12 results on '"Zapparelli, G"'
Search Results
2. Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer
- Author
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Zeuner, A., Francescangeli, F., Contavalli, P., Zapparelli, G., Apuzzo, T., Eramo, A., Baiocchi, M., De Angelis, M. L., Biffoni, M., Sette, G., Todaro, M., Stassi, G., De Maria Marchiano, R., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Zeuner, A., Francescangeli, F., Contavalli, P., Zapparelli, G., Apuzzo, T., Eramo, A., Baiocchi, M., De Angelis, M. L., Biffoni, M., Sette, G., Todaro, M., Stassi, G., De Maria Marchiano, R., and De Maria Marchiano, R. (ORCID:0000-0003-2255-0583)
- Abstract
Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL. In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC.
- Published
- 2014
3. Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer
- Author
-
Zeuner, A, Francescangeli, F, Contavalli, Paola, Zapparelli, G, Apuzzo, T, Eramo, A, Baiocchi, M, De Angelis, M. L, Biffoni, M, Sette, G, Todaro, M, Stassi, G, De Maria Marchiano, Ruggero, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Zeuner, A, Francescangeli, F, Contavalli, Paola, Zapparelli, G, Apuzzo, T, Eramo, A, Baiocchi, M, De Angelis, M. L, Biffoni, M, Sette, G, Todaro, M, Stassi, G, De Maria Marchiano, Ruggero, and De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583)
- Abstract
Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL. In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC.
- Published
- 2014
4. Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer.
- Author
-
Zeuner, A, Francescangeli, F, Contavalli, P, Zapparelli, G, Apuzzo, T, Eramo, A, Baiocchi, M, De Angelis, M L, Biffoni, M, Sette, G, Todaro, M, Stassi, G, and De Maria, R
- Subjects
CANCER stem cells ,BCL genes ,LUNG cancer & genetics ,NEOPLASTIC cell transformation ,CANCER chemotherapy - Abstract
Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-X
L is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL . In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC. [ABSTRACT FROM AUTHOR]- Published
- 2014
- Full Text
- View/download PDF
5. MSR45 Evaluation of the Future Impact of Immuno-Oncology Introduction on Cancer Mortality in Italy.
- Author
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Fiorentino, F., Mezzanotte, C., Patanè, G., Zapparelli, G., and Urbinati, D.
- Subjects
- *
CANCER-related mortality - Published
- 2023
- Full Text
- View/download PDF
6. Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer
- Author
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Matilde Todaro, Federica Francescangeli, M L De Angelis, Giovanni Sette, R De Maria, Giorgio Stassi, Tiziana Apuzzo, G Zapparelli, Paola Contavalli, Adriana Eramo, Ann Zeuner, Mauro Biffoni, Marta Baiocchi, Zeuner, A., Francescangeli, F., Contavalli, P., Zapparelli, G., Apuzzo, T., Eramo, A., Baiocchi, M., De Angelis, M., Biffoni, M., Sette, G., Todaro, M., Stassi, G., and De Maria, R.
- Subjects
Lung Neoplasms ,Mice, SCID ,Pharmacology ,Piperazines ,Antineoplastic Agent ,Nitrophenols ,Mice ,Mice, Inbred NOD ,Carcinoma, Non-Small-Cell Lung ,Cytotoxic T cell ,Non-Small-Cell Lung ,education.field_of_study ,Sulfonamides ,Tumor ,Animals ,Antineoplastic Agents ,Biphenyl Compounds ,Cell Line, Tumor ,Cell Proliferation ,Cell Survival ,Female ,Humans ,Neoplastic Stem Cells ,Tumor Burden ,Xenograft Model Antitumor Assays ,bcl-X Protein ,Molecular Biology ,Cell Biology ,Stem cell ,Human ,medicine.drug ,Xenograft Model Antitumor Assay ,Population ,Biology ,SCID ,Sulfonamide ,Cell Line ,Cancer stem cell ,medicine ,education ,Lung cancer ,Piperazine ,Settore MED/04 - Patologia Generale ,Original Paper ,Nitrophenol ,Animal ,Cell growth ,Carcinoma ,medicine.disease ,Gemcitabine ,Lung Neoplasm ,Cell culture ,Biphenyl Compound ,Cancer research ,Inbred NOD ,Neoplastic Stem Cell - Abstract
Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL. In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC.
- Published
- 2014
7. Prevention of chemotherapy-induced anemia and thrombocytopenia by constant administration of stem cell factor
- Author
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Matilde Todaro, Rosanna Dattilo, Giuseppina Zapparelli, Daniela Martinetti, Ann Zeuner, Ruggero De Maria, Mauro Biffoni, Monica Bartucci, Antonio Di Virgilio, Bartucci, M, Dattilo, R, Martineti, D, Todaro, M, Zapparelli, G, Di Virgilio, A, Biffoni, M, De Maria, R, and Zeuner, A
- Subjects
Cancer Research ,Anemia ,medicine.medical_treatment ,SCF, Bcl-2/Bcl-XL–positive ,Stem cell factor ,Antineoplastic Agents ,Bone Marrow Cells ,Inbred C57BL ,Drug Administration Schedule ,Mice ,Settore MED/04 - PATOLOGIA GENERALE ,medicine ,Animals ,Cisplatin ,Erythroid Precursor Cells ,Chemotherapy ,Stem Cell Factor ,business.industry ,medicine.disease ,Female ,Megakaryocytes ,Mice, Inbred C57BL ,Thrombocytopenia ,Oncology ,Haematopoiesis ,Cytokine ,medicine.anatomical_structure ,Erythropoietin ,Immunology ,Cancer research ,Bone marrow ,business ,medicine.drug - Abstract
Purpose: Chemotherapy-induced apoptosis of immature hematopoietic cells is a major cause of anemia and thrombocytopenia in cancer patients. Although hematopoietic growth factors such as erythropoietin and colony-stimulating factors cannot prevent the occurrence of drug-induced myelosuppression, stem cell factor (SCF) has been previously shown to protect immature erythroid and megakaryocytic cells in vitro from drug-induced apoptosis. However, the effect of SCF in vivo as a single myeloprotective agent has never been elucidated. Experimental Design: The ability of SCF to prevent the occurrence of chemotherapy-induced anemia and thrombocytopenia was tested in a mouse model of cisplatin-induced myelosuppression. To highlight the importance of maintaining a continuous antiapoptotic signal in immature hematopoietic cells, we compared two treatment schedules: in the first schedule, SCF administration was interrupted during chemotherapy treatment and resumed thereafter, whereas in the second schedule, SCF was administered without interruption for 7 days, including the day of chemotherapy treatment. Results: The administration of SCF to cisplatin-treated mice could preserve bone marrow integrity, inhibit apoptosis of erythroid and megakaryocytic precursors, prevent chemotherapy-induced anemia, and rapidly restore normal platelet production. Treatment with SCF increased the frequency of Bcl-2/Bcl-XL–positive bone marrow erythroid cells and sustained Akt activation in megakaryocytes. Myeloprotection was observed only when SCF was administered concomitantly with cisplatin and kept constantly present during the days following chemotherapy treatment. Conclusions: SCF treatment can prevent the occurrence of chemotherapy-induced anemia and thrombocytopenia in mice, indicating a potential use of this cytokine in the supportive therapy of cancer patients. Clin Cancer Res; 17(19); 6185–91. ©2011 AACR.
- Published
- 2011
8. Regolazione del prezzo e rimborso dei farmaci: comparatori, endpoint e ruolo della costo-efficacia.
- Author
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Jommi C, Apolone G, Scroccaro G, Acciai V, Addis A, Ardizzoni A, Bernardini R, Bortolami A, Brigido A, Buzzetti G, Canonico PL, Caprari F, Centanni S, Cernetti C, Cicchetti A, Corsico G, Damele F, de Braud F, Manurita S, Mennini FS, Olivi I, Parretta F, Pippo L, Pulimeno S, Riccaboni M, Rossi G, Saleri C, Sinibaldi A, Spandonaro F, Stefenoni C, Visentin E, Viale P, Zapparelli G, and Popoli P
- Abstract
Competing Interests: Conflict of interest: The authors declare no potential conflict of interest with respect to the research, authorship and/or publication of this article. The authors declare the following competing interests.
- Published
- 2022
- Full Text
- View/download PDF
9. Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer.
- Author
-
Zeuner A, Francescangeli F, Contavalli P, Zapparelli G, Apuzzo T, Eramo A, Baiocchi M, De Angelis ML, Biffoni M, Sette G, Todaro M, Stassi G, and De Maria R
- Subjects
- Animals, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung metabolism, Cell Line, Tumor, Cell Proliferation, Cell Survival drug effects, Female, Humans, Lung Neoplasms drug therapy, Lung Neoplasms metabolism, Mice, Inbred NOD, Mice, SCID, Neoplastic Stem Cells drug effects, Piperazines pharmacology, Tumor Burden, Xenograft Model Antitumor Assays, bcl-X Protein metabolism, Antineoplastic Agents pharmacology, Biphenyl Compounds pharmacology, Carcinoma, Non-Small-Cell Lung pathology, Lung Neoplasms pathology, Neoplastic Stem Cells physiology, Nitrophenols pharmacology, Sulfonamides pharmacology, bcl-X Protein antagonists & inhibitors
- Abstract
Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differently from gemcitabine, which preferentially eliminated proliferating LCSC, ABT-737 had an increased cytotoxic activity in vitro towards quiescent/slow-proliferating LCSC, which expressed high levels of Bcl-XL. In vivo, ABT-737 as a single agent was able to inhibit the growth of LCSC-derived xenografts and to reduce cancer stem cell content in treated tumors. Altogether, these results indicate that quiescent/slow-proliferating LCSC strongly depend on Bcl-XL for their survival and indicate Bcl-XL inhibition as a potential therapeutic avenue in NSCLC.
- Published
- 2014
- Full Text
- View/download PDF
10. Prevention of chemotherapy-induced anemia and thrombocytopenia by constant administration of stem cell factor.
- Author
-
Bartucci M, Dattilo R, Martinetti D, Todaro M, Zapparelli G, Di Virgilio A, Biffoni M, De Maria R, and Zeuner A
- Subjects
- Anemia chemically induced, Animals, Antineoplastic Agents adverse effects, Bone Marrow Cells drug effects, Drug Administration Schedule, Erythroid Precursor Cells drug effects, Female, Megakaryocytes drug effects, Mice, Mice, Inbred C57BL, Thrombocytopenia chemically induced, Anemia prevention & control, Cisplatin adverse effects, Stem Cell Factor administration & dosage, Thrombocytopenia prevention & control
- Abstract
Purpose: Chemotherapy-induced apoptosis of immature hematopoietic cells is a major cause of anemia and thrombocytopenia in cancer patients. Although hematopoietic growth factors such as erythropoietin and colony-stimulating factors cannot prevent the occurrence of drug-induced myelosuppression, stem cell factor (SCF) has been previously shown to protect immature erythroid and megakaryocytic cells in vitro from drug-induced apoptosis. However, the effect of SCF in vivo as a single myeloprotective agent has never been elucidated., Experimental Design: The ability of SCF to prevent the occurrence of chemotherapy-induced anemia and thrombocytopenia was tested in a mouse model of cisplatin-induced myelosuppression. To highlight the importance of maintaining a continuous antiapoptotic signal in immature hematopoietic cells, we compared two treatment schedules: in the first schedule, SCF administration was interrupted during chemotherapy treatment and resumed thereafter, whereas in the second schedule, SCF was administered without interruption for 7 days, including the day of chemotherapy treatment., Results: The administration of SCF to cisplatin-treated mice could preserve bone marrow integrity, inhibit apoptosis of erythroid and megakaryocytic precursors, prevent chemotherapy-induced anemia, and rapidly restore normal platelet production. Treatment with SCF increased the frequency of Bcl-2/Bcl-XL-positive bone marrow erythroid cells and sustained Akt activation in megakaryocytes. Myeloprotection was observed only when SCF was administered concomitantly with cisplatin and kept constantly present during the days following chemotherapy treatment., Conclusions: SCF treatment can prevent the occurrence of chemotherapy-induced anemia and thrombocytopenia in mice, indicating a potential use of this cytokine in the supportive therapy of cancer patients., (©2011 AACR)
- Published
- 2011
- Full Text
- View/download PDF
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