T-Lymphoblastoid Cell Line

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Guido Antonelli - One of the best experts on this subject based on the ideXlab platform.

  • The effects of prolonged treatment with zidovudine, lamivudine, and abacavir on a T-Lymphoblastoid Cell Line.
    AIDS research and human retroviruses, 2006
    Co-Authors: Ombretta Turriziani, P. Pagnotti, Alessandra Pierangeli, Federico Focher, Cinzia Baranello, Francesca Bellomi, Francesca Falasca, Jessica A. Morgan, John D. Schuetz, Guido Antonelli
    Abstract:

    A human T-Lymphoblastoid Cell Line that is resistant to the antiviral activity of zidovudine (ZDV) and moderately resistant to lamivudine (3TC) has been obtained as a result of prolonged treatment with a combination of three nucleoside analogues (NA), ZDV, 3TC, and abacavir (ABV). These Cells, called CEMZLA, are fully sensitive to ABV. The Cellular resistance of the CEMZLA Cells to ZDV correlates with significant reductions in thymidine kinase (TK) activity and in the amount of intraCellular TK protein. Interestingly, the reduction in TK activity led to impairment of the ability of CEMZLA to accumulate the triphosphate metabolite of ZDV. However, the moderately 3TC-resistant phenotype of CEMZLA cannot be ascribed to a similar reduction in deoxycytidine kinase activity. Compared to the parental CEM Cells, CEMZLA Cells express a high level of multidrug resistance protein 4 (MRP4), which could reduce the intraCellular concentration of 3TC. This study shows that the exposure of Cells to a combination of NAs i...

  • Impaired 2′,3′-dideoxy-3′-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11
    Biochemical Journal, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, John D. Schuetz, Carolina Scagnolari, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, Guido Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Selection of a T-Cell Line resistant to stavudine and zidovudine by prolonged treatment with stavudine.
    Antiviral therapy, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, Francesca Bellomi, Carolina Scagnolari, F. Bambacioni, Massimo Gentile, Guido Antonelli
    Abstract:

    It has been demonstrated that prolonged treatment with nucleoside analogues, such as 3'-azido-3'-deoxythymidine (zidovudine), 2',3'-dideoxycytidine (zalcitabine) and 9-(2-phosphonylmethoxyethyl) adenine (PMEA), may cause selection of Cells that are resistant to their anti-HIV activity. A human T-Lymphoblastoid Cell Line that is resistant to the antiviral and cytotoxic activity of 2',3'-didehydro-3'-deoxythymidine (stavudine) has developed as a result of prolonged treatment. These Cells, called CEMstavudine, are also less sensitive to zidovudine. The Cellular/pharmacological resistance acquired by the CEMstavudine Cells is relatively low and appears to correlate with a reduction in thymidine kinase (TK) activity, rather than with a decreased expression of TK mRNA.

Ombretta Turriziani - One of the best experts on this subject based on the ideXlab platform.

  • The effects of prolonged treatment with zidovudine, lamivudine, and abacavir on a T-Lymphoblastoid Cell Line.
    AIDS research and human retroviruses, 2006
    Co-Authors: Ombretta Turriziani, P. Pagnotti, Alessandra Pierangeli, Federico Focher, Cinzia Baranello, Francesca Bellomi, Francesca Falasca, Jessica A. Morgan, John D. Schuetz, Guido Antonelli
    Abstract:

    A human T-Lymphoblastoid Cell Line that is resistant to the antiviral activity of zidovudine (ZDV) and moderately resistant to lamivudine (3TC) has been obtained as a result of prolonged treatment with a combination of three nucleoside analogues (NA), ZDV, 3TC, and abacavir (ABV). These Cells, called CEMZLA, are fully sensitive to ABV. The Cellular resistance of the CEMZLA Cells to ZDV correlates with significant reductions in thymidine kinase (TK) activity and in the amount of intraCellular TK protein. Interestingly, the reduction in TK activity led to impairment of the ability of CEMZLA to accumulate the triphosphate metabolite of ZDV. However, the moderately 3TC-resistant phenotype of CEMZLA cannot be ascribed to a similar reduction in deoxycytidine kinase activity. Compared to the parental CEM Cells, CEMZLA Cells express a high level of multidrug resistance protein 4 (MRP4), which could reduce the intraCellular concentration of 3TC. This study shows that the exposure of Cells to a combination of NAs i...

  • Impaired 2′,3′-dideoxy-3′-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11
    Biochemical Journal, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, John D. Schuetz, Carolina Scagnolari, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, Guido Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Selection of a T-Cell Line resistant to stavudine and zidovudine by prolonged treatment with stavudine.
    Antiviral therapy, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, Francesca Bellomi, Carolina Scagnolari, F. Bambacioni, Massimo Gentile, Guido Antonelli
    Abstract:

    It has been demonstrated that prolonged treatment with nucleoside analogues, such as 3'-azido-3'-deoxythymidine (zidovudine), 2',3'-dideoxycytidine (zalcitabine) and 9-(2-phosphonylmethoxyethyl) adenine (PMEA), may cause selection of Cells that are resistant to their anti-HIV activity. A human T-Lymphoblastoid Cell Line that is resistant to the antiviral and cytotoxic activity of 2',3'-didehydro-3'-deoxythymidine (stavudine) has developed as a result of prolonged treatment. These Cells, called CEMstavudine, are also less sensitive to zidovudine. The Cellular/pharmacological resistance acquired by the CEMstavudine Cells is relatively low and appears to correlate with a reduction in thymidine kinase (TK) activity, rather than with a decreased expression of TK mRNA.

Federico Focher - One of the best experts on this subject based on the ideXlab platform.

  • The effects of prolonged treatment with zidovudine, lamivudine, and abacavir on a T-Lymphoblastoid Cell Line.
    AIDS research and human retroviruses, 2006
    Co-Authors: Ombretta Turriziani, P. Pagnotti, Alessandra Pierangeli, Federico Focher, Cinzia Baranello, Francesca Bellomi, Francesca Falasca, Jessica A. Morgan, John D. Schuetz, Guido Antonelli
    Abstract:

    A human T-Lymphoblastoid Cell Line that is resistant to the antiviral activity of zidovudine (ZDV) and moderately resistant to lamivudine (3TC) has been obtained as a result of prolonged treatment with a combination of three nucleoside analogues (NA), ZDV, 3TC, and abacavir (ABV). These Cells, called CEMZLA, are fully sensitive to ABV. The Cellular resistance of the CEMZLA Cells to ZDV correlates with significant reductions in thymidine kinase (TK) activity and in the amount of intraCellular TK protein. Interestingly, the reduction in TK activity led to impairment of the ability of CEMZLA to accumulate the triphosphate metabolite of ZDV. However, the moderately 3TC-resistant phenotype of CEMZLA cannot be ascribed to a similar reduction in deoxycytidine kinase activity. Compared to the parental CEM Cells, CEMZLA Cells express a high level of multidrug resistance protein 4 (MRP4), which could reduce the intraCellular concentration of 3TC. This study shows that the exposure of Cells to a combination of NAs i...

  • Impaired 2′,3′-dideoxy-3′-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11
    Biochemical Journal, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, John D. Schuetz, Carolina Scagnolari, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, Guido Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Selection of a T-Cell Line resistant to stavudine and zidovudine by prolonged treatment with stavudine.
    Antiviral therapy, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, Francesca Bellomi, Carolina Scagnolari, F. Bambacioni, Massimo Gentile, Guido Antonelli
    Abstract:

    It has been demonstrated that prolonged treatment with nucleoside analogues, such as 3'-azido-3'-deoxythymidine (zidovudine), 2',3'-dideoxycytidine (zalcitabine) and 9-(2-phosphonylmethoxyethyl) adenine (PMEA), may cause selection of Cells that are resistant to their anti-HIV activity. A human T-Lymphoblastoid Cell Line that is resistant to the antiviral and cytotoxic activity of 2',3'-didehydro-3'-deoxythymidine (stavudine) has developed as a result of prolonged treatment. These Cells, called CEMstavudine, are also less sensitive to zidovudine. The Cellular/pharmacological resistance acquired by the CEMstavudine Cells is relatively low and appears to correlate with a reduction in thymidine kinase (TK) activity, rather than with a decreased expression of TK mRNA.

F. Bambacioni - One of the best experts on this subject based on the ideXlab platform.

  • Impaired 2',3'-dideoxy-3'-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11.
    The Biochemical journal, 2002
    Co-Authors: O Turriziani, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, J D Schuetz, F Focher, C Scagnolari, G Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Impaired 2′,3′-dideoxy-3′-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11
    Biochemical Journal, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, John D. Schuetz, Carolina Scagnolari, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, Guido Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Selection of a T-Cell Line resistant to stavudine and zidovudine by prolonged treatment with stavudine.
    Antiviral therapy, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, Francesca Bellomi, Carolina Scagnolari, F. Bambacioni, Massimo Gentile, Guido Antonelli
    Abstract:

    It has been demonstrated that prolonged treatment with nucleoside analogues, such as 3'-azido-3'-deoxythymidine (zidovudine), 2',3'-dideoxycytidine (zalcitabine) and 9-(2-phosphonylmethoxyethyl) adenine (PMEA), may cause selection of Cells that are resistant to their anti-HIV activity. A human T-Lymphoblastoid Cell Line that is resistant to the antiviral and cytotoxic activity of 2',3'-didehydro-3'-deoxythymidine (stavudine) has developed as a result of prolonged treatment. These Cells, called CEMstavudine, are also less sensitive to zidovudine. The Cellular/pharmacological resistance acquired by the CEMstavudine Cells is relatively low and appears to correlate with a reduction in thymidine kinase (TK) activity, rather than with a decreased expression of TK mRNA.

Carolina Scagnolari - One of the best experts on this subject based on the ideXlab platform.

  • Impaired 2′,3′-dideoxy-3′-thiacytidine accumulation in T-Lymphoblastoid Cells as a mechanism of acquired resistance independent of multidrug resistant protein 4 with a possible role for ATP-binding cassette C11
    Biochemical Journal, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, John D. Schuetz, Carolina Scagnolari, F. Bambacioni, Janardhan Sampath, Masashi Adachi, Elisabetta Riva, Guido Antonelli
    Abstract:

    Cellular factors may contribute to the decreased efficacy of chemotherapy in HIV infection. Indeed, prolonged treatment with nucleoside analogues, such as azidothymidine (AZT), 2',3'-deoxycytidine or 9-(2-phosphonylmethoxyethyl)adenine, induces Cellular resistance. We have developed a human T lymphoblastoid Cell Line (CEM 3TC) that is selectively resistant to the antiproliferative effect of 2',3'-dideoxy-3'-thiacytidine (3TC) because the CEM 3TC Cells were equally sensitive to AZT, as well as the antimitotic agent, vinblastine. The anti-retroviral activity of 3TC against HIV-1 was also severely impaired in the CEM 3TC Cells. Despite similar deoxycytidine kinase activity and unchanged uptake of nucleosides such as AZT and 2'-deoxycytidine, CEM 3TC had profoundly impaired 3TC accumulation. Further studies indicated that CEM 3TC retained much less 3TC. However, despite a small overexpression of multidrug resistance protein (MRP) 4, additional studies with Cells specifically engineered to overexpress MRP4 demonstrated there was no impact on either 3TC accumulation or efflux. Finally, an increased expression of the MRP5 homologue, ATP-binding cassette C11 (ABCC11) was observed in the CEM 3TC Cells. We speculate that the decreased 3TC accumulation in the CEM 3TC might be due to the upregulation of ABCC11.

  • Selection of a T-Cell Line resistant to stavudine and zidovudine by prolonged treatment with stavudine.
    Antiviral therapy, 2002
    Co-Authors: Ombretta Turriziani, Federico Focher, Francesca Bellomi, Carolina Scagnolari, F. Bambacioni, Massimo Gentile, Guido Antonelli
    Abstract:

    It has been demonstrated that prolonged treatment with nucleoside analogues, such as 3'-azido-3'-deoxythymidine (zidovudine), 2',3'-dideoxycytidine (zalcitabine) and 9-(2-phosphonylmethoxyethyl) adenine (PMEA), may cause selection of Cells that are resistant to their anti-HIV activity. A human T-Lymphoblastoid Cell Line that is resistant to the antiviral and cytotoxic activity of 2',3'-didehydro-3'-deoxythymidine (stavudine) has developed as a result of prolonged treatment. These Cells, called CEMstavudine, are also less sensitive to zidovudine. The Cellular/pharmacological resistance acquired by the CEMstavudine Cells is relatively low and appears to correlate with a reduction in thymidine kinase (TK) activity, rather than with a decreased expression of TK mRNA.