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Article: Be mindful of potential pitfalls when using the Cre-LoxP system in cancer research.

Czarnota, Piotr / Cisowski, Jaroslaw

Oncoscience

2023 Volume 10, Page(s) 67–68

Language	English
Publishing date	2023-11-14
Publishing country	United States
Document type	Editorial
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.591
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Article: Correction: Current view of liver cancer cell-of-origin and proposed mechanisms precluding its proper determination.

Gromowski, Tomasz / Lukacs-Kornek, Veronika / Cisowski, Jaroslaw

Cancer cell international

2023 Volume 23, Issue 1, Page(s) 31

Language	English
Publishing date	2023-02-21
Publishing country	England
Document type	Published Erratum
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-023-02875-0
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Article: Current view of liver cancer cell-of-origin and proposed mechanisms precluding its proper determination.

Gromowski, Tomasz / Lukacs-Kornek, Veronika / Cisowski, Jaroslaw

Cancer cell international

2023 Volume 23, Issue 1, Page(s) 3

Abstract: Hepatocellular carcinoma and intrahepatic cholangiocarcinoma are devastating primary liver cancers with increasing prevalence in many parts of the world. Despite intense investigation, many aspects of their biology are still largely obscure. For example, ...

Abstract	Hepatocellular carcinoma and intrahepatic cholangiocarcinoma are devastating primary liver cancers with increasing prevalence in many parts of the world. Despite intense investigation, many aspects of their biology are still largely obscure. For example, numerous studies have tackled the question of the cell-of-origin of primary liver cancers using different experimental approaches; they have not, however, provided a clear and undisputed answer. Here, we will review the evidence from animal models supporting the role of all major types of liver epithelial cells: hepatocytes, cholangiocytes, and their common progenitor as liver cancer cell-of-origin. Moreover, we will also propose mechanisms that promote liver cancer cell plasticity (dedifferentiation, transdifferentiation, and epithelial-to-mesenchymal transition) which may contribute to misinterpretation of the results and which make the issue of liver cancer cell-of-origin particularly complex.
Language	English
Publishing date	2023-01-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-022-02843-0
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Article ; Online: What makes oncogenes mutually exclusive?

Cisowski, Jaroslaw / Bergo, Martin O

Small GTPases

2017 Volume 8, Issue 3, Page(s) 187–192

Abstract: Cancer is driven by mutations in genes whose products participate in major signaling pathways that fuel cell proliferation and survival. It is easy to assume that the more of these so-called driver mutations a tumor accumulates, the faster it progresses. ...

Abstract	Cancer is driven by mutations in genes whose products participate in major signaling pathways that fuel cell proliferation and survival. It is easy to assume that the more of these so-called driver mutations a tumor accumulates, the faster it progresses. However, this does not appear to be the case: Data from large-scale genome sequencing studies indicate that mutations in driver oncogenes often are mutually exclusive. The mechanisms underlying the mutual exclusivity of oncogenes are not completely understood, but recent reports suggest that the mechanisms may depend on the tumor type, and the nature of interacting oncogenes. Here we discuss our recent findings that the oncogenes KRAS
MeSH term(s)	Animals ; Cell Death/genetics ; Cellular Senescence/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes/genetics
Language	English
Publishing date	2017--03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2682247-7
ISSN	2154-1256 ; 2154-1248
ISSN (online)	2154-1256
ISSN	2154-1248
DOI	10.1080/21541248.2016.1212689
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Article ; Online: Percutaneous treatment of right heart endocarditis.

Sacha, Jerzy / Lipski, Przemysław / Bugajski, Jarosław / Marszalski, Maciej / Gwóźdź, Witold / Płonka, Joanna / Tomaszewski, Paweł / Cisowski, Marek / Gierlotka, Marek

Kardiologia polska

2023 Volume 81, Issue 10, Page(s) 1028–1029

MeSH term(s)	Humans ; Endocarditis/diagnostic imaging ; Endocarditis/surgery ; Endocarditis, Bacterial/diagnostic imaging ; Endocarditis, Bacterial/drug therapy ; Endocarditis, Bacterial/surgery ; Heart ; Treatment Outcome
Language	English
Publishing date	2023-08-04
Publishing country	Poland
Document type	Journal Article
ZDB-ID	411492-9
ISSN	1897-4279 ; 0022-9032
ISSN (online)	1897-4279
ISSN	0022-9032
DOI	10.33963/KP.a2023.0176
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Article ; Online: Knockout of the RAS endoprotease RCE1 accelerates myeloid leukemia by downregulating GADD45b.

Karlsson, Christin / Akula, Murali K / Staffas, Anna / Cisowski, Jaroslaw / Sayin, Volkan I / Ibrahim, Mohamed X / Lindahl, Per / Bergo, Martin O

Leukemia

2020 Volume 35, Issue 2, Page(s) 606–609

MeSH term(s)	Animals ; Antigens, Differentiation/chemistry ; Antigens, Differentiation/genetics ; Antigens, Differentiation/metabolism ; Down-Regulation ; Endopeptidases/physiology ; Leukemia, Myeloid/etiology ; Leukemia, Myeloid/metabolism ; Leukemia, Myeloid/pathology ; Mice ; Mice, Knockout
Chemical Substances	Antigens, Differentiation ; Gadd45b protein, mouse ; Endopeptidases (EC 3.4.-) ; Rce1 protein, mouse (EC 3.4.22)
Language	English
Publishing date	2020-05-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-020-0859-0
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Article ; Online: Overexpression of biliverdin reductase enhances resistance to chemotherapeutics.

Florczyk, Urszula / Golda, Slawomir / Zieba, Agata / Cisowski, Jaroslaw / Jozkowicz, Alicja / Dulak, Jozef

Cancer letters

2011 Volume 300, Issue 1, Page(s) 40–47

Abstract: Biliverdin reductase (BVR) converts biliverdin to bilirubin. Additionally, acting as a transcription factor and possessing a capacity of a serine/threonine kinase, it may modulate signaling pathways. In order to gain better understanding of BVR functions, ...

Abstract	Biliverdin reductase (BVR) converts biliverdin to bilirubin. Additionally, acting as a transcription factor and possessing a capacity of a serine/threonine kinase, it may modulate signaling pathways. In order to gain better understanding of BVR functions, we used genetically modified line of mouse fibroblasts with reversible overexpression of BVR. Current study revealed that enhanced activity of BVR may protect cells in stressful conditions arising from anti-cancer drugs, cisplatin and doxorubicin, the effect most probably related to PKC α/β activity, as its inhibition reversed BVR action. Therefore activity of BVR may be of significance in tumors and may influence the effectiveness of therapies.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Cisplatin/pharmacology ; Dose-Response Relationship, Drug ; Doxycycline/pharmacology ; Drug Resistance, Neoplasm ; Heme Oxygenase-1/genetics ; Membrane Proteins/genetics ; Mice ; NIH 3T3 Cells ; Oxidoreductases Acting on CH-CH Group Donors/physiology ; Protein Kinase C/physiology
Chemical Substances	Antineoplastic Agents ; Membrane Proteins ; Heme Oxygenase-1 (EC 1.14.14.18) ; Hmox1 protein, mouse (EC 1.14.14.18) ; Oxidoreductases Acting on CH-CH Group Donors (EC 1.3.-) ; biliverdin reductase (EC 1.3.1.24) ; Protein Kinase C (EC 2.7.11.13) ; Doxycycline (N12000U13O) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2011-01-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2010.09.003
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Article: Overexpression of biliverdin reductase enhances resistance to chemotherapeutics

Florczyk, Urszula / Golda, Slawomir / Zieba, Agata / Cisowski, Jaroslaw / Jozkowicz, Alicja / Dulak, Jozef

Cancer letters. 2011 Jan. 1, v. 300, no. 1

2011

Abstract	Biliverdin reductase (BVR) converts biliverdin to bilirubin. Additionally, acting as a transcription factor and possessing a capacity of a serine/threonine kinase, it may modulate signaling pathways. In order to gain better understanding of BVR functions, we used genetically modified line of mouse fibroblasts with reversible overexpression of BVR. Current study revealed that enhanced activity of BVR may protect cells in stressful conditions arising from anti-cancer drugs, cisplatin and doxorubicin, the effect most probably related to PKC α/β activity, as its inhibition reversed BVR action. Therefore activity of BVR may be of significance in tumors and may influence the effectiveness of therapies.
Keywords	bilirubin ; cisplatin ; doxorubicin ; fibroblasts ; mice ; neoplasms ; serine ; signal transduction ; threonine ; transcription factors
Language	English
Dates of publication	2011-0101
Size	p. 40-47.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2010.09.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Heme oxygenase-1 and the vascular bed: from molecular mechanisms to therapeutic opportunities.

Loboda, Agnieszka / Jazwa, Agnieszka / Grochot-Przeczek, Anna / Rutkowski, Andrzej J / Cisowski, Jaroslaw / Agarwal, Anupam / Jozkowicz, Alicja / Dulak, Jozef

Antioxidants & redox signaling

2008 Volume 10, Issue 10, Page(s) 1767–1812

Abstract: Heme oxygenase-1, an enzyme degrading heme to carbon monoxide, iron, and biliverdin, has been recognized as playing a crucial role in cellular defense against stressful conditions, not only related to heme release. HO-1 protects endothelial cells from ... ...

Abstract	Heme oxygenase-1, an enzyme degrading heme to carbon monoxide, iron, and biliverdin, has been recognized as playing a crucial role in cellular defense against stressful conditions, not only related to heme release. HO-1 protects endothelial cells from apoptosis, is involved in blood-vessel relaxation regulating vascular tone, attenuates inflammatory response in the vessel wall, and participates in blood-vessel formation by means of angiogenesis and vasculogenesis. The latter functions link HO-1 not only to cardiovascular ischemia but also to many other conditions that, like development, wound healing, or cancer, are dependent on neovascularization. The aim of this comprehensive review is to address the mechanisms of HO-1 regulation and function in cardiovascular physiology and pathology and to demonstrate some possible applications of the vast knowledge generated so far. Recent data provide powerful evidence for the involvement of HO-1 in the therapeutic effect of drugs used in cardiovascular diseases. Novel studies open the possibilities of application of HO-1 for gene and cell therapy. Therefore, research in forthcoming years should help to elucidate both the real role of HO-1 in the effect of drugs and the clinical feasibility of HO-1-based cell and gene therapy, creating the effective therapeutic avenues for this refined antioxidant system.
MeSH term(s)	Animals ; Apoptosis ; Biliverdine/metabolism ; Carbon Monoxide/metabolism ; Carbon Monoxide/pharmacology ; Carbon Monoxide/toxicity ; Cardiovascular Agents/pharmacology ; Cardiovascular Agents/therapeutic use ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/enzymology ; Cardiovascular Diseases/therapy ; Child ; Diabetes Complications/enzymology ; Diabetes Complications/prevention & control ; Diabetes Complications/therapy ; Endothelium, Vascular/enzymology ; Enzyme Induction/drug effects ; Enzyme Induction/radiation effects ; Female ; Genetic Therapy ; Heme/metabolism ; Heme Oxygenase-1/chemistry ; Heme Oxygenase-1/deficiency ; Heme Oxygenase-1/genetics ; Heme Oxygenase-1/physiology ; Humans ; Inflammation/enzymology ; Inflammation/therapy ; Iron/metabolism ; Male ; Mice ; Mice, Knockout ; Neovascularization, Physiologic ; Rabbits ; Rats ; Vasomotor System/drug effects
Chemical Substances	Cardiovascular Agents ; Heme (42VZT0U6YR) ; Carbon Monoxide (7U1EE4V452) ; Iron (E1UOL152H7) ; Heme Oxygenase-1 (EC 1.14.14.18) ; Biliverdine (O9MIA842K9)
Language	English
Publishing date	2008-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2008.2043
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Article ; Online: 15d-PGJ2 upregulates synthesis of IL-8 in endothelial cells through induction of oxidative stress.

Jozkowicz, Alicja / Was, Halina / Taha, Hevidar / Kotlinowski, Jerzy / Mleczko, Katarzyna / Cisowski, Jaroslaw / Weigel, Guenter / Dulak, Jozef

Antioxidants & redox signaling

2008 Volume 10, Issue 12, Page(s) 2035–2046

Abstract: 15-Deoxy-Delta(12,14)-prostaglandin-J(2) (15d-PGJ(2)) is a cyclopentenone prostaglandin regarded as antiinflammatory mediator, which can act through peroxisome proliferator-activated receptor-gamma (PPARgamma) or through G protein-coupled surface ... ...

Abstract	15-Deoxy-Delta(12,14)-prostaglandin-J(2) (15d-PGJ(2)) is a cyclopentenone prostaglandin regarded as antiinflammatory mediator, which can act through peroxisome proliferator-activated receptor-gamma (PPARgamma) or through G protein-coupled surface receptors. It has been demonstrated that 15d-PGJ(2) potently increases the generation of interleukin-8 (IL-8) in human microvascular endothelial cells (HMEC-1s); however, the mechanism of this induction is not known. The aim of the study was to find the pathway involved in 15d-PGJ(2)-mediated IL-8 stimulation. Our data confirmed that the effect of 15d-PGJ(2) is independent of PPARgamma. For the first time, we excluded the activation of G proteins and the contribution of G protein-coupled surface receptors in endothelial cells treated with 15d-PGJ(2). Instead, we demonstrated that stimulation of IL-8 involved induction of oxidative stress, activation of p38 kinases, and increase in stability of IL-8 mRNA. Upregulation of IL-8 promoter, although measurable, seemed to play a less-pronounced role. Additionally, our results indicate the involvement of cAMP elevation and may suggest a role for ATF2 transcription factor. Concomitant induction of heme oxygenase-1 in HMEC-1s did not influence the synthesis of IL-8. In summary, we showed that 15d-PGJ(2), acting through oxidative stress, may exert proinflammatory effects. The upregulation of IL-8 is mostly associated with p38-mediated stabilization of mRNA.
MeSH term(s)	Acetylcysteine/pharmacology ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/antagonists & inhibitors ; Cyclic AMP/metabolism ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Enzyme-Linked Immunosorbent Assay ; Ethacrynic Acid/pharmacology ; Ethylmaleimide/analogs & derivatives ; Ethylmaleimide/pharmacology ; Gene Expression/drug effects ; Hemin/pharmacology ; Humans ; Hydantoins/pharmacology ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Oxidative Stress/drug effects ; Prostaglandin D2/analogs & derivatives ; Prostaglandin D2/pharmacology ; Protein Kinase Inhibitors/pharmacology ; RNA Stability/drug effects ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reactive Oxygen Species/metabolism ; Receptors, Prostaglandin/agonists ; Receptors, Prostaglandin/antagonists & inhibitors ; Reverse Transcriptase Polymerase Chain Reaction ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Transfection ; Xanthones/pharmacology ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	15-deoxyprostaglandin J2 ; Hydantoins ; Interleukin-8 ; Protein Kinase Inhibitors ; RNA, Messenger ; Reactive Oxygen Species ; Receptors, Prostaglandin ; Xanthones ; prostanoid D receptor 1, human ; Colforsin (1F7A44V6OU) ; 6-isopropoxy-9-oxoxanthene-2-carboxylic acid (33458-93-4) ; Hemin (743LRP9S7N) ; BW 245C (75693-75-3) ; Cyclic AMP (E0399OZS9N) ; Superoxide Dismutase (EC 1.15.1.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Ethacrynic Acid (M5DP350VZV) ; Ethylmaleimide (O3C74ACM9V) ; Prostaglandin D2 (RXY07S6CZ2) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2008-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2008.2032
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