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Article ; Online: Targeting endogenous fatty acid synthesis stimulates the migration of ovarian cancer cells to adipocytes and promotes the transport of fatty acids from adipocytes to cancer cells.

Grunt, Thomas W / Wagner, Renate / Ries, Alexander / Berghoff, Anna S / Preusser, Matthias / Grusch, Michael / Valent, Peter

International journal of oncology

2024 Volume 64, Issue 3

Abstract: Despite significant advances in oncology, 1 of 108 female patients succumb to ovarian cancer (OC) each year. Improved novel treatments against this aggressive disease would be a major improvement. The growth of OC cells has been demonstrated to be highly ...

Abstract	Despite significant advances in oncology, 1 of 108 female patients succumb to ovarian cancer (OC) each year. Improved novel treatments against this aggressive disease would be a major improvement. The growth of OC cells has been demonstrated to be highly dependent on lipids. OC cells are abundantly present in the abdominal cavity and omentum, the main sites of OC expansion. Accordingly, it has been attempted not only to block the hyperactive synthesis of fatty acids (FAs) in cancer cells, but also to disrupt lipid supply. While either strategy has yielded promising results as monotherapy, the induction of resistance pathways diminishing the anticancer effects is yet conceivable. The endogenous regulation of lipid biosynthesis in OC has been extensively studied. However, the role of stromal cells in the modulation of the effects of anti‑lipogenic drugs has not yet been well documented. The present study thus examined the interaction between OC cells and associated stromal cells, when
MeSH term(s)	Humans ; Female ; Fatty Acids/metabolism ; Ovarian Neoplasms/pathology ; Cell Line, Tumor ; Adipocytes/metabolism ; Adipocytes/pathology ; Lipogenesis
Chemical Substances	Fatty Acids
Language	English
Publishing date	2024-01-12
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2024.5612
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Zs.A 3690: Show issues

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Article ; Online: Impact of mobile phone-specific electromagnetic fields on DNA damage caused by occupationally relevant exposures: results of ex vivo experiments with peripheral blood mononuclear cells from different demographic groups.

Mišík, Miroslav / Kundi, Michael / Worel, Nadine / Ferk, Franziska / Hutter, Hans-Peter / Grusch, Michael / Nersesyan, Armen / Herrera Morales, Denise / Knasmueller, Siegfried

Mutagenesis

2023 Volume 38, Issue 4, Page(s) 227–237

Abstract: The aim of this study was to investigate if age and body mass of humans have an impact on the DNA-damaging properties of high-frequency mobile phone-specific electromagnetic fields (HF-EMF, 1950 MHz, universal mobile telecommunications system, UMTS ... ...

Abstract	The aim of this study was to investigate if age and body mass of humans have an impact on the DNA-damaging properties of high-frequency mobile phone-specific electromagnetic fields (HF-EMF, 1950 MHz, universal mobile telecommunications system, UMTS signal) and if this form of radiation has an impact on the genotoxic effects of occupationally relevant exposures. Pooled peripheral blood mononuclear cells (PBMC) from three groups [young normal weight, young obese (YO), and older age normal weight individuals] were exposed to different doses of HF-EMF (0.25, 0.5, and 1.0 W/kg specific absorption rate-SAR) and simultaneously or sequentially to different chemicals which cause DNA damage (CrO3, NiCl2, benzo[a]pyrene diol epoxide-BPDE, and 4-nitroquinoline 1-oxide-4NQO) via different molecular mechanisms. We found no difference in regard to the background values in the three groups but a significant increase of DNA damage (81% without and 36% with serum) in cells from old participants after radiation with 1.0 W/kg SAR 16 h. In combined treatment experiments we found no impact of the UMTS signal on chemically induced DNA damage in the different groups in general. However, a moderate decrease of DNA damage was seen in simultaneous treatment experiments with BPDE and 1.0 W/kg SAR in the YO group (decline 18%). Taken together our findings indicate that HF-EMF cause DNA damage in PBMC from older subjects (69.1 years). Furthermore, they show that the radiation does not increase induction of DNA damage by occupationally relevant chemicals.
MeSH term(s)	Humans ; Electromagnetic Fields/adverse effects ; Leukocytes, Mononuclear ; 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide ; DNA Damage ; Cell Phone ; Demography
Chemical Substances	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide (55097-80-8)
Language	English
Publishing date	2023-07-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632903-2
ISSN	1464-3804 ; 0267-8357
ISSN (online)	1464-3804
ISSN	0267-8357
DOI	10.1093/mutage/gead022
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Zs.A 2189: Show issues

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Article ; Online: Effective targeting of breast cancer by the inhibition of P-glycoprotein mediated removal of toxic lipid peroxidation byproducts from drug tolerant persister cells.

Szebényi, Kornélia / Füredi, András / Bajtai, Eszter / Sama, Sai Nagender / Csiszar, Agnes / Gombos, Balázs / Szabó, Pál / Grusch, Michael / Szakács, Gergely

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

2023 Volume 71, Page(s) 101007

Abstract: Therapy resistance has long been considered to occur through the selection of pre-existing clones equipped to survive and quickly regrow, or through the acquisition of mutations during chemotherapy. Here we show that following in vitro treatment by ... ...

Abstract	Therapy resistance has long been considered to occur through the selection of pre-existing clones equipped to survive and quickly regrow, or through the acquisition of mutations during chemotherapy. Here we show that following in vitro treatment by chemotherapy, epithelial breast cancer cells adopt a transient drug tolerant phenotype characterized by cell cycle arrest, epithelial-to-mesenchymal transition (EMT) and the reversible upregulation of the multidrug resistance (MDR) efflux transporter P-glycoprotein (P-gp). The drug tolerant persister (DTP) state is reversible, as cells eventually resume proliferation, giving rise to a cell population resembling the initial, drug-naïve cell lines. However, recovery after doxorubicin treatment is almost completely eliminated when DTP cells are cultured in the presence of the P-gp inhibitor Tariquidar. Mechanistically, P-gp contributes to the survival of DTP cells by removing reactive oxygen species-induced lipid peroxidation products resulting from doxorubicin exposure. In vivo, prolonged administration of Tariquidar during doxorubicin treatment holidays resulted in a significant increase of the overall survival of Brca1
MeSH term(s)	Humans ; Animals ; Mice ; Female ; ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics ; Lipid Peroxidation ; Pharmaceutical Preparations ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; ATP Binding Cassette Transporter, Subfamily B/genetics ; Doxorubicin/pharmacology
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Pharmaceutical Preparations ; ATP Binding Cassette Transporter, Subfamily B ; Doxorubicin (80168379AG)
Language	English
Publishing date	2023-09-17
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1016/j.drup.2023.101007
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Zs.A 5099: Show issues

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Article ; Online: Impact of fibrinogen levels and modified Glasgow prognostic score on survival of stage III/N2 non-small cell lung cancer patients treated with neoadjuvant therapy and radical resection.

Sinn, Katharina / Mosleh, Berta / Grusch, Michael / Klepetko, Walter / Hoetzenecker, Konrad / Klikovits, Thomas / Gompelmann, Daniela / Hoda, Mir Alireza

BMC cancer

2022 Volume 22, Issue 1, Page(s) 1197

Abstract: Purpose: The prognostic value of pretreatment and preoperative fibrinogen plasma levels and the modified Glasgow prognostic score (mGPS) in stage III/N2 non-small cell lung cancer (NSCLC) patients who receive neoadjuvant treatment followed by radical ... ...

Abstract	Purpose: The prognostic value of pretreatment and preoperative fibrinogen plasma levels and the modified Glasgow prognostic score (mGPS) in stage III/N2 non-small cell lung cancer (NSCLC) patients who receive neoadjuvant treatment followed by radical surgery is yet unclear. Methods: Fibrinogen levels and mGPS of 84 patients with initial stage III/N2 NSCLC, who received neoadjuvant therapy followed by complete surgical resection from 2002 to 2014 were retrospectively analyzed and correlated with clinical parameters and overall survival (OS). Data were analyzed using log-rank and Cox regression analysis adjusted for clinical and pathological factors. Results: Median serum fibrinogen level after neoadjuvant treatment was 439 mg/dL (IQR 158 mg/dL). Elevated fibrinogen levels (> 400 mg/dL) after neoadjuvant treatment were significantly associated with poorer OS (28.2 months vs. 60.9 months, HR 0.562, p = 0.048). Importantly, a decrease in fibrinogen levels after neoadjuvant treatment (n = 34) was found to be an independent predictor for favorable OS in multivariate analysis (HR 0.994, p = 0.025). Out of 80 patients, 55, 19 and 6 patients had a mGPS of 0, 1 and 2, respectively. Moreover, elevated mGPS after neoadjuvant treatment (mGPS 1-2) showed a non-significant trend for poorer OS compared to mGPS 0 (28.2 vs. 46.5 months, HR 0.587, p = 0.066). Conclusion: Elevated fibrinogen levels after neoadjuvant therapy prior to surgery in stage III/N2 NSCLC patients are associated with significant disadvantage for OS. A decrease in fibrinogen levels after neoadjuvant therapy was found to be a predictor for superior OS in this retrospective patient cohort.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/surgery ; Neoadjuvant Therapy ; Prognosis ; Retrospective Studies ; Lung Neoplasms/surgery ; Fibrinogen
Chemical Substances	Fibrinogen (9001-32-5)
Language	English
Publishing date	2022-11-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-022-10298-9
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Article: Influence of the Fatty Acid Metabolism on the Mode of Action of a Cisplatin(IV) Complex with Phenylbutyrate as Axial Ligands.

Mendrina, Theresa / Poetsch, Isabella / Schueffl, Hemma / Baier, Dina / Pirker, Christine / Ries, Alexander / Keppler, Bernhard K / Kowol, Christian R / Gibson, Dan / Grusch, Michael / Berger, Walter / Heffeter, Petra

Pharmaceutics

2023 Volume 15, Issue 2

Abstract: For a variety of cancer types, platinum compounds are still among the best treatment options. However, their application is limited by side effects and drug resistance. Consequently, multi-targeted platinum(IV) prodrugs that target specific traits of the ...

Abstract	For a variety of cancer types, platinum compounds are still among the best treatment options. However, their application is limited by side effects and drug resistance. Consequently, multi-targeted platinum(IV) prodrugs that target specific traits of the malignant tissue are interesting new candidates. Recently, cisPt(PhB)
Language	English
Publishing date	2023-02-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics15020677
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Article ; Online: Targeting YB-1 via entinostat enhances cisplatin sensitivity of pleural mesothelioma in vitro and in vivo.

Schelch, Karin / Emminger, Dominik / Zitta, Benjamin / Johnson, Thomas G / Kopatz, Verena / Eder, Sebastian / Ries, Alexander / Stefanelli, Alessia / Heffeter, Petra / Hoda, Mir A / Hoetzenecker, Konrad / Dome, Balazs / Berger, Walter / Reid, Glen / Grusch, Michael

Cancer letters

2023 Volume 574, Page(s) 216395

Abstract: Pleural mesothelioma (PM) is characterized by poor prognosis and limited therapeutic options. Y-box-binding protein 1 (YB-1) was shown to drive growth and migration of PM cells. Here, we evaluated the effect of genetic and pharmacological targeting of YB- ...

Abstract	Pleural mesothelioma (PM) is characterized by poor prognosis and limited therapeutic options. Y-box-binding protein 1 (YB-1) was shown to drive growth and migration of PM cells. Here, we evaluated the effect of genetic and pharmacological targeting of YB-1 on PM growth and response to cisplatin and radiation treatment. YB-1 knockdown via siRNA resulted in reduced PM cell growth, which significantly correlated with wt BAP1 and mutant NF2 and P53 status. Entinostat inhibited YB-1 deacetylation and its efficacy correlated with YB-1 knockdown-induced growth inhibition in 20 PM cell lines. Tumor growth inhibition by siRNA as well as entinostat was confirmed in mouse xenotransplant models. Furthermore, both YBX1-targeting siRNA and entinostat enhanced sensitivity to cisplatin and radiation. In particular, entinostat showed strong synergistic interactions with cisplatin which was linked to significantly increased cellular platinum uptake in all investigated cell models. Importantly, in a mouse model, the combination of cisplatin and entinostat also resulted in stronger growth inhibition than each treatment alone. Our study highlights YB-1 as an attractive target in PM and demonstrates that targeting YB-1 via entinostat is a promising approach to enhance cisplatin and radiation sensitivity.
Language	English
Publishing date	2023-09-18
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2023.216395
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Zs.A 1177: Show issues

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Article ; Online: Activin A: an emerging target for improving cancer treatment?

Ries, Alexander / Schelch, Karin / Falch, David / Pany, Laura / Hoda, Mir Alireza / Grusch, Michael

Expert opinion on therapeutic targets

2020 Volume 24, Issue 10, Page(s) 985–996

Abstract: Introduction: Activin A is involved in the regulation of a surprisingly broad number of processes that are relevant for cancer development and treatment; it is implicated in cell autonomous functions and multiple regulatory functions in the tumor ... ...

Abstract	Introduction: Activin A is involved in the regulation of a surprisingly broad number of processes that are relevant for cancer development and treatment; it is implicated in cell autonomous functions and multiple regulatory functions in the tumor microenvironment. Areas covered: This article summarizes the current knowledge about activin A in cell growth and death, migration and metastasis, angiogenesis, stemness and drug resistance, regulation of antitumor immunity, and cancer cachexia. We explore the role of activin A as a biomarker and discuss strategies for using it as target for cancer therapy. Literature retrieved from Medline until 25 June 2020 was considered. Expert opinion: While many functions of activin A were investigated in preclinical models, there is currently limited experience from clinical trials. Activin A has growth- and migration-promoting effects, contributes to immune evasion and cachexia and is associated with shorter survival in several cancer types. Targeting activin A could offer the chance to simultaneously limit tumor growth and spreading, improve drug response, boost antitumor immune responses and improve cancer-associated or treatment-associated cachexia, bone loss, and anemia. Nevertheless, defining which patients have the highest likelihood of benefiting from these effects is challenging and will require further work.
MeSH term(s)	Activins/metabolism ; Animals ; Biomarkers, Tumor/metabolism ; Cachexia/pathology ; Cachexia/therapy ; Drug Resistance, Neoplasm ; Humans ; Molecular Targeted Therapy ; Neoplasms/pathology ; Neoplasms/therapy ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/therapy ; Tumor Microenvironment
Chemical Substances	Biomarkers, Tumor ; activin A ; Activins (104625-48-1)
Language	English
Publishing date	2020-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2020.1799350
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Zs.A 5244: Show issues

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Article ; Online: Epigenetic Biomarkers in Cancer.

Cheng, Yuen Yee / Jin, Hong Chuan / Chan, Michael W Y / Chu, Wai Kit / Grusch, Michael

Disease markers

2018 Volume 2018, Page(s) 4987103

MeSH term(s)	Biomarkers, Tumor/genetics ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2018-02-20
Publishing country	United States
Document type	Editorial ; Introductory Journal Article
ZDB-ID	604951-5
ISSN	1875-8630 ; 0278-0240
ISSN (online)	1875-8630
ISSN	0278-0240
DOI	10.1155/2018/4987103
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Zs.A 1856: 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)
Einzelsignatur: Show issues

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Article ; Online: The state of the art of biomedical applications of optogenetics.

Keshmiri Neghab, Hoda / Soheilifar, Mohammad Hasan / Grusch, Michael / Ortega, Manoela Marques / Esmaeeli Djavid, Gholamreza / Saboury, Ali Akbar / Goliaei, Bahram

Lasers in surgery and medicine

2021 Volume 54, Issue 2, Page(s) 202–216

Abstract: Background and objective: Optogenetics has opened new insights into biomedical research with the ability to manipulate and control cellular activity using light in combination with genetically engineered photosensitive proteins. By stimulating with ... ...

Abstract	Background and objective: Optogenetics has opened new insights into biomedical research with the ability to manipulate and control cellular activity using light in combination with genetically engineered photosensitive proteins. By stimulating with light, this method provides high spatiotemporal and high specificity resolution, which is in contrast to conventional pharmacological or electrical stimulation. Optogenetics was initially introduced to control neural activities but was gradually extended to other biomedical fields. Study design: In this paper, firstly, we summarize the current optogenetic tools stimulated by different light sources, including lasers, light-emitting diodes, and laser diodes. Second, we outline the variety of biomedical applications of optogenetics not only for neuronal circuits but also for various kinds of cells and tissues from cardiomyocytes to ganglion cells. Furthermore, we highlight the potential of this technique for treating neurological disorders, cardiac arrhythmia, visual impairment, hearing loss, and urinary bladder diseases as well as clarify the mechanisms underlying cancer progression and control of stem cell differentiation. Conclusion: We sought to summarize the various types of promising applications of optogenetics to treat a broad spectrum of disorders. It is conceivable to expect that optogenetics profits a growing number of patients suffering from a range of different diseases in the near future.
MeSH term(s)	Humans ; Lasers ; Neoplasms/metabolism ; Neurons/metabolism ; Optogenetics/methods
Language	English
Publishing date	2021-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604493-1
ISSN	1096-9101 ; 0196-8092
ISSN (online)	1096-9101
ISSN	0196-8092
DOI	10.1002/lsm.23463
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Zs.A 1603: Show issues

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Article: EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells.

Schelch, Karin / Vogel, Lisa / Schneller, Anja / Brankovic, Jelena / Mohr, Thomas / Mayer, Rupert L / Slany, Astrid / Gerner, Christopher / Grusch, Michael

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 634371

Abstract: Tumors and the tumor microenvironment produce multiple growth factors that influence cancer cell behavior via various signal transduction pathways. Growth factors, like transforming growth factor β (TGFβ) and epidermal growth factor (EGF), have been ... ...

Abstract	Tumors and the tumor microenvironment produce multiple growth factors that influence cancer cell behavior via various signal transduction pathways. Growth factors, like transforming growth factor β (TGFβ) and epidermal growth factor (EGF), have been shown to induce proliferation, migration, and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, the similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of treating A549 lung adenocarcinoma cells with TGFβ, EGF, and both in combination by applying videomicroscopy, functional assays, immunoblotting, real-time PCR, and proteomics. Treatment with both factors stimulated A549 migration to a similar extent, but with different kinetics. The combination had an additive effect. EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway. However, this pathway was dispensable for TGFβ-induced migration, despite a strong activation of this pathway by TGFβ. Proteome analysis (data are available via ProteomeXchange with identifier PXD023024) revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF. Further, only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF, in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, TGFβ treatment significantly increased the invasive capacity of A549 cells, while EGF treatment did not. Moreover, the addition of EGF failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF can partly compensate for each other for stimulation of cell migration, but abrogation of TGFβ signaling may be more suitable to suppress cell invasion.
Language	English
Publishing date	2021-03-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.634371
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