Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1

Karin Jöhrer; Katrin Janke; Jens Krugmann; Michael Fiegl; Richard Greil

doi:10.1158/1078-0432.CCR-1053-03

Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1

Karin Jöhrer, Katrin Janke, Jens Krugmann, Michael Fiegl, Richard Greil^* (Last author)

^*Corresponding author for this work

Department of Internal Medicine III - Division of Hematology, Medical Oncology, Hemostaseology, Rheumatology, Infectiology and Oncologic Center

Research output: Contribution to journal › Original Article › peer-review

69 Citations (Web of Science)

Original language	English
Pages (from-to)	1901-1910
Journal	CLINICAL CANCER RESEARCH
Volume	10
Issue number	6
DOIs	https://doi.org/10.1158/1078-0432.CCR-1053-03
Publication status	Published - 2004

Keywords

MARROW ENDOTHELIAL-CELLS
HUMAN BONE-MARROW
HUMAN MULTIPLE-MYELOMA
PLASMA-CELLS
FACTOR-ALPHA
EXPRESSION
BLOOD
CYTOKINES
SURVIVAL
ADHESION

Access to Document

10.1158/1078-0432.CCR-1053-03

Cite this

Jöhrer, K., Janke, K., Krugmann, J., Fiegl, M., & Greil, R. (2004). Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1. CLINICAL CANCER RESEARCH , 10(6), 1901-1910. https://doi.org/10.1158/1078-0432.CCR-1053-03

Jöhrer, Karin ; Janke, Katrin ; Krugmann, Jens et al. / Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1. In: CLINICAL CANCER RESEARCH 2004 ; Vol. 10, No. 6. pp. 1901-1910.

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keywords = "MARROW ENDOTHELIAL-CELLS, HUMAN BONE-MARROW, HUMAN MULTIPLE-MYELOMA, PLASMA-CELLS, FACTOR-ALPHA, EXPRESSION, BLOOD, CYTOKINES, SURVIVAL, ADHESION",

author = "Karin J{\"o}hrer and Katrin Janke and Jens Krugmann and Michael Fiegl and Richard Greil",

note = "Tyrolean Cancer Research Institute at the University of Innsbruck; Laboratory of Molecular Cytology, Department of Internal Medicine, Division of Hematology and Oncology, University Hospital Innsbruck; and Institute of Pathology, University of Innsbruck, Innsbruck, Austria",

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Jöhrer, K, Janke, K, Krugmann, J, Fiegl, M & Greil, R 2004, 'Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1', CLINICAL CANCER RESEARCH , vol. 10, no. 6, pp. 1901-1910. https://doi.org/10.1158/1078-0432.CCR-1053-03

Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1. / Jöhrer, Karin; Janke, Katrin; Krugmann, Jens et al.
In: CLINICAL CANCER RESEARCH , Vol. 10, No. 6, 2004, p. 1901-1910.

Research output: Contribution to journal › Original Article › peer-review

TY - JOUR

T1 - Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1

AU - Jöhrer, Karin

AU - Janke, Katrin

AU - Krugmann, Jens

AU - Fiegl, Michael

AU - Greil, Richard

N1 - Tyrolean Cancer Research Institute at the University of Innsbruck; Laboratory of Molecular Cytology, Department of Internal Medicine, Division of Hematology and Oncology, University Hospital Innsbruck; and Institute of Pathology, University of Innsbruck, Innsbruck, Austria

PY - 2004

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KW - MARROW ENDOTHELIAL-CELLS

KW - HUMAN BONE-MARROW

KW - HUMAN MULTIPLE-MYELOMA

KW - PLASMA-CELLS

KW - FACTOR-ALPHA

KW - EXPRESSION

KW - BLOOD

KW - CYTOKINES

KW - SURVIVAL

KW - ADHESION

U2 - 10.1158/1078-0432.CCR-1053-03

DO - 10.1158/1078-0432.CCR-1053-03

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C2 - 15041705

SN - 1078-0432

VL - 10

SP - 1901

EP - 1910

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Jöhrer K, Janke K, Krugmann J, Fiegl M, Greil R. Transendothelial migration of myeloma cells is increased by tumor necrosis factor (TNF)-alpha via TNF receptor 2 and autocrine up-regulation of MCP-1. CLINICAL CANCER RESEARCH . 2004;10(6):1901-1910. doi: 10.1158/1078-0432.CCR-1053-03