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1. Supplementary Figure 4 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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2. Supplementary Table 9 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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3. Supplementary Table 7 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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4. Data from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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5. Supplementary Figure 6 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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6. Supplementary Figure 2 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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7. Supplementary Table 4 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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8. Supplementary Table 2 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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9. Supplementary Table 5 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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10. Supplementary Methods, Figure Legend from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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11. Supplementary Figure 1 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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12. Supplementary Table 3 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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13. Supplementary Table 6 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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14. Supplementary Figure 5 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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15. Supplementary Table 10 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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16. Supplementary Figure 3 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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17. Supplementary Table 8 from Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, primary, Reijm, Esther A., primary, Simon, Iris, primary, Kerkhoven, Ron, primary, Droog, Marjolein, primary, Velds, Arno, primary, van Laere, Steven, primary, Dirix, Luc, primary, Alexi, Xanthippi, primary, Foekens, John A., primary, Wessels, Lodewyk, primary, Linn, Sabine C., primary, Berns, Els M.J.J., primary, and Zwart, Wilbert, primary

Published
2023
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29. IGF-1R pathway activation as putative biomarker for linsitinib therapy to revert tamoxifen resistance in ER-positive breast cancer

Author

Kruger, Dinja T., Alexi, Xanthippi, Opdam, Mark, Schuurman, Karianne, Voorwerk, Leonie, Sanders, Joyce, van der Noort, Vincent, Boven, Epie, Zwart, Wilbert, Linn, Sabine C., Kruger, Dinja T., Alexi, Xanthippi, Opdam, Mark, Schuurman, Karianne, Voorwerk, Leonie, Sanders, Joyce, van der Noort, Vincent, Boven, Epie, Zwart, Wilbert, and Linn, Sabine C.

Abstract

Preclinical studies indicate that activated IGF-1R can drive endocrine resistance in ER-positive (ER+) breast cancer, but its clinical relevance is unknown. We studied the effect of IGF-1R signaling on tamoxifen benefit in patients and we searched for approaches to overcome IGF-1R-mediated tamoxifen failure in cell lines. Primary tumor blocks from postmenopausal ER+ breast cancer patients randomized between adjuvant tamoxifen versus nil were recollected. Immunohistochemistry for IGF-1R, p-IGF-1R/InsR, p-ERα(Ser118), p-ERα(Ser167) and PI3K/MAPK pathway proteins was performed. Multivariate Cox models were employed to assess tamoxifen efficacy. The association between p-IGF-1R/InsR and PI3K/MAPK pathway activation in MCF-7 and T47D cells was analyzed with Western blots. Cell proliferation experiments were performed under various growth-stimulating and -inhibiting conditions. Patients with ER+, IGF-1R-positive breast cancer without p-IGF-1R/InsR staining (n = 242) had tamoxifen benefit (HR 0.41, p = 0.0038), while the results for p-IGF-1R/InsR-positive patients (n = 125) were not significant (HR 0.95, p = 0.3). High p-ERα(Ser118) or p-ERα(Ser167) expression was associated with less tamoxifen benefit. In MCF-7 cells, IGF-1R stimulation increased phosphorylation of PI3K/MAPK proteins and ERα(Ser167) regardless of IGF-1R overexpression. This could be abrogated by the dual IGF-1R/InsR inhibitor linsitinib, but not by the IGF-IR-selective antibody 1H7. In MCF-7 and T47D cells, stimulation of the IGF-1R/InsR pathway resulted in cell proliferation regardless of tamoxifen. Abrogation of cell growth was regained by addition of linsitinib. In conclusion, p-IGF-1R/InsR positivity in ER+ breast cancer is associated with reduced benefit from adjuvant tamoxifen in postmenopausal patients. In cell lines, stimulation rather than overexpression of IGF-1R is driving tamoxifen resistance to be abrogated by linsitinib.

Published
2020

31. Biological evaluation of isoflavonoids from Genista halacsyi using estrogen-target cells: Activities of glucosides compared to aglycones

Author

Fokialakis, Nikolas, primary, Alexi, Xanthippi, additional, Aligiannis, Nektarios, additional, Boulaka, Athina, additional, Meligova, Aggeliki K., additional, Lambrinidis, George, additional, Kalpoutzakis, Eleftherios, additional, Pratsinis, Harris, additional, Cheilari, Antigoni, additional, Mitsiou, Dimitra J., additional, Mitakou, Sofia, additional, and Alexis, Michael N., additional

Published
2019
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34. Biological and computational evaluation of resveratrol inhibitors against Alzheimer’s disease

Author

Koukoulitsa, Catherine, primary, Villalonga-Barber, Caroline, additional, Csonka, Robert, additional, Alexi, Xanthippi, additional, Leonis, Georgios, additional, Dellis, Dimitris, additional, Hamelink, Elizabeth, additional, Belda, Oscar, additional, Steele, Barry R., additional, Micha-Screttas, Maria, additional, Alexis, Michael N., additional, Papadopoulos, Manthos G., additional, and Mavromoustakos, Thomas, additional

Published
2015
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35. Hallmarks of Aromatase Inhibitor Drug Resistance Revealed by Epigenetic Profiling in Breast Cancer

Author

Jansen, Maurice P.H.M., primary, Knijnenburg, Theo, additional, Reijm, Esther A., additional, Simon, Iris, additional, Kerkhoven, Ron, additional, Droog, Marjolein, additional, Velds, Arno, additional, van Laere, Steven, additional, Dirix, Luc, additional, Alexi, Xanthippi, additional, Foekens, John A., additional, Wessels, Lodewyk, additional, Linn, Sabine C., additional, Berns, Els M.J.J., additional, and Zwart, Wilbert, additional

Published
2013
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36. Pharmacoproteomic Study of the Natural Product Ebenfuran III in DU-145 Prostate Cancer Cells: The Quantitative and Temporal Interrogation of Chemically Induced Cell Death at the Protein Level

Author

Roumeliotis, Theodoros I., primary, Halabalaki, Maria, additional, Alexi, Xanthippi, additional, Ankrett, Dyan, additional, Giannopoulou, Eugenia G., additional, Skaltsounis, Alexios-Leandros, additional, Sayan, Berna S., additional, Alexis, Michael N., additional, Townsend, Paul A., additional, and Garbis, Spiros D., additional

Published
2013
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37. The transcriptional co-factor RIP140 regulates mammary gland development by promoting the generation of key mitogenic signals

Author

Nautiyal, Jaya, primary, Steel, Jennifer H., additional, Mane, Meritxell Rosell, additional, Oduwole, Olayiwola, additional, Poliandri, Ariel, additional, Alexi, Xanthippi, additional, Wood, Nicholas, additional, Poutanen, Matti, additional, Zwart, Wilbert, additional, Stingl, John, additional, and Parker, Malcolm G., additional

Published
2013
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38. Biological and computational evaluation of resveratrol inhibitors against Alzheimer’s disease.

Author

Koukoulitsa, Catherine, Villalonga-Barber, Caroline, Csonka, Robert, Alexi, Xanthippi, Leonis, Georgios, Dellis, Dimitris, Hamelink, Elizabeth, Belda, Oscar, Steele, Barry R., Micha-Screttas, Maria, Alexis, Michael N., Papadopoulos, Manthos G., and Mavromoustakos, Thomas

Subjects
ALZHEIMER'S disease treatment, RESVERATROL, OXIDATIVE stress, NEURAL physiology, CELL death, SECRETASES, CHEMICAL derivatives
Abstract

It has been reported that beta amyloid induces production of radical oxygen species and oxidative stress in neuronal cells, which in turn upregulates β-secretase (BACE-1) expression and beta amyloid levels, thereby propagating oxidative stress and increasing neuronal injury. A series of resveratrol derivatives, known to be inhibitors of oxidative stress-induced neuronal cell death (oxytosis) were biologically evaluated against BACE-1 using homogeneous time-resolved fluorescence (TRF) assay. Correlation between oxytosis inhibitory and BACE-1 inhibitory activity of resveratrol derivatives was statistically significant, supporting the notion that BACE-1 may act as pivotal mediator of neuronal cell oxytosis. Four of the biologically evaluated resveratrol analogs demonstrated considerably higher activity than resveratrol in either assay. The discovery of some “hits” led us to initiate detailed docking studies associated with Molecular Dynamics in order to provide a plausible explanation for the experimental results and understand their molecular basis of action. [ABSTRACT FROM AUTHOR]

Published
2016
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42. Novel Dehydroepiandrosterone Derivatives with Antiapoptotic, Neuroprotective Activity

Author

Calogeropoulou, Theodora, primary, Avlonitis, Nicolaos, additional, Minas, Vassilios, additional, Alexi, Xanthippi, additional, Pantzou, Athanasia, additional, Charalampopoulos, Ioannis, additional, Zervou, Maria, additional, Vergou, Varvara, additional, Katsanou, Efrosini S., additional, Lazaridis, Iakovos, additional, Alexis, Michael N., additional, and Gravanis, Achille, additional

Published
2009
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46. Protein Kinase A-induced tamoxifen resistance is mediated by anchoring protein AKAP13.

Author

Toaldo, Cristiane Bentin, Alexi, Xanthippi, Beelen, Karin, Kok, Marleen, Hauptmann, Michael, Jansen, Maurice, Berns, Els, Neefjes, Jacques, Linn, Sabine, Michalides, Rob, and Zwart, Wilbert

Subjects
*CYCLIC-AMP-dependent protein kinase, *TAMOXIFEN, *DRUG resistance, *ESTROGEN receptors, *BREAST cancer patients, *BREAST cancer treatment, *HORMONE therapy
Abstract

Background: Estrogen Receptor alpha (ERα)-positive breast cancer patients receive endocrine therapy, often in the form of tamoxifen. However, resistance to tamoxifen is frequently observed. A signalling cascade that leads to tamoxifen resistance is dictated by activation of the Protein Kinase A (PKA) pathway, which leads to phosphorylation of ERα on Serine 305 and receptor activation, following tamoxifen binding. Thus far, it remains elusive what protein complexes enable the PKA-ERα interaction resulting in ERα Serine 305 phosphorylation. Methods: We performed immunohistochemistry to detect ERαSerine 305 phosphorylation in a cohort of breast cancer patients who received tamoxifen treatment in the metastatic setting. From the same tumor specimens, Agilent 44 K gene expression analyses were performed and integrated with clinicopathological data and survival information. In vitro analyses were performed using MCF7 breast cancer cells, which included immunoprecipitations and Fluorescence Resonance Energy Transfer (FRET) analyses to illustrate ERα complex formation. siRNA mediated knockdown experiments were performed to assess effects on ERαSerine 305 phosphorylation status, ERα/PKA interactions and downstream responsive gene activity. Results: Stratifying breast tumors on ERα Serine 305 phosphorylation status resulted in the identification of a gene network centered upon AKAP13. AKAP13 mRNA expression levels correlate with poor outcome in patients who received tamoxifen treatment in the metastatic setting. In addition, AKAP13 mRNA levels correlate with ERαSerine 305 phosphorylation in breast tumor samples, suggesting a functional connection between these two events. In a luminal breast cancer cell line, AKAP13 was found to interact with ERα as well as with a regulatory subunit of PKA. Knocking down of AKAP13 prevented PKA-mediated Serine 305 phosphorylation of ERα and abrogated PKA-driven tamoxifen resistance, illustrating that AKAP13 is an essential protein in this process. Conclusions: We show that the PKA-anchoring protein AKAP13 is essential for the phosphorylation of ERαS305, which leads to tamoxifen resistance both in cell lines and tamoxifen-treated breast cancer patients. [ABSTRACT FROM AUTHOR]

Published
2015
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47. Estrogenic Activity of Isoflavonoids fromOnobrychis ebenoides

Author

Halabalaki, Maria, primary, Alexi, Xanthippi, additional, Aligiannis, Nektarios, additional, Lambrinidis, George, additional, Pratsinis, Harris, additional, Florentin, Ida, additional, Mitakou, Sofia, additional, Mikros, Emmanuel, additional, Skaltsounis, Alexios-Leandros, additional, and Alexis, Michael, additional

Published
2006
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49. Erymildbraedin A and B, two novel cytotoxic dimethylpyrano-isoflavones from the stem bark of Erythrina mildbraedii: evaluation of their activity toward endocrine cancer cells.

Author

Tchokouaha, Ruben F., Alexi, Xanthippi, Chosson, Elizabeth, Besson, Thierry, Skaltsounis, Alexios-Leandros, Seguin, Elisabeth, Alexis, Michael N., and Wandji, Jean

Subjects
*ISOFLAVONES, *ERYTHRINA, *CANCER cells, *CELL lines, *CANCER invasiveness
Abstract

Two new dimethylpyrano-isoflavones, named erymildbraedin A ( 4) and B ( 5), were isolated from the stem bark of the Cameroonian medicinal plant Erythrina mildbraedii, along with four known ones, the linear congeners, scandenone ( 1), erysenegalinsein M ( 2), 5,4′-dihydroxy-2′-methoxy-8-(3,3-dimethylallyl)-2″,2″-dimethylpyrano[5,6:6,7]isoflavone ( 3), and the angular isoflavone eryvarin B ( 6), and two other compounds, fraxidin and scoparone. Their structures were elucidated by the usual spectroscopic methods and isoflavone effects on the growth of human breast, prostate, and endometrial adenocarcinoma cells were determined. Isoflavones 1, 3, and 6 strongly inhibited the growth of all three cell lines, supporting the notion that a non-oxidized isoprenyl group at C-8 is requisite for cytotoxic activity. [ABSTRACT FROM AUTHOR]

Published
2010
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