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1. Targeting chemoresistant colorectal cancer via systemic administration of a BMP7 variant

Author

Veschi, Veronica, Mangiapane, Laura R., Nicotra, Annalisa, Di Franco, Simone, Scavo, Emanuela, Apuzzo, Tiziana, Sardina, Davide S., Fiori, Micol, Benfante, Antonina, Colorito, Maria L., Cocorullo, Gianfranco, Giuliante, Felice, Cipolla, Calogero, Pistone, Giuseppe, Bongiorno, Maria Rita, Rizzo, Aroldo, Tate, Courtney M., Wu, Xiaohua, Rowlinson, Scott, Stancato, Louis F., Todaro, Matilde, De Maria, Ruggero, and Stassi, Giorgio

Published
2020
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2. Supplementary Figure S5 from IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

Author

Gaggianesi, Miriam, primary, Turdo, Alice, primary, Chinnici, Aurora, primary, Lipari, Elisa, primary, Apuzzo, Tiziana, primary, Benfante, Antonina, primary, Sperduti, Isabella, primary, Di Franco, Simone, primary, Meraviglia, Serena, primary, Lo Presti, Elena, primary, Dieli, Francesco, primary, Caputo, Valentina, primary, Militello, Gabriella, primary, Vieni, Salvatore, primary, Stassi, Giorgio, primary, and Todaro, Matilde, primary

Published
2023
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3. Data from IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

Author

Gaggianesi, Miriam, primary, Turdo, Alice, primary, Chinnici, Aurora, primary, Lipari, Elisa, primary, Apuzzo, Tiziana, primary, Benfante, Antonina, primary, Sperduti, Isabella, primary, Di Franco, Simone, primary, Meraviglia, Serena, primary, Lo Presti, Elena, primary, Dieli, Francesco, primary, Caputo, Valentina, primary, Militello, Gabriella, primary, Vieni, Salvatore, primary, Stassi, Giorgio, primary, and Todaro, Matilde, primary

Published
2023
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4. Supplementary information from IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

Author

Gaggianesi, Miriam, primary, Turdo, Alice, primary, Chinnici, Aurora, primary, Lipari, Elisa, primary, Apuzzo, Tiziana, primary, Benfante, Antonina, primary, Sperduti, Isabella, primary, Di Franco, Simone, primary, Meraviglia, Serena, primary, Lo Presti, Elena, primary, Dieli, Francesco, primary, Caputo, Valentina, primary, Militello, Gabriella, primary, Vieni, Salvatore, primary, Stassi, Giorgio, primary, and Todaro, Matilde, primary

Published
2023
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6. Supplementary Figures 1 through 9 from Activated Thyroid Hormone Promotes Differentiation and Chemotherapeutic Sensitization of Colorectal Cancer Stem Cells by Regulating Wnt and BMP4 Signaling

Author

Catalano, Veronica, primary, Dentice, Monica, primary, Ambrosio, Raffaele, primary, Luongo, Cristina, primary, Carollo, Rosachiara, primary, Benfante, Antonina, primary, Todaro, Matilde, primary, Stassi, Giorgio, primary, and Salvatore, Domenico, primary

Published
2023
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10. Circulating tumor DNA (ctDNA) and serum thymidine kinase 1 activity (TKa) matched dynamics in patients (pts) with hormone receptor–positive (HR+), human epidermal growth factor 2–negative (HER2-) advanced breast cancer (ABC) treated in first-line (1L) with ribociclib (RIB) and letrozole (LET) in the BioItaLEE trial.

Author

Arpino, Grazia, primary, Bianchini, Giampaolo, additional, Malorni, Luca, additional, Zambelli, Alberto, additional, Puglisi, Fabio, additional, Del Mastro, Lucia, additional, Colleoni, Marco, additional, Montemurro, Filippo, additional, Bianchi, Giulia Valeria, additional, Paris, Ida, additional, Allegrini, Giacomo, additional, Tamberi, Stefano, additional, Cazzaniga, Marina Elena, additional, Orditura, Michele, additional, Zamagni, Claudio, additional, Grasso, Donatella, additional, Benelli, Matteo, additional, Callari, Maurizio, additional, Benfante, Antonina, additional, and De Laurentiis, Michelino, additional

Published
2022
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12. Targeting chemoresistant colorectal cancer via systemic administration of a BMP7 variant

Author

Veschi, Veronica, primary, Mangiapane, Laura R., additional, Nicotra, Annalisa, additional, Di Franco, Simone, additional, Scavo, Emanuela, additional, Apuzzo, Tiziana, additional, Sardina, Davide S., additional, Fiori, Micol, additional, Benfante, Antonina, additional, Colorito, Maria L., additional, Cocorullo, Gianfranco, additional, Giuliante, Felice, additional, Cipolla, Calogero, additional, Pistone, Giuseppe, additional, Bongiorno, Maria Rita, additional, Rizzo, Aroldo, additional, Tate, Courtney M., additional, Wu, Xiaohua, additional, Rowlinson, Scott, additional, Stancato, Louis F., additional, Todaro, Matilde, additional, De Maria, Ruggero, additional, and Stassi, Giorgio, additional

Published
2019
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13. Additional file 1: Figure S1. of Combined platelet-rich plasma and lipofilling treatment provides great improvement in facial skin-induced lesion regeneration for scleroderma patients

Author

VirzĂŹ, Francesco, Bianca, Paola, Giammona, Alessandro, Apuzzo, Tiziana, Franco, Simone Di, Mangiapane, Laura, Colorito, Maria, Catalano, Dario, Scavo, Emanuela, Nicotra, Annalisa, Benfante, Antonina, Pistone, Giuseppe, Caputo, Valentina, Dieli, Francesco, Pirrello, Roberto, and Stassi, Giorgio

Abstract

showing AD-MSCs from both healthy subjects and SSc patients with increased levels of CD271 expression. Representative dot plot showing the expression of CD271 corresponding isotype match control in freshly isolated SVF and long-term propagated AD-MSCs from healthy subjects (upper panels) and SSc patients (lower panels), performed by flow cytometry. (PDF 205Â kb)

Published
2017
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14. Additional file 2: Figure S2. of Combined platelet-rich plasma and lipofilling treatment provides great improvement in facial skin-induced lesion regeneration for scleroderma patients

Author

VirzĂŹ, Francesco, Bianca, Paola, Giammona, Alessandro, Apuzzo, Tiziana, Franco, Simone Di, Mangiapane, Laura, Colorito, Maria, Catalano, Dario, Scavo, Emanuela, Nicotra, Annalisa, Benfante, Antonina, Pistone, Giuseppe, Caputo, Valentina, Dieli, Francesco, Pirrello, Roberto, and Stassi, Giorgio

Subjects
embryonic structures
Abstract

showing AD-MSCs from SSc patients with decreased levels of mesenchymal stem cell markers. Representative dot plot showing the expression of CD44, CD90, CD271, CD29, CD73, and CD9 in AD-MSCs from healthy subjects (upper panels) and SSc patients (lower panels). Small boxes show isotype match control staining. (PDF 316Â kb)

Published
2017
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15. PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

Author

Milella, Michele, Falcone, Italia, Conciatori, Fabiana, Matteoni, Silvia, Sacconi, Andrea, De Luca, Teresa, Bazzichetto, Chiara, Corbo, Vincenzo, Simbolo, Michele, Sperduti, Isabella, Benfante, Antonina, Del Curatolo, Anai, Cesta Incani, Ursula, Malusa, Federico, Eramo, Adriana, Sette, Giovanni, Scarpa, Aldo, Konopleva, Marina, Andreeff, Michael, Mccubrey, James Andrew, Blandino, Giovanni, Todaro, Matilde, Stassi, Giorgio, De Maria Marchiano, Ruggero, Cognetti, Francesco, Del Bufalo, Donatella, Ciuffreda, Ludovica, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Milella, Michele, Falcone, Italia, Conciatori, Fabiana, Matteoni, Silvia, Sacconi, Andrea, De Luca, Teresa, Bazzichetto, Chiara, Corbo, Vincenzo, Simbolo, Michele, Sperduti, Isabella, Benfante, Antonina, Del Curatolo, Anai, Cesta Incani, Ursula, Malusa, Federico, Eramo, Adriana, Sette, Giovanni, Scarpa, Aldo, Konopleva, Marina, Andreeff, Michael, Mccubrey, James Andrew, Blandino, Giovanni, Todaro, Matilde, Stassi, Giorgio, De Maria Marchiano, Ruggero, Cognetti, Francesco, Del Bufalo, Donatella, Ciuffreda, Ludovica, and De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583)

Abstract

Combined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether PTEN status determines the functional response to combined pathway inhibition. PTEN (gene, mRNA, and protein) status was extensively characterized in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmacologic interactions almost exclusively in PTEN-loss models. Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined pathway blockade. Proteomic analysis showed greater phosphoproteomic profile modification(s) in response to combined MEK/mTOR inhibition in PTEN-loss contexts and identified JAK1/STAT3 activation as a potential mediator of synergistic interactions. Overall, our results show that PTEN-loss is a crucial determinant of synergistic interactions between MAPK and PI3K pathway inhibitors, potentially exploitable for the selection of cancer patients at the highest chance of benefit from combined therapeutic strategies.

Published
2017

16. Combined platelet-rich plasma and lipofilling treatment provides great improvement in facial skin-induced lesion regeneration for scleroderma patients

Author

Virzì, Francesco, primary, Bianca, Paola, additional, Giammona, Alessandro, additional, Apuzzo, Tiziana, additional, Di Franco, Simone, additional, Mangiapane, Laura Rosa, additional, Colorito, Maria Luisa, additional, Catalano, Dario, additional, Scavo, Emanuela, additional, Nicotra, Annalisa, additional, Benfante, Antonina, additional, Pistone, Giuseppe, additional, Caputo, Valentina, additional, Dieli, Francesco, additional, Pirrello, Roberto, additional, and Stassi, Giorgio, additional

Published
2017
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17. IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

Author

Gaggianesi, Miriam, primary, Turdo, Alice, additional, Chinnici, Aurora, additional, Lipari, Elisa, additional, Apuzzo, Tiziana, additional, Benfante, Antonina, additional, Sperduti, Isabella, additional, Di Franco, Simone, additional, Meraviglia, Serena, additional, Lo Presti, Elena, additional, Dieli, Francesco, additional, Caputo, Valentina, additional, Militello, Gabriella, additional, Vieni, Salvatore, additional, Stassi, Giorgio, additional, and Todaro, Matilde, additional

Published
2017
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18. PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

Author

Milella, Michele, primary, Falcone, Italia, additional, Conciatori, Fabiana, additional, Matteoni, Silvia, additional, Sacconi, Andrea, additional, De Luca, Teresa, additional, Bazzichetto, Chiara, additional, Corbo, Vincenzo, additional, Simbolo, Michele, additional, Sperduti, Isabella, additional, Benfante, Antonina, additional, Del Curatolo, Anais, additional, Cesta Incani, Ursula, additional, Malusa, Federico, additional, Eramo, Adriana, additional, Sette, Giovanni, additional, Scarpa, Aldo, additional, Konopleva, Marina, additional, Andreeff, Michael, additional, McCubrey, James Andrew, additional, Blandino, Giovanni, additional, Todaro, Matilde, additional, Stassi, Giorgio, additional, De Maria, Ruggero, additional, Cognetti, Francesco, additional, Del Bufalo, Donatella, additional, and Ciuffreda, Ludovica, additional

Published
2017
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19. BMP7v induces cancer stem cells differentiation and enhances chemotherapy response in colorectal cancer

Author

BENFANTE, Antonina, Benfante, ., and DIELI, FRANCESCO

Subjects
Settore MED/04 - Patologia Generale, Cancer stem cell, Bone Morphogenetic Proteins (BMPs), Colorectal cancer
Abstract

Cancer stem cells (CSCs), characterized by high levels of ATP-binding cassette, anti-apoptotic molecules, active DNA-repair and slow replication capacities, surviving to conventional anti-cancer therapies, able to eradicate only the highly proliferating tumor cells, represent the elective target for new therapies. Colorectal CSCs (CR-CSCs) represent a powerful tool for preclinical validation of target therapies. In particular the elucidation of the mechanisms that govern stem cell survival and differentiation appears very essential for the identification of new molecular targets in cancer therapy. Among the molecules that govern these processes there are the Bone Morphogenetic Proteins (BMPs), members of the TGF-b superfamily. Here we propose that a BMP7 variant (BMP7v) have an important antitumoral and anti angiogenetic effect on CR-CSCs inducing a differentiation program and making these cells more sensitive to conventional chemotherapy drugs. BMP7v in vitro administration, activates the BMP signaling pathway in CR-CSCs, reducing the percentage of stem cell marker expression and enhancing epithelial colonic differentiation marker expression. BMP7v reduces self-renewal of CR-CSCs inducing their exit from quiescence and, reducing their typical mesenchymal trait, decreases their invasive and endothelial cord formation capacity. In vivo, BMP7v decreases tumor growth and stem cell marker expression, enhancing differentiation compared with control mice and in combination with CRC standard chemotherapy reduces tumor growth, inducing a differentiative and antiproliferative effect, associated with a strong antiangiogenic role. In addition, BMP7v as second-line of treatment also showed a significant anti-tumor activity in xenografts refractory to chemotherapy. Our data support the use of BMP7v as differentiative agent in combination with cytotoxic drugs for the treatment of CRC, and the use of BMP7v provides a potentially powerful and novel approach for the treatment of tumor disease.

Published
2014

21. ΔNp63 drives metastasis in breast cancer cellsviaPI3K/CD44v6 axis

Author

Di Franco, Simone, primary, Turdo, Alice, additional, Benfante, Antonina, additional, Colorito, Maria L., additional, Gaggianesi, Miriam, additional, Apuzzo, Tiziana, additional, Kandimalla, Raju, additional, Chinnici, Aurora, additional, Barcaroli, Daniela, additional, Mangiapane, Laura Rosa, additional, Pistone, Giuseppe, additional, Vieni, Salvatore, additional, Gulotta, Eliana, additional, Dieli, Francesco, additional, Medema, Jan Paul, additional, Stassi, Giorgio, additional, De Laurenzi, Vincenzo, additional, and Todaro, Matilde, additional

Published
2016
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24. A BMP7 variant inhibits tumor angiogenesis in vitro and in vivo through direct modulation of endothelial cell biology

Author

Tate, Courtney M., Mc Entire, Jacquelyn, Pallini, Roberto, Vakana, Eliza, Wyss, Lisa, Blosser, Wayne, Ricci-Vitiani, Lucia, D'Alessandris, Quintino Giorgio, Morgante, Liliana, Giannetti, Stefano, Larocca, Luigi Maria, Todaro, Matilde, Benfante, Antonina, Colorito, Maria Luisa, Stassi, Giorgio, De Maria Marchiano, Ruggero, Rowlinson, Scott, Stancato, Louis, Pallini, Roberto (ORCID:0000-0002-4611-8827), D'Alessandris, Quintino Giorgio (ORCID:0000-0002-2953-9291), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Larocca, Luigi Maria (ORCID:0000-0003-1739-4758), De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Tate, Courtney M., Mc Entire, Jacquelyn, Pallini, Roberto, Vakana, Eliza, Wyss, Lisa, Blosser, Wayne, Ricci-Vitiani, Lucia, D'Alessandris, Quintino Giorgio, Morgante, Liliana, Giannetti, Stefano, Larocca, Luigi Maria, Todaro, Matilde, Benfante, Antonina, Colorito, Maria Luisa, Stassi, Giorgio, De Maria Marchiano, Ruggero, Rowlinson, Scott, Stancato, Louis, Pallini, Roberto (ORCID:0000-0002-4611-8827), D'Alessandris, Quintino Giorgio (ORCID:0000-0002-2953-9291), Giannetti, Stefano (ORCID:0000-0002-9456-8865), Larocca, Luigi Maria (ORCID:0000-0003-1739-4758), and De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583)

Abstract

Bone morphogenetic proteins (BMPs), members of the TGF-Î2 superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating a direct effect on endothelial cell function. BMP7v activated the canonical SMAD signaling pathway in endothelial cells but targeted gene knockdown using shRNA directed against SMAD4 suggests this pathway is not required to mediate the anti-angiogenic effect. In contrast to SMAD activation, BMP7v selectively decreased ERK and AKT activation, significantly decreased endothelial cell migration and down-regulated expression of critical RTKs involved in VEGF and FGF angiogenic signaling, VEGFR2 and FGFR1 respectively. Importantly, in an in vivo angiogenic plug assay that serves as a measurement of angiogenesis, BMP7v significantly decreased hemoglobin content indicating inhibition of neoangiogenesis. In addition, BMP7v significantly decreased angiogenesis in glioblastoma stem-like cell (GSLC) Matrigel plugs and significantly impaired in vivo growth of a GSLC xenograft with a concomitant reduction in microvessel density. These data support BMP7v as a potent anti-angiogenic molecule that is effective in the context of tumor angiogenesis.

Published
2015

25. Abstract LB-143: DNp63 governs metastatic outgrowth of breast cancer stem cells

Author

Turdo, Alice, primary, Di Franco, Simone, additional, Benfante, Antonina, additional, Colorito, Maria Luisa, additional, Bonanno, Marco, additional, Gaggianesi, Miriam, additional, Barcaroli, Daniela, additional, Dieli, Francesco, additional, Medema, Jan Paul, additional, De Laurenzi, Vincenzo, additional, Stassi, Giorgio, additional, and Todaro, Matilde, additional

Published
2015
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26. ErbB-3 activation by NRG-1β sustains growth and promotes vemurafenib resistance in BRAF-V600E colon cancer stem cells (CSCs)

Author

Prasetyanti, Pramudita R., primary, Capone, Emily, additional, Barcaroli, Daniela, additional, D’Agostino, Daniela, additional, Volpe, Silvia, additional, Benfante, Antonina, additional, van Hooff, Sander, additional, Iacobelli, Valentina, additional, Rossi, Cosmo, additional, Iacobelli, Stefano, additional, Medema, Jan Paul, additional, De Laurenzi, Vincenzo, additional, and Sala, Gianluca, additional

Published
2015
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27. Cancer Stem Cells Sensitivity Assay (STELLA) in Patients with Advanced Lung and Colorectal Cancer: A Feasibility Study

Author

D’Arcangelo, Manolo, primary, Todaro, Matilde, additional, Salvini, Jessica, additional, Benfante, Antonina, additional, Colorito, Maria Luisa, additional, D’Incecco, Armida, additional, Landi, Lorenza, additional, Apuzzo, Tiziana, additional, Rossi, Elisa, additional, Sani, Spartaco, additional, Stassi, Giorgio, additional, and Cappuzzo, Federico, additional

Published
2015
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28. A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

Author

Tate, Courtney M., primary, Mc Entire, Jacquelyn, additional, Pallini, Roberto, additional, Vakana, Eliza, additional, Wyss, Lisa, additional, Blosser, Wayne, additional, Ricci-Vitiani, Lucia, additional, D’Alessandris, Quintino Giorgio, additional, Morgante, Liliana, additional, Giannetti, Stefano, additional, Maria Larocca, Luigi, additional, Todaro, Matilde, additional, Benfante, Antonina, additional, Colorito, Maria Luisa, additional, Stassi, Giorgio, additional, De Maria, Ruggero, additional, Rowlinson, Scott, additional, and Stancato, Louis, additional

Published
2015
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29. CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis

Author

Todaro, Matilde, Gaggianesi, Miriam, Catalano, Veronica, Benfante, Antonina, Iovino, Flora, Biffoni, Mauro, Apuzzo, Tiziana, Sperduti, Isabella, Volpe, Silvia, Cocorullo, Gianfranco, Gulotta, Gaspare, Dieli, Francesco, De Maria Marchiano, Ruggero, Stassi, Giorgio, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Todaro, Matilde, Gaggianesi, Miriam, Catalano, Veronica, Benfante, Antonina, Iovino, Flora, Biffoni, Mauro, Apuzzo, Tiziana, Sperduti, Isabella, Volpe, Silvia, Cocorullo, Gianfranco, Gulotta, Gaspare, Dieli, Francesco, De Maria Marchiano, Ruggero, Stassi, Giorgio, and De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583)

Abstract

Cancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/Î2-catenin pathway, which promotes migration and metastasis. CD44v6- progenitor cells do not give rise to metastatic lesions but, when treated with cytokines, acquire CD44v6 expression and metastatic capacity. Importantly, phosphatidylinositol 3-kinase (PI3K) inhibition selectively killed CD44v6 CR-CSCs and reduced metastatic growth. In patient cohorts, low levels of CD44v6 predict increased probability of survival. Thus, the metastatic process in colorectal cancer is initiated by CSCs through the expression of CD44v6, which is both a functional biomarker and therapeutic target. © 2014 Elsevier Inc.

Published
2014

30. Lipid Droplets: A New Player in Colorectal Cancer Stem Cells Unveiled by Spectroscopic Imaging

Author

Tirinato, Luca, primary, Liberale, Carlo, additional, Di Franco, Simone, additional, Candeloro, Patrizio, additional, Benfante, Antonina, additional, La Rocca, Rosanna, additional, Potze, Lisette, additional, Marotta, Roberto, additional, Ruffilli, Roberta, additional, Rajamanickam, Vijayakumar P., additional, Malerba, Mario, additional, De Angelis, Francesco, additional, Falqui, Andrea, additional, Carbone, Ennio, additional, Todaro, Matilde, additional, Medema, Jan Paul, additional, Stassi, Giorgio, additional, and Di Fabrizio, Enzo, additional

Published
2014
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32. CD44v6 Is a Marker of Constitutive and Reprogrammed Cancer Stem Cells Driving Colon Cancer Metastasis

Author

Todaro, Matilde, primary, Gaggianesi, Miriam, additional, Catalano, Veronica, additional, Benfante, Antonina, additional, Iovino, Flora, additional, Biffoni, Mauro, additional, Apuzzo, Tiziana, additional, Sperduti, Isabella, additional, Volpe, Silvia, additional, Cocorullo, Gianfranco, additional, Gulotta, Gaspare, additional, Dieli, Francesco, additional, De Maria, Ruggero, additional, and Stassi, Giorgio, additional

Published
2014
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33. Abstract B5: A BMP7 variant inhibits angiogenesis in vitro and in vivo in part by downregulating VEGFR2 and FGFR1 expression in endothelial cells.

Author

Tate, Courtney, primary, McEntire, Jacquelyn, additional, Pallini, Roberto, additional, Wyss, Lisa, additional, Blosser, Wayne, additional, Vakana, Eliza, additional, D'Alessandris, Giorgio, additional, Morgante, Liliana, additional, Giannetti, Stefano, additional, Larocca, Luigi, additional, Stassi, Giorgio, additional, Benfante, Antonina, additional, Colorito, Maria, additional, De Maria, Ruggero, additional, Rowlinson, Scott, additional, and Stancato, Louis, additional

Published
2013
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34. Stem Cells and Colon Cancer

Author

Di Franco, Simone, primary, Benfante, Antonina, additional, Iovino, Flora, additional, Bonventre, Sebastiano, additional, Dieli, Francesco, additional, Stassi, Giorgio, additional, and Todaro, Matilde, additional

Published
2012
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36. Lipid Droplets: A New Player in Colorectal Cancer Stem Cells Unveiled by Spectroscopic Imaging.

Author

Tirinato, Luca, Liberale, Carlo, Di Franco, Simone, Candeloro, Patrizio, Benfante, Antonina, La Rocca, Rosanna, Potze, Lisette, Marotta, Roberto, Ruffilli, Roberta, Rajamanickam, Vijayakumar P., Malerba, Mario, De Angelis, Francesco, Falqui, Andrea, Carbone, Ennio, Todaro, Matilde, Medema, Jan Paul, Stassi, Giorgio, and Di Fabrizio, Enzo

Subjects
COLON cancer, CANCER cells, DIAGNOSTIC imaging, DISEASE relapse, RAMAN spectroscopy, XENOTRANSPLANTATION
Abstract

The cancer stem cell (CSC) model is describing tumors as a hierarchical organized system and CSCs are suggested to be responsible for cancer recurrence after therapy. The identification of specific markers of CSCs is therefore of paramount importance. Here, we show that high levels of lipid droplets (LDs) are a distinctive mark of CSCs in colorectal (CR) cancer. This increased lipid content was clearly revealed by label-free Raman spectroscopy and it directly correlates with well-accepted CR-CSC markers as CD133 and Wnt pathway activity. By xenotransplantation experiments, we have finally demonstrated that CR-CSCs overexpressing LDs retain most tumorigenic potential. A relevant conceptual advance in this work is the demonstration that a cellular organelle, the LD, is a signature of CSCs, in addition to molecular markers. A further functional characterization of LDs could lead soon to design new target therapies against CR-CSCs. S tem C ells 2015;33:35-44 [ABSTRACT FROM AUTHOR]

Published
2015
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37. Activated Thyroid Hormone Promotes Differentiation and Chemotherapeutic Sensitization of Colorectal Cancer Stem Cells by Regulating Wnt and BMP4 Signaling

Author

Raffaele Ambrosio, Cristina Luongo, Matilde Todaro, Domenico Salvatore, R. Carollo, Antonina Benfante, Giorgio Stassi, Veronica Catalano, Monica Dentice, Catalano, Veronica, Dentice, Monica, Ambrosio, Raffaele, Luongo, Cristina, Carollo, Rosachiara, Benfante, Antonina, Todaro, Matilde, Stassi, Giorgio, Salvatore, Domenico, Catalano, V., Dentice, M., Ambrosio, R., Luongo, C., Carollo, R., Benfante, A., Todaro, M., Stassi, G., and Salvatore, D.

Subjects
Male, 0301 basic medicine, Thyroid Hormones, endocrine system, Cancer Research, medicine.medical_specialty, endocrine system diseases, Cellular differentiation, Deiodinase, Bone Morphogenetic Protein 4, Colorectal Neoplasm, Mice, 03 medical and health sciences, Cancer stem cell, Cell Line, Tumor, Internal medicine, medicine, Animals, Humans, Thyroid Hormone, Wnt Signaling Pathway, Hormone activity, Thyroid hormone receptor, biology, Animal, Thyroid, Wnt signaling pathway, Cell Differentiation, Middle Aged, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, Oncology, Neoplastic Stem Cells, Cancer research, biology.protein, Neoplastic Stem Cell, Colorectal Neoplasms, Human, Signal Transduction, Hormone
Abstract

Thyroid hormone is a pleiotropic factor that controls many cellular processes in multiple cell types such as cancer stem cells (CSC). Thyroid hormone concentrations in the blood are stable, but the action of the deiodinases (D2–D3) provides cell-specific regulation of thyroid hormone activity. Deregulation of deiodinase function and thyroid hormone status has been implicated in tumorigenesis. Therefore, we investigated the role of thyroid hormone metabolism and signaling in colorectal CSCs (CR-CSC), where deiodinases control cell division and chemosensitivity. We found that increased intracellular thyroid hormone concentration through D3 depletion induced cell differentiation and sharply mitigated tumor formation. Upregulated BMP4 expression and concomitantly attenuated Wnt signaling accompanied these effects. Furthermore, we demonstrate that BMP4 is a direct thyroid hormone target and is involved in a positive autoregulatory feedback loop that modulates thyroid hormone signaling. Collectively, our findings highlight a cell-autonomous metabolic mechanism by which CR-CSCs exploit thyroid hormone signaling to facilitate their self-renewal potential and suggest that drug-induced cell differentiation may represent a promising therapy for preventing CSC expansion and tumor progression. Cancer Res; 76(5); 1237–44. ©2015 AACR.

Published
2016
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38. ΔNp63 drives metastasis in breast cancer cells via PI3K/CD44v6 axis.

Author

Di Franco S, Turdo A, Benfante A, Colorito ML, Gaggianesi M, Apuzzo T, Kandimalla R, Chinnici A, Barcaroli D, Mangiapane LR, Pistone G, Vieni S, Gulotta E, Dieli F, Medema JP, Stassi G, De Laurenzi V, and Todaro M

Subjects
Aged, Aged, 80 and over, Animals, Breast Neoplasms genetics, Drug Resistance, Neoplasm, Epithelial-Mesenchymal Transition, Female, Humans, Mice, Middle Aged, Neoplasm Metastasis, Proto-Oncogene Proteins c-akt physiology, Signal Transduction physiology, Tumor Microenvironment, Breast Neoplasms pathology, Hyaluronan Receptors physiology, Membrane Proteins physiology, Phosphatidylinositol 3-Kinases physiology
Abstract

P63 is a transcription factor belonging to the family of p53, essential for the development and differentiation of epithelia. In recent years, it has become clear that altered expression of the different isoforms of this gene can play an important role in carcinogenesis. The p63 gene encodes for two main isoforms known as TA and ΔN p63 with different functions. The role of these different isoforms in sustaining tumor progression and metastatic spreading however has not entirely been clarified. Here we show that breast cancer initiating cells express ΔNp63 isoform that supports a more mesenchymal phenotype associated with a higher tumorigenic and metastatic potential. On the contrary, the majority of cells within the tumor appears to express predominantly TAp63 isoform. While ΔNp63 exerts its effects by regulating a PI3K/CD44v6 pathway, TAp63 modulates this pathway in an opposite fashion. As a result, tumorigenicity and invasive capacity of breast cancer cells is a balance of the two isoforms. Finally, we found that tumor microenvironmental cytokines significantly contribute to the establishment of breast cancer cell phenotype by positively regulating ΔNp63 and CD44v6 expression.

Published
2016
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39. Cancer Stem Cells Sensitivity Assay (STELLA) in Patients with Advanced Lung and Colorectal Cancer: A Feasibility Study.

Author

D'Arcangelo M, Todaro M, Salvini J, Benfante A, Colorito ML, D'Incecco A, Landi L, Apuzzo T, Rossi E, Sani S, Stassi G, and Cappuzzo F

Subjects
Aged, Aged, 80 and over, Colorectal Neoplasms pathology, Drug Combinations, Feasibility Studies, Female, Humans, Liver Neoplasms pathology, Lung Neoplasms pathology, Lymphatic Metastasis pathology, Male, Middle Aged, Neoplastic Stem Cells pathology, Pleural Effusion pathology, Time Factors, Antineoplastic Agents pharmacology, Cell Separation methods, Drug Screening Assays, Antitumor methods, Neoplastic Stem Cells drug effects
Abstract

Background: Cancer stem cells represent a population of immature tumor cells found in most solid tumors. Their peculiar features make them ideal models for studying drug resistance and sensitivity. In this study, we investigated whether cancer stem cells isolation and in vitro sensitivity assay are feasible in a clinical setting., Methods: Cancer stem cells were isolated from effusions or fresh cancer tissue of 23 patients who progressed after standard therapy failure. Specific culture conditions selected for immature tumor cells that express markers of stemness. These cells were exposed in vitro to chemotherapeutic and targeted agents., Results: Cancer stem cells were extracted from liver metastases in 6 cases (25%), lung nodules in 2 (8%), lymph node metastases in 3 (12.5%) and pleural/peritoneal/pericardial effusion in 13 (54%). Cancer stem cells were successfully isolated in 15 patients (63%), including 14 with lung cancer (93.3%). A sensitivity assay was successfully performed in 7 patients (30.4%), with a median of 15 drugs/combinations tested (range 5-28) and a median time required for results of 51 days (range 37-95)., Conclusion: The approach used for the STELLA trial allowed isolation of cancer stem cells in a consistent proportion of patients. The low percentage of cases completing the full procedure and the long median time for obtaining results highlights the need for a more efficient procedure., Trial Registration: ClinalTrials.gov NCT01483001.

Published
2015
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