Reversible lymphomagenesis in conditionally c-MYC expressing mice
Apstrakt
It is well documented that deregulation of MYC leads to tumor development, yet many aspects of this process are only partially understood. We have established a transgenic mouse model in which c-MYC is conditionally expressed in lymphoid cells using the tetracycline-regulated system of gene regulation. Mice with continuously expressed transgenic c-MYC died of invasive T- or B-cell lymphomas within 4 months. Lymphomas developing in transgenic mice were c-MYC dependent since doxycycline treatment led to tumor regression. Using transplantation of established tumor cell lines labeled with GFP, we followed the fate of neoplastic cells in recipients upon MYC inactivation. This approach allowed us to elucidate both apoptosis and differentiation as mechanisms of tumor elimination. Comparative genomic hybridization (CGH) and FISH analyses were performed in order to analyze possible chromosomal aberrations induced by c-MYC. We observed that overexpression of c-MYC is sufficient to induce recurre...nt patterns of genomic instability. The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy.
Ključne reči:
MYC / lymphomas / genomic instabilityIzvor:
International Journal of Cancer, 2004, 110, 3, 336-342Izdavač:
- Wiley, Hoboken
DOI: 10.1002/ijc.20099
ISSN: 0020-7136
PubMed: 15095297
WoS: 000221374600004
Scopus: 2-s2.0-2442595901
Institucija/grupa
rFASPERTY - JOUR AU - Marinković, Dragan AU - Marinković, Tatjana AU - Mahr, B AU - Hess, J AU - Wirth, Thomas PY - 2004 UR - http://rfasper.fasper.bg.ac.rs/handle/123456789/35 AB - It is well documented that deregulation of MYC leads to tumor development, yet many aspects of this process are only partially understood. We have established a transgenic mouse model in which c-MYC is conditionally expressed in lymphoid cells using the tetracycline-regulated system of gene regulation. Mice with continuously expressed transgenic c-MYC died of invasive T- or B-cell lymphomas within 4 months. Lymphomas developing in transgenic mice were c-MYC dependent since doxycycline treatment led to tumor regression. Using transplantation of established tumor cell lines labeled with GFP, we followed the fate of neoplastic cells in recipients upon MYC inactivation. This approach allowed us to elucidate both apoptosis and differentiation as mechanisms of tumor elimination. Comparative genomic hybridization (CGH) and FISH analyses were performed in order to analyze possible chromosomal aberrations induced by c-MYC. We observed that overexpression of c-MYC is sufficient to induce recurrent patterns of genomic instability. The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy. PB - Wiley, Hoboken T2 - International Journal of Cancer T1 - Reversible lymphomagenesis in conditionally c-MYC expressing mice EP - 342 IS - 3 SP - 336 VL - 110 DO - 10.1002/ijc.20099 ER -
@article{ author = "Marinković, Dragan and Marinković, Tatjana and Mahr, B and Hess, J and Wirth, Thomas", year = "2004", abstract = "It is well documented that deregulation of MYC leads to tumor development, yet many aspects of this process are only partially understood. We have established a transgenic mouse model in which c-MYC is conditionally expressed in lymphoid cells using the tetracycline-regulated system of gene regulation. Mice with continuously expressed transgenic c-MYC died of invasive T- or B-cell lymphomas within 4 months. Lymphomas developing in transgenic mice were c-MYC dependent since doxycycline treatment led to tumor regression. Using transplantation of established tumor cell lines labeled with GFP, we followed the fate of neoplastic cells in recipients upon MYC inactivation. This approach allowed us to elucidate both apoptosis and differentiation as mechanisms of tumor elimination. Comparative genomic hybridization (CGH) and FISH analyses were performed in order to analyze possible chromosomal aberrations induced by c-MYC. We observed that overexpression of c-MYC is sufficient to induce recurrent patterns of genomic instability. The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy.", publisher = "Wiley, Hoboken", journal = "International Journal of Cancer", title = "Reversible lymphomagenesis in conditionally c-MYC expressing mice", pages = "342-336", number = "3", volume = "110", doi = "10.1002/ijc.20099" }
Marinković, D., Marinković, T., Mahr, B., Hess, J.,& Wirth, T.. (2004). Reversible lymphomagenesis in conditionally c-MYC expressing mice. in International Journal of Cancer Wiley, Hoboken., 110(3), 336-342. https://doi.org/10.1002/ijc.20099
Marinković D, Marinković T, Mahr B, Hess J, Wirth T. Reversible lymphomagenesis in conditionally c-MYC expressing mice. in International Journal of Cancer. 2004;110(3):336-342. doi:10.1002/ijc.20099 .
Marinković, Dragan, Marinković, Tatjana, Mahr, B, Hess, J, Wirth, Thomas, "Reversible lymphomagenesis in conditionally c-MYC expressing mice" in International Journal of Cancer, 110, no. 3 (2004):336-342, https://doi.org/10.1002/ijc.20099 . .