Hypoxia-induced p38 MAPK activation reduces Mcl-1 expression and facilitates sensitivity towards BH3 mimetics in chronic lymphocytic leukemia.
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
M F
MF
Huelsemann
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
M
M
Patz
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
L
L
Beckmann
1] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany [2] Institute for Medical Microbiology, Immunology and Hygiene, University Hospital of Cologne, Cologne, Germany.
K
K
Brinkmann
Institute of Physiology, University of Duisburg-Essen, Essen, Germany.
T
T
Otto
Institute of Physiology, University of Duisburg-Essen, Essen, Germany.
J
J
Fandrey
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany.
H J
HJ
Becker
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany.
S
S
Theurich
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany.
M
M
von Bergwelt-Baildon
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
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CP
Pallasch
Leibniz-Institute for Analytical Sciences-ISAS-e.V., Dortmund, Germany.
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RP
Zahedi
1] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany [2] Institute for Medical Microbiology, Immunology and Hygiene, University Hospital of Cologne, Cologne, Germany.
H
H
Kashkar
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
H C
HC
Reinhardt
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
M
M
Hallek
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany [4] Department I of Internal Medicine, Klinikum Schwabing, Munich, Germany.
C M
CM
Wendtner
1] Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany [2] Center of Integrated Oncology, University Hospital of Cologne, Cologne, Germany [3] Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne, Cologne, Germany.
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LP
Frenzel
D000970:Antineoplastic Agents / Q000494:pharmacology*; D001402:B-Lymphocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000069461:Bendamustine Hydrochloride; D001713:Biphenyl Compounds / Q000494:pharmacology*; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology*; D023201:CD40 Ligand / Q000235:genetics / Q000378:metabolism; D015687:Cell Hypoxia; D002478:Cells, Cultured; D019008:Drug Resistance, Neoplasm; D004789:Enzyme Activation; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D064549:Myeloid Cell Leukemia Sequence 1 Protein / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D009588:Nitrogen Mustard Compounds / Q000494:pharmacology; D009596:Nitrophenols / Q000494:pharmacology*; D010100:Oxygen / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013449:Sulfonamides / Q000494:pharmacology*; D014740:Vidarabine / Q000031:analogs & derivatives / Q000494:pharmacology; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics* / Q000378:metabolism
C501332:ABT-737; D000970:Antineoplastic Agents; C000595707:BCL2 protein, human; D001713:Biphenyl Compounds; D019086:Bridged Bicyclo Compounds, Heterocyclic; C579095:MCL1 protein, human; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D009588:Nitrogen Mustard Compounds; D009596:Nitrophenols; D010879:Piperazines; D019253:Proto-Oncogene Proteins c-bcl-2; D013449:Sulfonamides; D051020:bcl-X Protein; D023201:CD40 Ligand; D000069461:Bendamustine Hydrochloride; D048051:p38 Mitogen-Activated Protein Kinases; D014740:Vidarabine; C579720:venetoclax; C024352:fludarabine; D010100:Oxygen