Search for druggable upregulated proteins in therapy-resistant AML cells
- Prosjektnummer
- 911979
- Ansvarlig person
- Stein Ove Døskeland
- Institusjon
- Helse Bergen HF
- Prosjektkategori
- Åpen prosjektstøtte
- Helsekategori
- Blood, Cancer, Cardiovascular
- Forskningsaktivitet
- 1. Underpinning, 5. Treatment Developement
The end-users are patients with AML. The project leader and many of the project participants have contact with cancer patients and their relatives, as well as others interested in cancer, in part through popular science lectures organised by DNK. The project participants have also close contact with Drs. Ø. Bruserud and BT Gjertsen, who treat AML patients on daily basis and receive their inputs. A subproject not commented in this report (due to space considerations) is to understand how hydroxy-urea and thio-guanine interact to kill AML cells, based on their beneficial effects in clinical studies, and the apparently high user-satisfaction (low grade of side effects, also in weak and elderly patients) reported by the patients undergoing such therapy (B.T. Gjertsen, pers. communic.)
Epac1 null mice have nephrogenic diabetes insipidus with deficient corticopapillary osmotic gradient and weaker collecting duct tight junctions.
Acta Physiol (Oxf) 2020 05;229(1):e13442. Epub 2020 feb 3
PMID: 31943825
Proteome and Phosphoproteome Changes Associated with Prognosis in Acute Myeloid Leukemia.
Cancers (Basel) 2020 Mar 17;12(3). Epub 2020 mar 17
PMID: 32192169
The Progression of Acute Myeloid Leukemia from First Diagnosis to Chemoresistant Relapse: A Comparison of Proteomic and Phosphoproteomic Profiles.
Cancers (Basel) 2020 Jun 04;12(6). Epub 2020 jun 4
PMID: 32512867
Epac1 Is Crucial for Maintenance of Endothelial Barrier Function through A Mechanism Partly Independent of Rac1.
Cells 2020 09 25;9(10). Epub 2020 sep 25
PMID: 32992982
A Kinase Inhibitor with Anti-Pim Kinase Activity is a Potent and Selective Cytotoxic Agent Toward Acute Myeloid Leukemia.
Mol Cancer Ther 2019 03;18(3):567-578. Epub 2019 jan 24
PMID: 30679386
Fusion pore regulation by cAMP/Epac2 controls cargo release during insulin exocytosis.
Elife 2019 05 20;8(). Epub 2019 mai 20
PMID: 31099751
Mice depleted for Exchange Proteins Directly Activated by cAMP (Epac) exhibit irregular liver regeneration in response to partial hepatectomy.
Sci Rep 2019 Sep 24;9(1):13789. Epub 2019 sep 24
PMID: 31551444
Epac1
Acta Physiol (Oxf) 2019 03;225(3):e13199. Epub 2018 nov 2
PMID: 30300965
Deletion of exchange proteins directly activated by cAMP (Epac) causes defects in hippocampal signaling in female mice.
PLoS One 2018;13(7):e0200935. Epub 2018 jul 26
PMID: 30048476
Mathematical Modelling of Nitric Oxide/Cyclic GMP/Cyclic AMP Signalling in Platelets.
Int J Mol Sci 2018 Feb 19;19(2). Epub 2018 feb 19
PMID: 29462984
Preservation Method and Phosphate Buffered Saline Washing Affect the Acute Myeloid Leukemia Proteome.
Int J Mol Sci 2018 Jan 19;19(1). Epub 2018 jan 19
PMID: 29351208
Enhancement of iodinin solubility by encapsulation into cyclodextrin nanoparticles.
J Enzyme Inhib Med Chem 2018 Dec;33(1):370-375.
PMID: 29336193
Epac1-deficient mice have bleeding phenotype and thrombocytes with decreased GPIbβ expression.
Sci Rep 2017 Aug 18;7(1):8725. Epub 2017 aug 18
PMID: 28821815
Total synthesis and antileukemic evaluations of the phenazine 5,10-dioxide natural products iodinin, myxin and their derivatives.
Bioorg Med Chem 2017 04 01;25(7):2285-2293. Epub 2017 feb 28
PMID: 28284865
Increased microvascular permeability in mice lacking Epac1 (Rapgef3).
Acta Physiol (Oxf) 2017 Feb;219(2):441-452. Epub 2016 mai 17
PMID: 27096875
Long-term consumption of an obesogenic high fat diet prior to ischemia-reperfusion mediates cardioprotection via Epac1-dependent signaling.
Nutr Metab (Lond) 2016;13():87. Epub 2016 nov 28
PMID: 27933093
Synthesis and activities of new indolopyrrolobenzodiazepine derivatives toward acute myeloid leukemia cells.
Bioorg Med Chem 2015 Nov 15;23(22):7313-23. Epub 2015 okt 24
PMID: 26526744
Cell Death Inducing Microbial Protein Phosphatase Inhibitors--Mechanisms of Action.
Mar Drugs 2015 Oct;13(10):6505-20. Epub 2015 okt 22
PMID: 26506362
B56d-related protein phosphatase 2A dysfunction identified in patients with intellectual disability.
J Clin Invest 2015 Aug 3;125(8):3051-62. Epub 2015 jul 13
PMID: 26168268
cAMP-Dependent Protein Kinase A (PKA)-Mediated c-Myc Degradation Is Dependent on the Relative Proportion of PKA-I and PKA-II Isozymes.
Mol Pharmacol 2015 Sep;88(3):469-76. Epub 2015 jun 23
PMID: 26104548
Assessing Cyclic Nucleotide Recognition in Cells: Opportunities and Pitfalls for selective Receptor activation
hapter 4. pp 61 - 80 in: In CRC series on Methods in Signal Transduction, Vol. title “Cyclic nucleotide signaling”. Editor: Xiaodong Cheng. CRC Press, Taylor & Francis, Boca Raton, London, New York. isbn = 1482235560, 2015
Exchange proteins directly activated by cAMP
- Disputert:
- september 2017
- Hovedveileder:
- Marit Bakke
Physiological roles of Epac: characterisation of gene knockout models
- Disputert:
- juni 2017
- Hovedveileder:
- Marit Bakke
Cell death induction by free and encapsulated cancer drug candidates
- Disputert:
- oktober 2015
- Hovedveileder:
- Stein Ove Døskeland
- Jens Waschke Leder av forskningsgruppe
- Marc Le Borgne Leder av forskningsgruppe
- Pål Rongved Prosjektdeltaker
- Rune Kleppe Prosjektdeltaker
- Haruna Muwonge Ph.d.-kandidat
- Marit Bakke Prosjektdeltaker
- Emmet Mc Cormack Prosjektdeltaker
- Lars Herfindal Leder av forskningsgruppe
- Ronja Bjørnstad Ph.d.-kandidat
- Emmet Martin Mc Cormack Leder av forskningsgruppe
- Kathrine Sivertsen åsrud Prosjektdeltaker
- Tuyen Thi Van Hoang Prosjektdeltaker
- Nina Lied Larsen Prosjektdeltaker
- Andrea Trentani Prosjektdeltaker
- Stein Ove Døskeland Prosjektleder
- Frode Selheim Prosjektdeltaker
- Elise Aasebø Prosjektdeltaker
- Bjørn Tore Gjertsen Prosjektdeltaker
- Øystein Bruserud Prosjektdeltaker
- Lene Elisabeth Myhren Ph.d.-kandidat
- Rolf K. Reed Leder av forskningsgruppe
eRapport er utarbeidet av Sølvi Lerfald og Reidar Thorstensen, Regionalt kompetansesenter for klinisk forskning, Helse Vest RHF, og videreutvikles av de fire RHF-ene i fellesskap, med støtte fra Helse Vest IKT
Alle henvendelser rettes til Faglig rapportering, Helse Vest