in many tumors, is known to inhibit apoptotic signals. Overexpression of ErbB2 causes anoikis resistance that contributes to luminal filling in three-dimensional mammary epithelial acinar structures in vitro. Given that integrins and growth factor receptors are highly interdependent for function, we examined the role of integrin subunits in ErbB2-mediated survival signaling. Here, we show that MCF-10A cells overexpressing ErbB2 upregulate integrin α5 via the MAP-kinase pathway in three-dimensional acini and found elevated integrin α5 levels associated with ErbB2 status in human breast cancer. Integrin α5 is required for ErbB2-mediated anoikis resistance and for optimal ErbB2 signaling to the Mek-Erk-Bim axis as depletion of integrin α5 reverses anoikis resistance and Bim inhibition. Integrin α5 is required for full activation of ErbB2 tyrosine phosphorylation on Y877 and ErbB2 phosphorylation is associated with increased activity of Src in the absence of adhesion. Indeed, we show that blocking elevated Src activity during cell detachment reverses ErbB2-mediated survival and Bim repression. Thus, integrin α5 serves as a key mediator of Src and ErbB2-survival signaling in low adhesion states, which are necessary to block the pro-anoikis mediator Bim, and we suggest that this pathway represents a potential novel therapeutic target in ErbB2-positive tumors.
Language	English
Dates of publication	2010-0415
Size	p. 1373-1382.
Publishing place	The Company of Biologists Limited
Document type	Article
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
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Article: The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor.

Schlisio, Susanne / Kenchappa, Rajappa S / Vredeveld, Liesbeth C W / George, Rani E / Stewart, Rodney / Greulich, Heidi / Shahriari, Kristina / Nguyen, Nguyen V / Pigny, Pascal / Dahia, Patricia L / Pomeroy, Scott L / Maris, John M / Look, A Thomas / Meyerson, Matthew / Peeper, Daniel S / Carter, Bruce D / Kaelin, William G

Genes & development

2008 Volume 22, Issue 7, Page(s) 884–893

Abstract: VHL, NF-1, c-Ret, and Succinate Dehydrogenase Subunits B and D act on a developmental apoptotic pathway that is activated when nerve growth factor (NGF) becomes limiting for neuronal progenitor cells and requires the EglN3 prolyl hydroxylase as a ... ...

Abstract	VHL, NF-1, c-Ret, and Succinate Dehydrogenase Subunits B and D act on a developmental apoptotic pathway that is activated when nerve growth factor (NGF) becomes limiting for neuronal progenitor cells and requires the EglN3 prolyl hydroxylase as a downstream effector. Germline mutations of these genes cause familial pheochromocytoma and other neural crest-derived tumors. Using an unbiased shRNA screen we found that the kinesin KIF1Bbeta acts downstream from EglN3 and is both necessary and sufficient for neuronal apoptosis when NGF becomes limiting. KIF1Bbeta maps to chromosome 1p36.2, which is frequently deleted in neural crest-derived tumors including neuroblastomas. We identified inherited loss-of-function KIF1Bbeta missense mutations in neuroblastomas and pheochromocytomas and an acquired loss-of-function mutation in a medulloblastoma, arguing that KIF1Bbeta is a pathogenic target of these deletions.
MeSH term(s)	Animals ; Animals, Newborn ; Apoptosis ; Cells, Cultured ; Child ; Chromosome Mapping ; Chromosomes, Mammalian/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor-Proline Dioxygenases ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Immunoblotting ; Kinesin/genetics ; Kinesin/metabolism ; Medulloblastoma/genetics ; Medulloblastoma/pathology ; Mice ; Mice, Knockout ; Models, Biological ; Mutation, Missense ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neuroblastoma/genetics ; Neuroblastoma/pathology ; Neurons/cytology ; Neurons/metabolism ; PC12 Cells ; Pheochromocytoma/genetics ; Pheochromocytoma/pathology ; Procollagen-Proline Dioxygenase ; RNA Interference ; Rats ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Immediate-Early Proteins ; Kif1b protein, mouse ; Nerve Tissue Proteins ; Tumor Suppressor Proteins ; Procollagen-Proline Dioxygenase (EC 1.14.11.2) ; Egln1 protein, mouse (EC 1.14.11.29) ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2008-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.1648608
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Article ; Online: 5th International Symposium on Focused Ultrasound

Menashe Zaaroor / Alon Sinai / Dorit Goldsher / Ayelet Eran / Maria Nassar / Ilana Schlesinger / Jonathon Parker / Vinod Ravikumar / Pejman Ghanouni / Sherman Stein / Casey Halpern / Vibhor Krishna / Amelia Hargrove / Punit Agrawal / Barbara Changizi / Eric Bourekas / Michael Knopp / Ali Rezai / Brian Mead /

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Journal of Therapeutic Ultrasound, Vol 4, Iss S1, Pp 1-

2016 Volume 113

Keywords	Medical physics. Medical radiology. Nuclear medicine ; R895-920
Language	English
Publishing date	2016-11-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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