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8 results on '"Monteiro, Madalena N"'

1. Malignant T cells induce skin barrier defects through cytokine-mediated JAK/STAT signaling in cutaneous T-cell lymphoma

Author

Gluud, Maria, Pallesen, Emil M. H., Buus, Terkild B., Gjerdrum, Lise Mette Rahbek, Lindahl, Lise M., Kamstrup, Maria R., Bzorek, Michael, Danielsen, Maria, Bech, Rikke, Monteiro, Madalena N., Blümel, Edda, Willerslev-Olsen, Andreas, Lykkebo-Valløe, Anders, Vadivel, Chella Krishna, Krejsgaard, Thorbjørn, Bonefeld, Charlotte Menne, Geisler, Carsten, Becker, Jürgen C., Koralov, Sergei B., Iversen, Lars, Litman, Thomas, Woetmann, Anders, and Ødum, Niels

Published
2023
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2. Abstract CC03-01: Exosome pathway inhibition as therapeutic strategy in colorectal cancer

Author

Monteiro, Madalena N., primary, Almeida-Marques, Catarina, additional, de Wit, Meike, additional, Dusseldorp, Valerie, additional, Bishop-Currey, Logan, additional, Piersma, Sander R., additional, Pham, Thang V., additional, Knol, Jaco C., additional, Sadeghi, Hanieh, additional, Meijer, Gerrit, additional, Fijneman, Remond J. A., additional, Hausser, Angelika, additional, Bijnsdorp, Irene V., additional, and Jimenez, Connie R., additional

Published
2021
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3. Lipopolysaccharide‐regulated secretion of soluble and vesicle‐based proteins from a panel of colorectal cancer cell lines

Author

Garcia de Durango, Cira R., primary, Monteiro, Madalena N., additional, Bijnsdorp, Irene V., additional, Pham, Thang V., additional, De Wit, Meike, additional, Piersma, Sander Rogier, additional, Knol, Jaco C., additional, Pérez‐Gordo, Marina, additional, Fijneman, Remond J. A., additional, Vidal‐Vanaclocha, Fernando, additional, and Jimenez, Connie R., additional

Published
2021
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4. Expression and function of Kv1.3 channel in malignant T cells in Sézary syndrome

Author

Hu, Tengpeng, Buus, Terkild Brink, Krejsgaard, Thorbjørn, Nansen, Anneline, Lundholt, Betina Kerstin, Spee, Pieter, Fredholm, Simon, Petersen, David Leander, Blümel, Edda, Gluud, Maria, Monteiro, Madalena N, Willerslev-Olsen, Andreas, Andersen, Mads Hald, Straten, Per Thor, Met, Özcan, Stolearenco, Veronica, Fogh, Hanne, Gniadecki, Robert, Nastasi, Claudia, Litman, Thomas, Woetmann, Anders, Gjerdrum, Lise Mette Rahbek, Ødum, Niels, Hu, Tengpeng, Buus, Terkild Brink, Krejsgaard, Thorbjørn, Nansen, Anneline, Lundholt, Betina Kerstin, Spee, Pieter, Fredholm, Simon, Petersen, David Leander, Blümel, Edda, Gluud, Maria, Monteiro, Madalena N, Willerslev-Olsen, Andreas, Andersen, Mads Hald, Straten, Per Thor, Met, Özcan, Stolearenco, Veronica, Fogh, Hanne, Gniadecki, Robert, Nastasi, Claudia, Litman, Thomas, Woetmann, Anders, Gjerdrum, Lise Mette Rahbek, and Ødum, Niels

Abstract

The voltage-gated potassium channel Kv1.3 (KCNA3) is expressed by a subset of chronically activated memory T cells and plays an important role in their activation and proliferation. Here, we show that primary malignant T cells isolated from patients with Sézary syndrome (SS) express Kv1.3 and are sensitive to potent Kv1.3 inhibitors ShK and Vm24, but not sensitive to a less potent inhibitor [N17A/F32T]-AnTx. Kv1.3 blockade inhibits CD3/CD28-induced proliferation and IL-9 expression by SS cells in a concentration-dependent manner. In parallel, CD3/CD28-mediated CD25 induction is inhibited, whereas Kv1.3 blockade has no effect on apoptosis or cell death as judged by Annexin V and PI staining. In conclusion, we provide the first evidence that malignant T cells in SS express functional Kv1.3 channels and that Kv1.3 blockade inhibits activation-induced proliferation as well as cytokine and cytokine receptor expression in malignant T cells, suggesting that Kv1.3 is a potential target for therapy in SS.

Published
2019

5. Expression and function of Kv1.3 channel in malignant T cells in Sézary syndrome

Author

Hu, Tengpeng, primary, Buus, Terkild Brink, additional, Krejsgaard, Thorbjørn, additional, Nansen, Anneline, additional, Lundholt, Betina Kerstin, additional, Spee, Pieter, additional, Fredholm, Simon, additional, Petersen, David Leander, additional, Blümel, Edda, additional, Gluud, Maria, additional, Monteiro, Madalena N., additional, Willerslev-Olsen, Andreas, additional, Andersen, Mads Hald, additional, Straten, Per thor, additional, Met, Özcan, additional, Stolearenco, Veronica, additional, Fogh, Hanne, additional, Gniadecki, Robert, additional, Nastasi, Claudia, additional, Litman, Thomas, additional, Woetmann, Anders, additional, Gjerdrum, Lise Mette Rahbek, additional, and Ødum, Niels, additional

Published
2019
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6. New inhibitor of the TAp73 interaction with MDM2 and mutant p53 with promising antitumor activity against neuroblastoma

Author

Gomes, Sara, primary, Raimundo, Liliana, additional, Soares, Joana, additional, Loureiro, Joana B., additional, Leão, Mariana, additional, Ramos, Helena, additional, Monteiro, Madalena N., additional, Lemos, Agostinho, additional, Moreira, Joana, additional, Pinto, Madalena, additional, Chlapek, Petr, additional, Veselska, Renata, additional, Sousa, Emília, additional, and Saraiva, Lucília, additional

Published
2019
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7. Malignant T cells induce skin barrier defects through cytokine-mediated JAK/STAT signaling in cutaneous T-cell lymphoma

Author

Gluud, Maria, Pallesen, Emil M.H., Buus, Terkild B., Gjerdrum, Lise Mette Rahbek, Lindahl, Lise M., Kamstrup, Maria R., Bzorek, Michael, Danielsen, Maria, Bech, Rikke, Monteiro, Madalena N., Blümel, Edda, Willerslev-Olsen, Andreas, Lykkebo-Valløe, Anders, Vadivel, Chella Krishna, Krejsgaard, Thorbjørn, Bonefeld, Charlotte Menne, Geisler, Carsten, Becker, Jürgen C., Koralov, Sergei B., Iversen, Lars, Litman, Thomas, Woetmann, Anders, and Ødum, Niels

Abstract

Cutaneous T-cell lymphoma (CTCL) is a devastating lymphoid malignancy characterized by the accumulation of malignant T cells in the dermis and epidermis. Skin lesions cause serious symptoms that hamper quality of life and are entry sites for bacterial infection, a major cause of morbidity and mortality in advanced diseases. The mechanism driving the pathological processes that compromise the skin barrier remains unknown. Here, we report increased transepidermal water loss and compromised expression of the skin barrier proteins filaggrin and filaggrin-2 in areas adjacent to TOX-positive T cells in CTCL skin lesions. Malignant T cells secrete mediators (including cytokines such as interleukin 13 [IL-13], IL-22, and oncostatin M) that activate STAT3 signaling and downregulate filaggrin and filaggrin-2 expression in human keratinocytes and reconstructed human epithelium. Consequently, the repression of filaggrins can be counteracted by a cocktail of antibodies targeting these cytokines/receptors, small interfering RNA–mediated knockdown of JAK1/STAT3, and JAK1 inhibitors. Notably, we show that treatment with a clinically approved JAK inhibitor, tofacitinib, increases filaggrin expression in lesional skin from patients with mycosis fungoides. Taken together, these findings indicate that malignant T cells secrete cytokines that induce skin barrier defects via a JAK1/STAT3-dependent mechanism. As clinical grade JAK inhibitors largely abrogate the negative effect of malignant T cells on skin barrier proteins, our findings suggest that such inhibitors provide novel treatment options for patients with CTCL with advanced disease and a compromised skin barrier.

Published
2022
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8. Lipopolysaccharide-regulated secretion of soluble and vesicle-based proteins from a panel of colorectal cancer cell lines.

Author

Garcia de Durango CR, Monteiro MN, Bijnsdorp IV, Pham TV, De Wit M, Piersma SR, Knol JC, Pérez-Gordo M, Fijneman RJA, Vidal-Vanaclocha F, and Jimenez CR

Subjects
Humans, Cell Line, Tumor, Extracellular Vesicles metabolism, Proteomics, Secretome metabolism, Solubility, NF-kappa B metabolism, Colorectal Neoplasms metabolism, Colorectal Neoplasms pathology, Lipopolysaccharides pharmacology
Abstract

Purpose: To mimic the perioperative microenvironment where bacterial products get in contact with colorectal cancer (CRC) cells and study its impact on protein release, we exposed six CRC cell lines to lipopolysaccharide (LPS) and investigated the effect on the secretome using in-depth mass spectrometry-based proteomics., Experimental Design: Cancer cell secretome was harvested in bio-duplicate after LPS treatment, and separated in EV and soluble secretome (SS) fractions. Gel-fractionated proteins were analysed by label-free nano-liquid chromatography coupled to tandem mass spectrometry. NF-κB activation, triggered upon LPS treatment, was evaluated., Results: We report a CRC secretome dataset of 5601 proteins. Comparison of all LPS-treated cells with controls revealed 37 proteins with altered abundance in the SS, including RPS25; and 13 in EVs, including HMGB1. Comparing controls and LPS-treated samples per cell line, revealed 564 significant differential proteins with fold-change >3. The LPS-induced release of RPS25 was validated by western blot., Conclusions and Clinical Relevance: Bacterial endotoxin has minor impact on the global CRC cell line secretome, yet it may alter protein release in a cell line-specific manner. This modulation might play a role in orchestrating the development of a permissive environment for CRC liver metastasis, especially through EV-communication., (© 2021 Wiley-VCH GmbH.)

Published
2021
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